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https://oercommons.org/courseware/lesson/15489/overview	Inventors of the Age Overview By the end of this section, you will be able to: - Explain how the ideas and products of late nineteenth-century inventors contributed to the rise of big business - Explain how the inventions of the late nineteenth century changed everyday American life The late nineteenth century was an energetic era of inventions and entrepreneurial spirit. Building upon the mid-century Industrial Revolution in Great Britain, as well as answering the increasing call from Americans for efficiency and comfort, the country found itself in the grip of invention fever, with more people working on their big ideas than ever before. In retrospect, harnessing the power of steam and then electricity in the nineteenth century vastly increased the power of man and machine, thus making other advances possible as the century progressed. Facing an increasingly complex everyday life, Americans sought the means by which to cope with it. Inventions often provided the answers, even as the inventors themselves remained largely unaware of the life-changing nature of their ideas. To understand the scope of this zeal for creation, consider the U.S. Patent Office, which, in 1790—its first decade of existence—recorded only 276 inventions. By 1860, the office had issued a total of 60,000 patents. But between 1860 and 1890, that number exploded to nearly 450,000, with another 235,000 in the last decade of the century. While many of these patents came to naught, some inventions became lynchpins in the rise of big business and the country’s move towards an industrial-based economy, in which the desire for efficiency, comfort, and abundance could be more fully realized by most Americans. AN EXPLOSION OF INVENTIVE ENERGY From corrugated rollers that could crack hard, homestead-grown wheat into flour to refrigerated train cars and garment-sewing machines (Figure), new inventions fueled industrial growth around the country. As late as 1880, fully one-half of all Americans still lived and worked on farms, whereas fewer than one in seven—mostly men, except for long-established textile factories in which female employees tended to dominate—were employed in factories. However, the development of commercial electricity by the close of the century, to complement the steam engines that already existed in many larger factories, permitted more industries to concentrate in cities, away from the previously essential water power. In turn, newly arrived immigrants sought employment in new urban factories. Immigration, urbanization, and industrialization coincided to transform the face of American society from primarily rural to significantly urban. From 1880 to 1920, the number of industrial workers in the nation quadrupled from 2.5 million to over 10 million, while over the same period urban populations doubled, to reach one-half of the country’s total population. In offices, worker productivity benefited from the typewriter, invented in 1867, the cash register, invented in 1879, and the adding machine, invented in 1885. These tools made it easier than ever to keep up with the rapid pace of business growth. Inventions also slowly transformed home life. The vacuum cleaner arrived during this era, as well as the flush toilet. These indoor “water closets” improved public health through the reduction in contamination associated with outhouses and their proximity to water supplies and homes. Tin cans and, later, Clarence Birdseye’s experiments with frozen food, eventually changed how women shopped for, and prepared, food for their families, despite initial health concerns over preserved foods. With the advent of more easily prepared food, women gained valuable time in their daily schedules, a step that partially laid the groundwork for the modern women’s movement. Women who had the means to purchase such items could use their time to seek other employment outside of the home, as well as broaden their knowledge through education and reading. Such a transformation did not occur overnight, as these inventions also increased expectations for women to remain tied to the home and their domestic chores; slowly, the culture of domesticity changed. Perhaps the most important industrial advancement of the era came in the production of steel. Manufacturers and builders preferred steel to iron, due to its increased strength and durability. After the Civil War, two new processes allowed for the creation of furnaces large enough and hot enough to melt the wrought iron needed to produce large quantities of steel at increasingly cheaper prices. The Bessemer process, named for English inventor Henry Bessemer, and the open-hearth process, changed the way the United States produced steel and, in doing so, led the country into a new industrialized age. As the new material became more available, builders eagerly sought it out, a demand that steel mill owners were happy to supply. In 1860, the country produced thirteen thousand tons of steel. By 1879, American furnaces were producing over one million tons per year; by 1900, this figure had risen to ten million. Just ten years later, the United States was the top steel producer in the world, at over twenty-four million tons annually. As production increased to match the overwhelming demand, the price of steel dropped by over 80 percent. When quality steel became cheaper and more readily available, other industries relied upon it more heavily as a key to their growth and development, including construction and, later, the automotive industry. As a result, the steel industry rapidly became the cornerstone of the American economy, remaining the primary indicator of industrial growth and stability through the end of World War II. ALEXANDER GRAHAM BELL AND THE TELEPHONE Advancements in communications matched the pace of growth seen in industry and home life. Communication technologies were changing quickly, and they brought with them new ways for information to travel. In 1858, British and American crews laid the first transatlantic cable lines, enabling messages to pass between the United States and Europe in a matter of hours, rather than waiting the few weeks it could take for a letter to arrive by steamship. Although these initial cables worked for barely a month, they generated great interest in developing a more efficient telecommunications industry. Within twenty years, over 100,000 miles of cable crisscrossed the ocean floors, connecting all the continents. Domestically, Western Union, which controlled 80 percent of the country’s telegraph lines, operated nearly 200,000 miles of telegraph routes from coast to coast. In short, people were connected like never before, able to relay messages in minutes and hours rather than days and weeks. One of the greatest advancements was the telephone, which Alexander Graham Bell patented in 1876 (Figure). While he was not the first to invent the concept, Bell was the first one to capitalize on it; after securing the patent, he worked with financiers and businessmen to create the National Bell Telephone Company. Western Union, which had originally turned down Bell’s machine, went on to commission Thomas Edison to invent an improved version of the telephone. It is actually Edison’s version that is most like the modern telephone used today. However, Western Union, fearing a costly legal battle they were likely to lose due to Bell’s patent, ultimately sold Edison’s idea to the Bell Company. With the communications industry now largely in their control, along with an agreement from the federal government to permit such control, the Bell Company was transformed into the American Telephone and Telegraph Company, which still exists today as AT&T. By 1880, fifty thousand telephones were in use in the United States, including one at the White House. By 1900, that number had increased to 1.35 million, and hundreds of American cities had obtained local service for their citizens. Quickly and inexorably, technology was bringing the country into closer contact, changing forever the rural isolation that had defined America since its beginnings. Visit the Library of Congress to examine the controversy over the invention of the telephone. While Alexander Graham Bell is credited with the invention, several other inventors played a role in its development; however, Bell was the first to patent the device. THOMAS EDISON AND ELECTRIC LIGHTING Although Thomas Alva Edison (Figure) is best known for his contributions to the electrical industry, his experimentation went far beyond the light bulb. Edison was quite possibly the greatest inventor of the turn of the century, saying famously that he “hoped to have a minor invention every ten days and a big thing every month or so.” He registered 1,093 patents over his lifetime and ran a world-famous laboratory, Menlo Park, which housed a rotating group of up to twenty-five scientists from around the globe. Edison became interested in the telegraph industry as a boy, when he worked aboard trains selling candy and newspapers. He soon began tinkering with telegraph technology and, by 1876, had devoted himself full time to lab work as an inventor. He then proceeded to invent a string of items that are still used today: the phonograph, the mimeograph machine, the motion picture projector, the dictaphone, and the storage battery, all using a factory-oriented assembly line process that made the rapid production of inventions possible. In 1879, Edison invented the item that has led to his greatest fame: the incandescent light bulb. He allegedly explored over six thousand different materials for the filament, before stumbling upon tungsten as the ideal substance. By 1882, with financial backing largely from financier J. P. Morgan, he had created the Edison Electric Illuminating Company, which began supplying electrical current to a small number of customers in New York City. Morgan guided subsequent mergers of Edison’s other enterprises, including a machine works firm and a lamp company, resulting in the creation of the Edison General Electric Company in 1889. The next stage of invention in electric power came about with the contribution of George Westinghouse. Westinghouse was responsible for making electric lighting possible on a national scale. While Edison used “direct current” or DC power, which could only extend two miles from the power source, in 1886, Westinghouse invented “alternating current” or AC power, which allowed for delivery over greater distances due to its wavelike patterns. The Westinghouse Electric Company delivered AC power, which meant that factories, homes, and farms—in short, anything that needed power—could be served, regardless of their proximity to the power source. A public relations battle ensued between the Westinghouse and Edison camps, coinciding with the invention of the electric chair as a form of prisoner execution. Edison publicly proclaimed AC power to be best adapted for use in the chair, in the hope that such a smear campaign would result in homeowners becoming reluctant to use AC power in their houses. Although Edison originally fought the use of AC power in other devices, he reluctantly adapted to it as its popularity increased. Not all of Edison’s ventures were successful. Read about Edison’s Folly to learn the story behind his greatest failure. Was there some benefit to his efforts? Or was it wasted time and money? Section Summary Inventors in the late nineteenth century flooded the market with new technological advances. Encouraged by Great Britain’s Industrial Revolution, and eager for economic development in the wake of the Civil War, business investors sought the latest ideas upon which they could capitalize, both to transform the nation as well as to make a personal profit. These inventions were a key piece of the massive shift towards industrialization that followed. For both families and businesses, these inventions eventually represented a fundamental change in their way of life. Although the technology spread slowly, it did spread across the country. Whether it was a company that could now produce ten times more products with new factories, or a household that could communicate with distant relations, the old way of doing things was disappearing. Communication technologies, electric power production, and steel production were perhaps the three most significant developments of the time. While the first two affected both personal lives and business development, the latter influenced business growth first and foremost, as the ability to produce large steel elements efficiently and cost-effectively led to permanently changes in the direction of industrial growth. Review Questions Which of these was not a successful invention of the era? - high-powered sewing machines - movies with sound - frozen foods - typewriters Hint: B What was the major advantage of Westinghouse’s “alternating current” power invention? - It was less prone to fire. - It cost less to produce. - It allowed machines to be farther from the power source. - It was not under Edison’s control. Hint: C How did the burst of new inventions during this era fuel the process of urbanization? Hint: New inventions fueled industrial growth, and the development of commercial electricity—along with the use of steam engines—allowed industries that had previously situated themselves close to sources of water power to shift away from those areas and move their production into cities. Immigrants sought employment in these urban factories and settled nearby, transforming the country’s population from mostly rural to largely urban.	oercommons	2025-03-18T00:37:00.304408	null	{ "license": "Creative Commons - Attribution - https://creativecommons.org/licenses/by/4.0/", "url": "https://oercommons.org/courseware/lesson/15489/overview", "title": "U.S. History, Industrialization and the Rise of Big Business, 1870-1900", "author": null }
https://oercommons.org/courseware/lesson/15490/overview	From Invention to Industrial Growth Overview By the end of this section, you will be able to: - Explain how the inventions of the late nineteenth century contributed directly to industrial growth in America - Identify the contributions of Andrew Carnegie, John Rockefeller, and J. P. Morgan to the new industrial order emerging in the late nineteenth century - Describe the visions, philosophies, and business methods of the leaders of the new industrial order As discussed previously, new processes in steel refining, along with inventions in the fields of communications and electricity, transformed the business landscape of the nineteenth century. The exploitation of these new technologies provided opportunities for tremendous growth, and business entrepreneurs with financial backing and the right mix of business acumen and ambition could make their fortunes. Some of these new millionaires were known in their day as robber barons, a negative term that connoted the belief that they exploited workers and bent laws to succeed. Regardless of how they were perceived, these businessmen and the companies they created revolutionized American industry. RAILROADS AND ROBBER BARONS Earlier in the nineteenth century, the first transcontinental railroad and subsequent spur lines paved the way for rapid and explosive railway growth, as well as stimulated growth in the iron, wood, coal, and other related industries. The railroad industry quickly became the nation’s first “big business.” A powerful, inexpensive, and consistent form of transportation, railroads accelerated the development of virtually every other industry in the country. By 1890, railroad lines covered nearly every corner of the United States, bringing raw materials to industrial factories and finished goods to consumer markets. The amount of track grew from 35,000 miles at the end of the Civil War to over 200,000 miles by the close of the century. Inventions such as car couplers, air brakes, and Pullman passenger cars allowed the volume of both freight and people to increase steadily. From 1877 to 1890, both the amount of goods and the number of passengers traveling the rails tripled. Financing for all of this growth came through a combination of private capital and government loans and grants. Federal and state loans of cash and land grants totaled $150 million and 185 million acres of public land, respectively. Railroads also listed their stocks and bonds on the New York Stock Exchange to attract investors from both within the United States and Europe. Individual investors consolidated their power as railroads merged and companies grew in size and power. These individuals became some of the wealthiest Americans the country had ever known. Midwest farmers, angry at large railroad owners for their exploitative business practices, came to refer to them as “robber barons,” as their business dealings were frequently shady and exploitative. Among their highly questionable tactics was the practice of differential shipping rates, in which larger business enterprises received discounted rates to transport their goods, as opposed to local producers and farmers whose higher rates essentially subsidized the discounts. Jay Gould was perhaps the first prominent railroad magnate to be tarred with the “robber baron” brush. He bought older, smaller, rundown railroads, offered minimal improvements, and then capitalized on factory owners’ desires to ship their goods on this increasingly popular and more cost-efficient form of transportation. His work with the Erie Railroad was notorious among other investors, as he drove the company to near ruin in a failed attempt to attract foreign investors during a takeover attempt. His model worked better in the American West, where the railroads were still widely scattered across the country, forcing farmers and businesses to pay whatever prices Gould demanded in order to use his trains. In addition to owning the Union Pacific Railroad that helped to construct the original transcontinental railroad line, Gould came to control over ten thousand miles of track across the United States, accounting for 15 percent of all railroad transportation. When he died in 1892, Gould had a personal worth of over $100 million, although he was a deeply unpopular figure. In contrast to Gould’s exploitative business model, which focused on financial profit more than on tangible industrial contributions, Commodore Cornelius Vanderbilt was a “robber baron” who truly cared about the success of his railroad enterprise and its positive impact on the American economy. Vanderbilt consolidated several smaller railroad lines, called trunk lines, to create the powerful New York Central Railroad Company, one of the largest corporations in the United States at the time (Figure). He later purchased stock in the major rail lines that would connect his company to Chicago, thus expanding his reach and power while simultaneously creating a railroad network to connect Chicago to New York City. This consolidation provided more efficient connections from Midwestern suppliers to eastern markets. It was through such consolidation that, by 1900, seven major railroad tycoons controlled over 70 percent of all operating lines. Vanderbilt’s personal wealth at his death (over $100 million in 1877), placed him among the top three wealthiest individuals in American history. GIANTS OF WEALTH: CARNEGIE, ROCKEFELLER, AND MORGAN The post-Civil War inventors generated ideas that transformed the economy, but they were not big businessmen. The evolution from technical innovation to massive industry took place at the hands of the entrepreneurs whose business gambles paid off, making them some of the richest Americans of their day. Steel magnate Andrew Carnegie, oil tycoon John D. Rockefeller, and business financier J. P. Morgan were all businessmen who grew their respective businesses to a scale and scope that were unprecedented. Their companies changed how Americans lived and worked, and they themselves greatly influenced the growth of the country. Andrew Carnegie and The Gospel of Wealth Andrew Carnegie, steel magnate, has the prototypical rags-to-riches story. Although such stories resembled more myth than reality, they served to encourage many Americans to seek similar paths to fame and fortune. In Carnegie, the story was one of few derived from fact. Born in Scotland, Carnegie immigrated with his family to Pennsylvania in 1848. Following a brief stint as a “bobbin boy,” changing spools of thread at a Pittsburgh clothing manufacturer at age thirteen, he subsequently became a telegram messenger boy. As a messenger, he spent much of his time around the Pennsylvania Railroad office and developed parallel interests in railroads, bridge building, and, eventually, the steel industry. Ingratiating himself to his supervisor and future president of the Pennsylvania Railroad, Tom Scott, Carnegie worked his way into a position of management for the company and subsequently began to invest some of his earnings, with Scott’s guidance. One particular investment, in the booming oil fields of northwest Pennsylvania in 1864, resulted in Carnegie earning over $1 million in cash dividends, thus providing him with the capital necessary to pursue his ambition to modernize the iron and steel industries, transforming the United States in the process. Having seen firsthand during the Civil War, when he served as Superintendent of Military Railways and telegraph coordinator for the Union forces, the importance of industry, particularly steel, to the future growth of the country, Carnegie was convinced of his strategy. His first company was the J. Edgar Thompson Steel Works, and, a decade later, he bought out the newly built Homestead Steel Works from the Pittsburgh Bessemer Steel Company. By the end of the century, his enterprise was running an annual profit in excess of $40 million (Figure). Although not a scientific expert in steel, Carnegie was an excellent promoter and salesman, able to locate financial backing for his enterprise. He was also shrewd in his calculations on consolidation and expansion, and was able to capitalize on smart business decisions. Always thrifty with the profits he earned, a trait owed to his upbringing, Carnegie saved his profits during prosperous times and used them to buy out other steel companies at low prices during the economic recessions of the 1870s and 1890s. He insisted on up-to-date machinery and equipment, and urged the men who worked at and managed his steel mills to constantly think of innovative ways to increase production and reduce cost. Carnegie, more than any other businessman of the era, championed the idea that America’s leading tycoons owed a debt to society. He believed that, given the circumstances of their successes, they should serve as benefactors to the less fortunate public. For Carnegie, poverty was not an abstract concept, as his family had been a part of the struggling masses. He desired to set an example of philanthropy for all other prominent industrialists of the era to follow. Carnegie’s famous essay, The Gospel of Wealth, featured below, expounded on his beliefs. In it, he borrowed from Herbert Spencer’s theory of social Darwinism, which held that society developed much like plant or animal life through a process of evolution in which the most fit and capable enjoyed the greatest material and social success. Andrew Carnegie on Wealth Carnegie applauded American capitalism for creating a society where, through hard work, ingenuity, and a bit of luck, someone like himself could amass a fortune. In return for that opportunity, Carnegie wrote that the wealthy should find proper uses for their wealth by funding hospitals, libraries, colleges, the arts, and more. The Gospel of Wealth spelled out that responsibility. Poor and restricted are our opportunities in this life; narrow our horizon; our best work most imperfect; but rich men should be thankful for one inestimable boon. They have it in their power during their lives to busy themselves in organizing benefactions from which the masses of their fellows will derive lasting advantage, and thus dignify their own lives. . . . This, then, is held to be the duty of the man of Wealth: First, to set an example of modest, unostentatious living, shunning display or extravagance; to provide moderately for the legitimate wants of those dependent upon him; and after doing so to consider all surplus revenues which come to him simply as trust funds, which he is called upon to administer, and strictly bound as a matter of duty to administer in the manner which, in his judgment, is best calculated to produce the most beneficial results for the community—the man of wealth thus becoming the mere agent and trustee for his poorer brethren, bringing to their service his superior wisdom, experience and ability to administer, doing for them better than they would or could do for themselves. . . . In bestowing charity, the main consideration should be to help those who will help themselves; to provide part of the means by which those who desire to improve may do so; to give those who desire to use the aids by which they may rise; to assist, but rarely or never to do all. Neither the individual nor the race is improved by alms-giving. Those worthy of assistance, except in rare cases, seldom require assistance. The really valuable men of the race never do, except in cases of accident or sudden change. Every one has, of course, cases of individuals brought to his own knowledge where temporary assistance can do genuine good, and these he will not overlook. But the amount which can be wisely given by the individual for individuals is necessarily limited by his lack of knowledge of the circumstances connected with each. He is the only true reformer who is as careful and as anxious not to aid the unworthy as he is to aid the worthy, and, perhaps, even more so, for in alms-giving more injury is probably done by rewarding vice than by relieving virtue. —Andrew Carnegie, The Gospel of Wealth Social Darwinism added a layer of pseudoscience to the idea of the self-made man, a desirable thought for all who sought to follow Carnegie’s example. The myth of the rags-to-riches businessman was a potent one. Author Horatio Alger made his own fortune writing stories about young enterprising boys who beat poverty and succeeded in business through a combination of “luck and pluck.” His stories were immensely popular, even leading to a board game (Figure) where players could hope to win in the same way that his heroes did. John D. Rockefeller and Business Integration Models Like Carnegie, John D. Rockefeller was born in 1839 of modest means, with a frequently absent traveling salesman of a father who sold medicinal elixirs and other wares. Young Rockefeller helped his mother with various chores and earned extra money for the family through the sale of family farm products. When the family moved to a suburb of Cleveland in 1853, he had an opportunity to take accounting and bookkeeping courses while in high school and developed a career interest in business. While living in Cleveland in 1859, he learned of Colonel Edwin Drake who had struck “black gold,” or oil, near Titusville, Pennsylvania, setting off a boom even greater than the California Gold Rush of the previous decade. Many sought to find a fortune through risky and chaotic “wildcatting,” or drilling exploratory oil wells, hoping to strike it rich. But Rockefeller chose a more certain investment: refining crude oil into kerosene, which could be used for both heating and lamps. As a more efficient source of energy, as well as less dangerous to produce, kerosene quickly replaced whale oil in many businesses and homes. Rockefeller worked initially with family and friends in the refining business located in the Cleveland area, but by 1870, Rockefeller ventured out on his own, consolidating his resources and creating the Standard Oil Company of Ohio, initially valued at $1 million. Rockefeller was ruthless in his pursuit of total control of the oil refining business. As other entrepreneurs flooded the area seeking a quick fortune, Rockefeller developed a plan to crush his competitors and create a true monopoly in the refining industry. Beginning in 1872, he forged agreements with several large railroad companies to obtain discounted freight rates for shipping his product. He also used the railroad companies to gather information on his competitors. As he could now deliver his kerosene at lower prices, he drove his competition out of business, often offering to buy them out for pennies on the dollar. He hounded those who refused to sell out to him, until they were driven out of business. Through his method of growth via mergers and acquisitions of similar companies—known as horizontal integration —Standard Oil grew to include almost all refineries in the area. By 1879, the Standard Oil Company controlled nearly 95 percent of all oil refining businesses in the country, as well as 90 percent of all the refining businesses in the world. Editors of the New York World lamented of Standard Oil in 1880 that, “When the nineteenth century shall have passed into history, the impartial eyes of the reviewers will be amazed to find that the U.S. . . . tolerated the presence of the most gigantic, the most cruel, impudent, pitiless and grasping monopoly that ever fastened itself upon a country.” Seeking still more control, Rockefeller recognized the advantages of controlling the transportation of his product. He next began to grow his company through vertical integration, wherein a company handles all aspects of a product’s lifecycle, from the creation of raw materials through the production process to the delivery of the final product. In Rockefeller’s case, this model required investment and acquisition of companies involved in everything from barrel-making to pipelines, tanker cars to railroads. He came to own almost every type of business and used his vast power to drive competitors from the market through intense price wars. Although vilified by competitors who suffered from his takeovers and considered him to be no better than a robber baron, several observers lauded Rockefeller for his ingenuity in integrating the oil refining industry and, as a result, lowering kerosene prices by as much as 80 percent by the end of the century. Other industrialists quickly followed suit, including Gustavus Swift, who used vertical integration to dominate the U.S. meatpacking industry in the late nineteenth century. In order to control the variety of interests he now maintained in industry, Rockefeller created a new legal entity, known as a trust. In this arrangement, a small group of trustees possess legal ownership of a business that they operate for the benefit of other investors. In 1882, all thirty-seven stockholders in the various Standard Oil enterprises gave their stock to nine trustees who were to control and direct all of the company’s business ventures. State and federal challenges arose, due to the obvious appearance of a monopoly, which implied sole ownership of all enterprises composing an entire industry. When the Ohio Supreme Court ruled that the Standard Oil Company must dissolve, as its monopoly control over all refining operations in the U.S. was in violation of state and federal statutes, Rockefeller shifted to yet another legal entity, called a holding company model. The holding company model created a central corporate entity that controlled the operations of multiple companies by holding the majority of stock for each enterprise. While not technically a “trust” and therefore not vulnerable to anti-monopoly laws, this consolidation of power and wealth into one entity was on par with a monopoly; thus, progressive reformers of the late nineteenth century considered holding companies to epitomize the dangers inherent in capitalistic big business, as can be seen in the political cartoon below (Figure). Impervious to reformers’ misgivings, other businessmen followed Rockefeller’s example. By 1905, over three hundred business mergers had occurred in the United States, affecting more than 80 percent of all industries. By that time, despite passage of federal legislation such as the Sherman Anti-Trust Act in 1890, 1 percent of the country’s businesses controlled over 40 percent of the nation’s economy. The PBS video on Robber Barons or Industrial Giants presents a lively discussion of whether the industrialists of the nineteenth century were really “robber barons” or if they were “industrial giants.” J. Pierpont Morgan Unlike Carnegie and Rockefeller, J. P. Morgan was no rags-to-riches hero. He was born to wealth and became much wealthier as an investment banker, making wise financial decisions in support of the hard-working entrepreneurs building their fortunes. Morgan’s father was a London banker, and Morgan the son moved to New York in 1857 to look after the family’s business interests there. Once in America, he separated from the London bank and created the J. Pierpont Morgan and Company financial firm. The firm bought and sold stock in growing companies, investing the family’s wealth in those that showed great promise, turning an enormous profit as a result. Investments from firms such as his were the key to the success stories of up-and-coming businessmen like Carnegie and Rockefeller. In return for his investment, Morgan and other investment bankers demanded seats on the companies’ boards, which gave them even greater control over policies and decisions than just investment alone. There were many critics of Morgan and these other bankers, particularly among members of a U.S. congressional subcommittee who investigated the control that financiers maintained over key industries in the country. The subcommittee referred to Morgan’s enterprise as a form of “money trust” that was even more powerful than the trusts operated by Rockefeller and others. Morgan argued that his firm, and others like it, brought stability and organization to a hypercompetitive capitalist economy, and likened his role to a kind of public service. Ultimately, Morgan’s most notable investment, and greatest consolidation, was in the steel industry, when he bought out Andrew Carnegie in 1901. Initially, Carnegie was reluctant to sell, but after repeated badgering by Morgan, Carnegie named his price: an outrageously inflated sum of $500 million. Morgan agreed without hesitation, and then consolidated Carnegie’s holdings with several smaller steel firms to create the U.S. Steel Corporation. U.S. Steel was subsequently capitalized at $1.4 billion. It was the country’s first billion-dollar firm. Lauded by admirers for the efficiency and modernization he brought to investment banking practices, as well as for his philanthropy and support of the arts, Morgan was also criticized by reformers who subsequently blamed his (and other bankers’) efforts for contributing to the artificial bubble of prosperity that eventually burst in the Great Depression of the 1930s. What none could doubt was that Morgan’s financial aptitude and savvy business dealings kept him in good stead. A subsequent U.S. congressional committee, in 1912, reported that his firm held 341 directorships in 112 corporations that controlled over $22 billion in assets. In comparison, that amount of wealth was greater than the assessed value of all the land in the United States west of the Mississippi River. Section Summary As the three tycoons profiled in this section illustrate, the end of the nineteenth century was a period in history that offered tremendous financial rewards to those who had the right combination of skill, ambition, and luck. Whether self-made millionaires like Carnegie or Rockefeller, or born to wealth like Morgan, these men were the lynchpins that turned inventors’ ideas into industrial growth. Steel production, in particular, but also oil refining techniques and countless other inventions, changed how industries in the country could operate, allowing them to grow in scale and scope like never before. It is also critical to note how these different men managed their businesses and ambition. Where Carnegie felt strongly that it was the job of the wealthy to give back in their lifetime to the greater community, his fellow tycoons did not necessarily agree. Although he contributed to many philanthropic efforts, Rockefeller’s financial success was built on the backs of ruined and bankrupt companies, and he came to be condemned by progressive reformers who questioned the impact on the working class as well as the dangers of consolidating too much power and wealth into one individual’s hands. Morgan sought wealth strictly through the investment in, and subsequent purchase of, others’ hard work. Along the way, the models of management they adopted—horizontal and vertical integration, trusts, holding companies, and investment brokerages—became commonplace in American businesses. Very quickly, large business enterprises fell under the control of fewer and fewer individuals and trusts. In sum, their ruthlessness, their ambition, their generosity, and their management made up the workings of America’s industrial age. Review Questions Which of the following “robber barons” was notable for the exploitative way he made his fortune in railroads? - Jay Gould - Cornelius Vanderbilt - Andrew Carnegie - J. Pierpont Morgan Hint: A Which of the following does not represent one of the management strategies that John D. Rockefeller used in building his empire? - horizontal integration - vertical integration - social Darwinism - the holding company model Hint: C Why was Rockefeller’s use of horizontal integration such an effective business tool at this time? Were his choices legal? Why or why not? Hint: Horizontal integration enabled Rockefeller to gain tremendous control over the oil industry and use that power to influence vendors and competitors. For example, he could pressure railroads into giving him lower rates because of the volume of his products. He undercut competitors, forcing them to set their prices so low that they could barely stay in business—at which point he could buy them out. Through horizontal integration, he was able to create a virtual monopoly and set the terms for business. While his business model of a holding company was technically legal, it held as much power as a monopoly and did not allow for other businesses to grow and compete. What differentiated a “robber baron” from other “captains of industry” in late nineteenth-century America? Hint: “Captains of industry” (such as Carnegie or Rockefeller) are noted for their new business models, entrepreneurial approaches, and, to varying degrees, philanthropic efforts, all of which transformed late nineteenth-century America. “Robber barons” (such as Gould) are noted for their self-centered drive for profit at the expense of workers and the general public, who seldom benefitted to any great degree. The terms, however, remain a gray area, as one could characterize the ruthless business practices of Rockefeller, or some of Carnegie’s tactics with regard to workers’ efforts to organize, as similar to the methods of robber barons. Nevertheless, “captains of industry” are noted for contributions that fundamentally changed and typically improved the nation, whereas “robber barons” can seldom point to such concrete contributions.	oercommons	2025-03-18T00:37:00.336975	null	{ "license": "Creative Commons - Attribution - https://creativecommons.org/licenses/by/4.0/", "url": "https://oercommons.org/courseware/lesson/15490/overview", "title": "U.S. History, Industrialization and the Rise of Big Business, 1870-1900", "author": null }
https://oercommons.org/courseware/lesson/15491/overview	Building Industrial America on the Backs of Labor Overview By the end of this section, you will be able to: - Explain the qualities of industrial working-class life in the late nineteenth century - Analyze both workers’ desire for labor unions and the reasons for unions’ inability to achieve their goals The growth of the American economy in the last half of the nineteenth century presented a paradox. The standard of living for many American workers increased. As Carnegie said in The Gospel of Wealth, “the poor enjoy what the rich could not before afford. What were the luxuries have become the necessaries of life. The laborer has now more comforts than the landlord had a few generations ago.” In many ways, Carnegie was correct. The decline in prices and the cost of living meant that the industrial era offered many Americans relatively better lives in 1900 than they had only decades before. For some Americans, there were also increased opportunities for upward mobility. For the multitudes in the working class, however, conditions in the factories and at home remained deplorable. The difficulties they faced led many workers to question an industrial order in which a handful of wealthy Americans built their fortunes on the backs of workers. WORKING-CLASS LIFE Between the end of the Civil War and the turn of the century, the American workforce underwent a transformative shift. In 1865, nearly 60 percent of Americans still lived and worked on farms; by the early 1900s, that number had reversed itself, and only 40 percent still lived in rural areas, with the remainder living and working in urban and early suburban areas. A significant number of these urban and suburban dwellers earned their wages in factories. Advances in farm machinery allowed for greater production with less manual labor, thus leading many Americans to seek job opportunities in the burgeoning factories in the cities. Not surprisingly, there was a concurrent trend of a decrease in American workers being self-employed and an increase of those working for others and being dependent on a factory wage system for their living. Yet factory wages were, for the most part, very low. In 1900, the average factory wage was approximately twenty cents per hour, for an annual salary of barely six hundred dollars. According to some historical estimates, that wage left approximately 20 percent of the population in industrialized cities at, or below, the poverty level. An average factory work week was sixty hours, ten hours per day, six days per week, although in steel mills, the workers put in twelve hours per day, seven days a week. Factory owners had little concern for workers’ safety. According to one of the few available accurate measures, as late as 1913, nearly 25,000 Americans lost their lives on the job, while another 700,000 workers suffered from injuries that resulted in at least one missed month of work. Another element of hardship for workers was the increasingly dehumanizing nature of their work. Factory workers executed repetitive tasks throughout the long hours of their shifts, seldom interacting with coworkers or supervisors. This solitary and repetitive work style was a difficult adjustment for those used to more collaborative and skill-based work, whether on farms or in crafts shops. Managers embraced Fredrick Taylor’s principles of scientific management, also called “stop-watch management,” where he used stop-watch studies to divide manufacturing tasks into short, repetitive segments. A mechanical engineer by training, Taylor encouraged factory owners to seek efficiency and profitability over any benefits of personal interaction. Owners adopted this model, effectively making workers cogs in a well-oiled machine. One result of the new breakdown of work processes was that factory owners were able to hire women and children to perform many of the tasks. From 1870 through 1900, the number of women working outside the home tripled. By the end of this period, five million American women were wage earners, with one-quarter of them working factory jobs. Most were young, under twenty-five, and either immigrants themselves or the daughters of immigrants. Their foray into the working world was not seen as a step towards empowerment or equality, but rather a hardship born of financial necessity. Women’s factory work tended to be in clothing or textile factories, where their appearance was less offensive to men who felt that heavy industry was their purview. Other women in the workforce worked in clerical positions as bookkeepers and secretaries, and as salesclerks. Not surprisingly, women were paid less than men, under the pretense that they should be under the care of a man and did not require a living wage. Factory owners used the same rationale for the exceedingly low wages they paid to children. Children were small enough to fit easily among the machines and could be hired for simple work for a fraction of an adult man’s pay. The image below (Figure) shows children working the night shift in a glass factory. From 1870 through 1900, child labor in factories tripled. Growing concerns among progressive reformers over the safety of women and children in the workplace would eventually result in the development of political lobby groups. Several states passed legislative efforts to ensure a safe workplace, and the lobby groups pressured Congress to pass protective legislation. However, such legislation would not be forthcoming until well into the twentieth century. In the meantime, many working-class immigrants still desired the additional wages that child and women labor produced, regardless of the harsh working conditions. WORKER PROTESTS AND VIOLENCE Workers were well aware of the vast discrepancy between their lives and the wealth of the factory owners. Lacking the assets and legal protection needed to organize, and deeply frustrated, some working communities erupted in spontaneous violence. The coal mines of eastern Pennsylvania and the railroad yards of western Pennsylvania, central to both respective industries and home to large, immigrant, working enclaves, saw the brunt of these outbursts. The combination of violence, along with several other factors, blunted any significant efforts to organize workers until well into the twentieth century. Business owners viewed organization efforts with great mistrust, capitalizing upon widespread anti-union sentiment among the general public to crush unions through open shops, the use of strikebreakers, yellow-dog contracts (in which the employee agrees to not join a union as a pre-condition of employment), and other means. Workers also faced obstacles to organization associated with race and ethnicity, as questions arose on how to address the increasing number of low-paid African American workers, in addition to the language and cultural barriers introduced by the large wave of southeastern European immigration to the United States. But in large part, the greatest obstacle to effective unionization was the general public’s continued belief in a strong work ethic and that an individual work ethic—not organizing into radical collectives—would reap its own rewards. As violence erupted, such events seemed only to confirm widespread popular sentiment that radical, un-American elements were behind all union efforts. In the 1870s, Irish coal miners in eastern Pennsylvania formed a secret organization known as the Molly Maguires, named for the famous Irish patriot. Through a series of scare tactics that included kidnappings, beatings, and even murder, the Molly Maguires sought to bring attention to the miners’ plight, as well as to cause enough damage and concern to the mine owners that the owners would pay attention to their concerns. Owners paid attention, but not in the way that the protesters had hoped. They hired detectives to pose as miners and mingle among the workers to obtain the names of the Molly Maguires. By 1875, they had acquired the names of twenty-four suspected Maguires, who were subsequently convicted of murder and violence against property. All were convicted and ten were hanged in 1876, at a public “Day of the Rope.” This harsh reprisal quickly crushed the remaining Molly Maguires movement. The only substantial gain the workers had from this episode was the knowledge that, lacking labor organization, sporadic violent protest would be met by escalated violence. Public opinion was not sympathetic towards labor’s violent methods as displayed by the Molly Maguires. But the public was further shocked by some of the harsh practices employed by government agents to crush the labor movement, as seen the following year in the Great Railroad Strike of 1877. After incurring a significant pay cut earlier that year, railroad workers in West Virginia spontaneously went on strike and blocked the tracks (Figure). As word spread of the event, railroad workers across the country joined in sympathy, leaving their jobs and committing acts of vandalism to show their frustration with the ownership. Local citizens, who in many instances were relatives and friends, were largely sympathetic to the railroad workers’ demands. The most significant violent outbreak of the railroad strike occurred in Pittsburgh, beginning on July 19. The governor ordered militiamen from Philadelphia to the Pittsburgh roundhouse to protect railroad property. The militia opened fire to disperse the angry crowd and killed twenty individuals while wounding another twenty-nine. A riot erupted, resulting in twenty-four hours of looting, violence, fire, and mayhem, and did not die down until the rioters wore out in the hot summer weather. In a subsequent skirmish with strikers while trying to escape the roundhouse, militiamen killed another twenty individuals. Violence erupted in Maryland and Illinois as well, and President Hayes eventually sent federal troops into major cities to restore order. This move, along with the impending return of cooler weather that brought with it the need for food and fuel, resulted in striking workers nationwide returning to the railroad. The strike had lasted for forty-five days, and they had gained nothing but a reputation for violence and aggression that left the public less sympathetic than ever. Dissatisfied laborers began to realize that there would be no substantial improvement in their quality of life until they found a way to better organize themselves. WORKER ORGANIZATION AND THE STRUGGLES OF UNIONS Prior to the Civil War, there were limited efforts to create an organized labor movement on any large scale. With the majority of workers in the country working independently in rural settings, the idea of organized labor was not largely understood. But, as economic conditions changed, people became more aware of the inequities facing factory wage workers. By the early 1880s, even farmers began to fully recognize the strength of unity behind a common cause. Models of Organizing: The Knights of Labor and American Federation of Labor In 1866, seventy-seven delegates representing a variety of different occupations met in Baltimore to form the National Labor Union (NLU). The NLU had ambitious ideas about equal rights for African Americans and women, currency reform, and a legally mandated eight-hour workday. The organization was successful in convincing Congress to adopt the eight-hour workday for federal employees, but their reach did not progress much further. The Panic of 1873 and the economic recession that followed as a result of overspeculation on railroads and the subsequent closing of several banks—during which workers actively sought any employment regardless of the conditions or wages—as well as the death of the NLU’s founder, led to a decline in their efforts. A combination of factors contributed to the debilitating Panic of 1873, which triggered what the public referred to at the time as the “Great Depression” of the 1870s. Most notably, the railroad boom that had occurred from 1840 to 1870 was rapidly coming to a close. Overinvestment in the industry had extended many investors’ capital resources in the form of railroad bonds. However, when several economic developments in Europe affected the value of silver in America, which in turn led to a de facto gold standard that shrunk the U.S. monetary supply, the amount of cash capital available for railroad investments rapidly declined. Several large business enterprises were left holding their wealth in all but worthless railroad bonds. When Jay Cooke & Company, a leader in the American banking industry, declared bankruptcy on the eve of their plans to finance the construction of a new transcontinental railroad, the panic truly began. A chain reaction of bank failures culminated with the New York Stock Exchange suspending all trading for ten days at the end of September 1873. Within a year, over one hundred railroad enterprises had failed; within two years, nearly twenty thousand businesses had failed. The loss of jobs and wages sent workers throughout the United States seeking solutions and clamoring for scapegoats. Although the NLU proved to be the wrong effort at the wrong time, in the wake of the Panic of 1873 and the subsequent frustration exhibited in the failed Molly Maguires uprising and the national railroad strike, another, more significant, labor organization emerged. The Knights of Labor (KOL) was more able to attract a sympathetic following than the Molly Maguires and others by widening its base and appealing to more members. Philadelphia tailor Uriah Stephens grew the KOL from a small presence during the Panic of 1873 to an organization of national importance by 1878. That was the year the KOL held their first general assembly, where they adopted a broad reform platform, including a renewed call for an eight-hour workday, equal pay regardless of gender, the elimination of convict labor, and the creation of greater cooperative enterprises with worker ownership of businesses. Much of the KOL’s strength came from its concept of “One Big Union”—the idea that it welcomed all wage workers, regardless of occupation, with the exception of doctors, lawyers, and bankers. It welcomed women, African Americans, Native Americans, and immigrants, of all trades and skill levels. This was a notable break from the earlier tradition of craft unions, which were highly specialized and limited to a particular group. In 1879, a new leader, Terence V. Powderly, joined the organization, and he gained even more followers due to his marketing and promotional efforts. Although largely opposed to strikes as effective tactics, through their sheer size, the Knights claimed victories in several railroad strikes in 1884–1885, including one against notorious “robber baron” Jay Gould, and their popularity consequently rose among workers. By 1886, the KOL had a membership in excess of 700,000. In one night, however, the KOL’s popularity—and indeed the momentum of the labor movement as a whole—plummeted due to an event known as the Haymarket affair, which occurred on May 4, 1886, in Chicago’s Haymarket Square (Figure). There, an anarchist group had gathered in response to a death at an earlier nationwide demonstration for the eight-hour workday. At the earlier demonstration, clashes between police and strikers at the International Harvester Company of Chicago led to the death of a striking worker. The anarchist group decided to hold a protest the following night in Haymarket Square, and, although the protest was quiet, the police arrived armed for conflict. Someone in the crowd threw a bomb at the police, killing one officer and injuring another. The seven anarchists speaking at the protest were arrested and charged with murder. They were sentenced to death, though two were later pardoned and one committed suicide in prison before his execution. The press immediately blamed the KOL as well as Powderly for the Haymarket affair, despite the fact that neither the organization nor Powderly had anything to do with the demonstration. Combined with the American public’s lukewarm reception to organized labor as a whole, the damage was done. The KOL saw its membership decline to barely 100,000 by the end of 1886. Nonetheless, during its brief success, the Knights illustrated the potential for success with their model of “industrial unionism,” which welcomed workers from all trades. The Haymarket Rally On May 1, 1886, recognized internationally as a day for labor celebration, labor organizations around the country engaged in a national rally for the eight-hour workday. While the number of striking workers varied around the country, estimates are that between 300,000 and 500,000 workers protested in New York, Detroit, Chicago, and beyond. In Chicago, clashes between police and protesters led the police to fire into the crowd, resulting in fatalities. Afterward, angry at the deaths of the striking workers, organizers quickly organized a “mass meeting,” per the poster below (Figure). While the meeting was intended to be peaceful, a large police presence made itself known, prompting one of the event organizers to state in his speech, “There seems to prevail the opinion in some quarters that this meeting has been called for the purpose of inaugurating a riot, hence these warlike preparations on the part of so-called ‘law and order.’ However, let me tell you at the beginning that this meeting has not been called for any such purpose. The object of this meeting is to explain the general situation of the eight-hour movement and to throw light upon various incidents in connection with it.” The mayor of Chicago later corroborated accounts of the meeting, noted that it was a peaceful rally, but as it was winding down, the police marched into the crowd, demanding they disperse. Someone in the crowd threw a bomb, killing one policeman immediately and wounding many others, some of whom died later. Despite the aggressive actions of the police, public opinion was strongly against the striking laborers. The New York Times, after the events played out, reported on it with the headline “Rioting and Bloodshed in the Streets of Chicago: Police Mowed Down with Dynamite.” Other papers echoed the tone and often exaggerated the chaos, undermining organized labor’s efforts and leading to the ultimate conviction and hanging of the rally organizers. Labor activists considered those hanged after the Haymarket affair to be martyrs for the cause and created an informal memorial at their gravesides in Park Forest, Illinois. This article about the “Rioting and Bloodshed in the Streets of Chicago” reveals how the New York Times reported on the Haymarket affair. Assess whether the article gives evidence of the information it lays out. Consider how it portrays the events, and how different, more sympathetic coverage might have changed the response of the general public towards immigrant workers and labor unions. During the effort to establish industrial unionism in the form of the KOL, craft unions had continued to operate. In 1886, twenty different craft unions met to organize a national federation of autonomous craft unions. This group became the American Federation of Labor (AFL), led by Samuel Gompers from its inception until his death in 1924. More so than any of its predecessors, the AFL focused almost all of its efforts on economic gains for its members, seldom straying into political issues other than those that had a direct impact upon working conditions. The AFL also kept a strict policy of not interfering in each union’s individual business. Rather, Gompers often settled disputes between unions, using the AFL to represent all unions of matters of federal legislation that could affect all workers, such as the eight-hour workday. By 1900, the AFL had 500,000 members; by 1914, its numbers had risen to one million, and by 1920 they claimed four million working members. Still, as a federation of craft unions, it excluded many factory workers and thus, even at its height, represented only 15 percent of the nonfarm workers in the country. As a result, even as the country moved towards an increasingly industrial age, the majority of American workers still lacked support, protection from ownership, and access to upward mobility. The Decline of Labor: The Homestead and Pullman Strikes While workers struggled to find the right organizational structure to support a union movement in a society that was highly critical of such worker organization, there came two final violent events at the close of the nineteenth century. These events, the Homestead Steel Strike of 1892 and the Pullman Strike of 1894, all but crushed the labor movement for the next forty years, leaving public opinion of labor strikes lower than ever and workers unprotected. At the Homestead factory of the Carnegie Steel Company, workers represented by the Amalgamated Association of Iron and Steel Workers enjoyed relatively good relations with management until Henry C. Frick became the factory manager in 1889. When the union contract was up for renewal in 1892, Carnegie—long a champion of living wages for his employees—had left for Scotland and trusted Frick—noted for his strong anti-union stance—to manage the negotiations. When no settlement was reached by June 29, Frick ordered a lockout of the workers and hired three hundred Pinkerton detectives to protect company property. On July 6, as the Pinkertons arrived on barges on the river, union workers along the shore engaged them in a gunfight that resulted in the deaths of three Pinkertons and six workers. One week later, the Pennsylvania militia arrived to escort strike-breakers into the factory to resume production. Although the lockout continued until November, it ended with the union defeated and individual workers asking for their jobs back. A subsequent failed assassination attempt by anarchist Alexander Berkman on Frick further strengthened public animosity towards the union. Two years later, in 1894, the Pullman Strike was another disaster for unionized labor. The crisis began in the company town of Pullman, Illinois, where Pullman “sleeper” cars were manufactured for America’s railroads. When the depression of 1893 unfolded in the wake of the failure of several northeastern railroad companies, mostly due to overconstruction and poor financing, company owner George Pullman fired three thousand of the factory’s six thousand employees, cut the remaining workers’ wages by an average of 25 percent, and then continued to charge the same high rents and prices in the company homes and store where workers were required to live and shop. Workers began the strike on May 11, when Eugene V. Debs, the president of the American Railway Union, ordered rail workers throughout the country to stop handling any trains that had Pullman cars on them. In practicality, almost all of the trains fell into this category, and, therefore, the strike created a nationwide train stoppage, right on the heels of the depression of 1893. Seeking justification for sending in federal troops, President Grover Cleveland turned to his attorney general, who came up with a solution: Attach a mail car to every train and then send in troops to ensure the delivery of the mail. The government also ordered the strike to end; when Debs refused, he was arrested and imprisoned for his interference with the delivery of U.S. mail. The image below (Figure) shows the standoff between federal troops and the workers. The troops protected the hiring of new workers, thus rendering the strike tactic largely ineffective. The strike ended abruptly on July 13, with no labor gains and much lost in the way of public opinion. George Estes on the Order of Railroad Telegraphers The following excerpt is a reflection from George Estes, an organizer and member of the Order of Railroad Telegraphers, a labor organization at the end of the nineteenth century. His perspective on the ways that labor and management related to each other illustrates the difficulties at the heart of their negotiations. He notes that, in this era, the two groups saw each other as enemies and that any gain by one was automatically a loss by the other. I have always noticed that things usually have to get pretty bad before they get any better. When inequities pile up so high that the burden is more than the underdog can bear, he gets his dander up and things begin to happen. It was that way with the telegraphers’ problem. These exploited individuals were determined to get for themselves better working conditions—higher pay, shorter hours, less work which might not properly be classed as telegraphy, and the high and mighty Mr. Fillmore [railroad company president] was not going to stop them. It was a bitter fight. At the outset, Mr. Fillmore let it be known, by his actions and comments, that he held the telegraphers in the utmost contempt. With the papers crammed each day with news of labor strife—and with two great labor factions at each other’s throats, I am reminded of a parallel in my own early and more active career. Shortly before the turn of the century, in 1898 and 1899 to be more specific, I occupied a position with regard to a certain class of skilled labor, comparable to that held by the Lewises and Greens of today. I refer, of course, to the telegraphers and station agents. These hard-working gentlemen—servants of the public—had no regular hours, performed a multiplicity of duties, and, considering the service they rendered, were sorely and inadequately paid. A telegrapher’s day included a considerable number of chores that present-day telegraphers probably never did or will do in the course of a day’s work. He used to clean and fill lanterns, block lights, etc. Used to do the janitor work around the small town depot, stoke the pot-bellied stove of the waiting-room, sweep the floors, picking up papers and waiting-room litter. . . . Today, capital and labor seem to understand each other better than they did a generation or so ago. Capital is out to make money. So is labor—and each is willing to grant the other a certain amount of tolerant leeway, just so he doesn’t go too far. In the old days there was a breach as wide as the Pacific separating capital and labor. It wasn’t money altogether in those days, it was a matter of principle. Capital and labor couldn’t see eye to eye on a single point. Every gain that either made was at the expense of the other, and was fought tooth and nail. No difference seemed ever possible of amicable settlement. Strikes were riots. Murder and mayhem was common. Railroad labor troubles were frequent. The railroads, in the nineties, were the country’s largest employers. They were so big, so powerful, so perfectly organized themselves—I mean so in accord among themselves as to what treatment they felt like offering the man who worked for them—that it was extremely difficult for labor to gain a single advantage in the struggle for better conditions. —George Estes, interview with Andrew Sherbert, 1938 Section Summary After the Civil War, as more and more people crowded into urban areas and joined the ranks of wage earners, the landscape of American labor changed. For the first time, the majority of workers were employed by others in factories and offices in the cities. Factory workers, in particular, suffered from the inequity of their positions. Owners had no legal restrictions on exploiting employees with long hours in dehumanizing and poorly paid work. Women and children were hired for the lowest possible wages, but even men’s wages were barely enough upon which to live. Poor working conditions, combined with few substantial options for relief, led workers to frustration and sporadic acts of protest and violence, acts that rarely, if ever, gained them any lasting, positive effects. Workers realized that change would require organization, and thus began early labor unions that sought to win rights for all workers through political advocacy and owner engagement. Groups like the National Labor Union and Knights of Labor both opened their membership to any and all wage earners, male or female, black or white, regardless of skill. Their approach was a departure from the craft unions of the very early nineteenth century, which were unique to their individual industries. While these organizations gained members for a time, they both ultimately failed when public reaction to violent labor strikes turned opinion against them. The American Federation of Labor, a loose affiliation of different unions, grew in the wake of these universal organizations, although negative publicity impeded their work as well. In all, the century ended with the vast majority of American laborers unrepresented by any collective or union, leaving them vulnerable to the power wielded by factory ownership. Review Questions What was one of the key goals for which striking workers fought in the late nineteenth century? - health insurance - disability pay - an eight-hour workday - women’s right to hold factory jobs Hint: C Which of the following was not a key goal of the Knights of Labor? - an end to convict labor - a graduated income tax on personal wealth - equal pay regardless of gender - the creation of cooperative business enterprises Hint: B What were the core differences in the methods and agendas of the Knights of Labor and the American Federation of Labor? Hint: The Knights of Labor (KOL) had a broad and open base, inviting all types of workers, including women and African Americans, into their ranks. The KOL also sought political gains for workers throughout the country, regardless of their membership. In contrast, the American Federation of Labor (AFL) was a loose affiliation of separate unions, with each group remaining intact and distinct. The AFL did not advocate for national labor issues, but restricted its efforts to helping improve economic conditions for its members.	oercommons	2025-03-18T00:37:00.371726	null	{ "license": "Creative Commons - Attribution - https://creativecommons.org/licenses/by/4.0/", "url": "https://oercommons.org/courseware/lesson/15491/overview", "title": "U.S. History, Industrialization and the Rise of Big Business, 1870-1900", "author": null }
https://oercommons.org/courseware/lesson/15492/overview	A New American Consumer Culture Overview By the end of this section, you will be able to: - Describe the characteristics of the new consumer culture that emerged at the end of the nineteenth century Despite the challenges workers faced in their new roles as wage earners, the rise of industry in the United States allowed people to access and consume goods as never before. The rise of big business had turned America into a culture of consumers desperate for time-saving and leisure commodities, where people could expect to find everything they wanted in shops or by mail order. Gone were the days where the small general store was the only option for shoppers; at the end of the nineteenth century, people could take a train to the city and shop in large department stores like Macy’s in New York, Gimbel’s in Philadelphia, and Marshall Fields in Chicago. Chain stores, like A&P and Woolworth’s, both of which opened in the 1870s, offered options to those who lived farther from major urban areas and clearly catered to classes other than the wealthy elite. Industrial advancements contributed to this proliferation, as new construction techniques permitted the building of stores with higher ceilings for larger displays, and the production of larger sheets of plate glass lent themselves to the development of larger store windows, glass countertops, and display cases where shoppers could observe a variety of goods at a glance. L. Frank Baum, of Wizard of Oz fame, later founded the National Association of Window Trimmers in 1898, and began publishing The Store Window journal to advise businesses on space usage and promotion. Even families in rural America had new opportunities to purchase a greater variety of products than ever before, at ever decreasing prices. Those far from chain stores could benefit from the newly developed business of mail-order catalogs, placing orders by telephone. Aaron Montgomery Ward established the first significant mail-order business in 1872, with Sears, Roebuck & Company following in 1886. Sears distributed over 300,000 catalogs annually by 1897, and later broke the one million annual mark in 1907. Sears in particular understood that farmers and rural Americans sought alternatives to the higher prices and credit purchases they were forced to endure at small-town country stores. By clearly stating the prices in his catalog, Richard Sears steadily increased his company’s image of their catalog serving as “the consumer’s bible.” In the process, Sears, Roebuck & Company supplied much of America’s hinterland with products ranging from farm supplies to bicycles, toilet paper to automobiles, as seen below in a page from the catalog (Figure). The tremendous variety of goods available for sale required businesses to compete for customers in ways they had never before imagined. Suddenly, instead of a single option for clothing or shoes, customers were faced with dozens, whether ordered by mail, found at the local chain store, or lined up in massive rows at department stores. This new level of competition made advertising a vital component of all businesses. By 1900, American businesses were spending almost $100 million annually on advertising. Competitors offered “new and improved” models as frequently as possible in order to generate interest. From toothpaste and mouthwash to books on entertaining guests, new goods were constantly offered. Newspapers accommodated the demand for advertising by shifting their production to include full-page advertisements, as opposed to the traditional column width, agate-type advertisements that dominated mid-nineteenth century newspapers (similar to classified advertisements in today’s publications). Likewise, professional advertising agencies began to emerge in the 1880s, with experts in consumer demand bidding for accounts with major firms. It may seem strange that, at a time when wages were so low, people began buying readily; however, the slow emergence of a middle class by the end of the century, combined with the growing practice of buying on credit, presented more opportunities to take part in the new consumer culture. Stores allowed people to open accounts and purchase on credit, thus securing business and allowing consumers to buy without ready cash. Then, as today, the risks of buying on credit led many into debt. As advertising expert Roland Marchand described in his Parable on the Democracy of Goods, in an era when access to products became more important than access to the means of production, Americans quickly accepted the notion that they could live a better lifestyle by purchasing the right clothes, the best hair cream, and the shiniest shoes, regardless of their class. For better or worse, American consumerism had begun. Advertising in the Industrial Age: Credit, Luxury, and the Advent of “New and Improved” Before the industrial revolution, most household goods were either made at home or purchased locally, with limited choices. By the end of the nineteenth century, factors such as the population’s move towards urban centers and the expansion of the railroad changed how Americans shopped for, and perceived, consumer goods. As mentioned above, advertising took off, as businesses competed for customers. Many of the elements used widely in nineteenth-century advertisements are familiar. Companies sought to sell luxury, safety, and, as the ad for the typewriter below shows (Figure), the allure of the new-and-improved model. One advertising tactic that truly took off in this era was the option to purchase on credit. For the first time, mail order and mass production meant that the aspiring middle class could purchase items that could only be owned previously by the wealthy. While there was a societal stigma for buying everyday goods on credit, certain items, such as fine furniture or pianos, were considered an investment in the move toward entry into the middle class. Additionally, farmers and housewives purchased farm equipment and sewing machines on credit, considering these items investments rather than luxuries. For women, the purchase of a sewing machine meant that a shirt could be made in one hour, instead of fourteen. The Singer Sewing Machine Company was one of the most aggressive at pushing purchase on credit. They advertised widely, and their “Dollar Down, Dollar a Week” campaign made them one of the fastest-growing companies in the country. For workers earning lower wages, these easy credit terms meant that the middle-class lifestyle was within their reach. Of course, it also meant they were in debt, and changes in wages, illness, or other unexpected expenses could wreak havoc on a household’s tenuous finances. Still, the opportunity to own new and luxurious products was one that many Americans, aspiring to improve their place in society, could not resist. Section Summary While tensions between owners and workers continued to grow, and wage earners struggled with the challenges of industrial work, the culture of American consumerism was changing. Greater choice, easier access, and improved goods at lower prices meant that even lower-income Americans, whether rural and shopping via mail order, or urban and shopping in large department stores, had more options. These increased options led to a rise in advertising, as businesses competed for customers. Furthermore, the opportunity to buy on credit meant that Americans could have their goods, even without ready cash. The result was a population that had a better standard of living than ever before, even as they went into debt or worked long factory hours to pay for it. Review Questions Which of the following did not contribute to the growth of a consumer culture in the United States at the close of the nineteenth century? - personal credit - advertising - greater disposable income - mail-order catalogs Hint: C Briefly explain Roland Marchand’s argument in the Parable of the Democracy of Goods. Hint: Marchand argues that in the new era of consumerism, workers’ desire for access to consumer goods replaces their desire for access to the means of production of those goods. So long as Americans could buy products that advertisers convinced them would make them look and feel wealthy, they did not need to fight for access to the means of wealth. Critical Thinking Questions Consider the fact that the light bulb and the telephone were invented only three years apart. Although it took many more years for such devices to find their way into common household use, they eventually wrought major changes in a relatively brief period of time. What effects did these inventions have on the lives of those who used them? Are there contemporary analogies in your lifetime of significant changes due to inventions or technological innovations? Industrialization, immigration, and urbanization all took place on an unprecedented scale during this era. What were the relationships of these processes to one another? How did each process serve to catalyze and fuel the others? Describe the various attempts at labor organization in this era, from the Molly Maguires to the Knights of Labor and American Federation of Labor. How were the goals, philosophies, and tactics of these groups similar and different? How did their agendas represent the concerns and grievances of their members and of workers more generally? Describe the various violent clashes between labor and management that occurred during this era. What do these events reveal about how each group had come to view the other? How did the new industrial order represent both new opportunities and new limitations for rural and working-class urban Americans? How did the emergent consumer culture change what it meant to be “American” at the turn of the century?	oercommons	2025-03-18T00:37:00.398654	null	{ "license": "Creative Commons - Attribution - https://creativecommons.org/licenses/by/4.0/", "url": "https://oercommons.org/courseware/lesson/15492/overview", "title": "U.S. History, Industrialization and the Rise of Big Business, 1870-1900", "author": null }
https://oercommons.org/courseware/lesson/15456/overview	Introduction Overview - Political Corruption in Postbellum America - Key Political Issues: Patronage, Tariffs, and Gold - Farmers Revolt in the Populist Era - Social and Labor Unrest in the 1890s Nine new slave states entered the Union between 1789 and 1860, rapidly expanding and transforming the South into a region of economic growth built on slave labor. In the image above (Figure), innumerable slaves load cargo onto a steamship in the Port of New Orleans, the commercial center of the antebellum South, while two well-dressed white men stand by talking. Commercial activity extends as far as the eye can see. By the mid-nineteenth century, southern commercial centers like New Orleans had become home to the greatest concentration of wealth in the United States. While most white southerners did not own slaves, they aspired to join the ranks of elite slaveholders, who played a key role in the politics of both the South and the nation. Meanwhile, slavery shaped the culture and society of the South, which rested on a racial ideology of white supremacy and a vision of the United States as a white man’s republic. Slaves endured the traumas of slavery by creating their own culture and using the Christian message of redemption to find hope for a world of freedom without violence.	oercommons	2025-03-18T00:37:00.414749	null	{ "license": "Creative Commons - Attribution - https://creativecommons.org/licenses/by/4.0/", "url": "https://oercommons.org/courseware/lesson/15456/overview", "title": "U.S. History, Cotton is King: The Antebellum South, 1800–1860", "author": null }
https://oercommons.org/courseware/lesson/15457/overview	The Economics of Cotton Overview By the end of this section, you will be able to: - Explain the labor-intensive processes of cotton production - Describe the importance of cotton to the Atlantic and American antebellum economy In the antebellum era—that is, in the years before the Civil War—American planters in the South continued to grow Chesapeake tobacco and Carolina rice as they had in the colonial era. Cotton, however, emerged as the antebellum South’s major commercial crop, eclipsing tobacco, rice, and sugar in economic importance. By 1860, the region was producing two-thirds of the world’s cotton. In 1793, Eli Whitney revolutionized the production of cotton when he invented the cotton gin, a device that separated the seeds from raw cotton. Suddenly, a process that was extraordinarily labor-intensive when done by hand could be completed quickly and easily. American plantation owners, who were searching for a successful staple crop to compete on the world market, found it in cotton. As a commodity, cotton had the advantage of being easily stored and transported. A demand for it already existed in the industrial textile mills in Great Britain, and in time, a steady stream of slave-grown American cotton would also supply northern textile mills. Southern cotton, picked and processed by American slaves, helped fuel the nineteenth-century Industrial Revolution in both the United States and Great Britain. KING COTTON Almost no cotton was grown in the United States in 1787, the year the federal constitution was written. However, following the War of 1812, a huge increase in production resulted in the so-called cotton boom, and by midcentury, cotton became the key cash crop (a crop grown to sell rather than for the farmer’s sole use) of the southern economy and the most important American commodity. By 1850, of the 3.2 million slaves in the country’s fifteen slave states, 1.8 million were producing cotton; by 1860, slave labor was producing over two billion pounds of cotton per year. Indeed, American cotton soon made up two-thirds of the global supply, and production continued to soar. By the time of the Civil War, South Carolina politician James Hammond confidently proclaimed that the North could never threaten the South because “cotton is king.” The crop grown in the South was a hybrid: Gossypium barbadense, known as Petit Gulf cotton, a mix of Mexican, Georgia, and Siamese strains. Petit Gulf cotton grew extremely well in different soils and climates. It dominated cotton production in the Mississippi River Valley—home of the new slave states of Louisiana, Mississippi, Arkansas, Tennessee, Kentucky, and Missouri—as well as in other states like Texas. Whenever new slave states entered the Union, white slaveholders sent armies of slaves to clear the land in order to grow and pick the lucrative crop. The phrase “to be sold down the river,” used by Harriet Beecher Stowe in her 1852 novel Uncle Tom’s Cabin, refers to this forced migration from the upper southern states to the Deep South, lower on the Mississippi, to grow cotton. The slaves who built this cotton kingdom with their labor started by clearing the land. Although the Jeffersonian vision of the settlement of new U.S. territories entailed white yeoman farmers single-handedly carving out small independent farms, the reality proved quite different. Entire old-growth forests and cypress swamps fell to the axe as slaves labored to strip the vegetation to make way for cotton. With the land cleared, slaves readied the earth by plowing and planting. To ambitious white planters, the extent of new land available for cotton production seemed almost limitless, and many planters simply leapfrogged from one area to the next, abandoning their fields every ten to fifteen years after the soil became exhausted. Theirs was a world of mobility and restlessness, a constant search for the next area to grow the valuable crop. Slaves composed the vanguard of this American expansion to the West. Cotton planting took place in March and April, when slaves planted seeds in rows around three to five feet apart. Over the next several months, from April to August, they carefully tended the plants. Weeding the cotton rows took significant energy and time. In August, after the cotton plants had flowered and the flowers had begun to give way to cotton bolls (the seed-bearing capsule that contains the cotton fiber), all the plantation’s slaves—men, women, and children—worked together to pick the crop (Figure). On each day of cotton picking, slaves went to the fields with sacks, which they would fill as many times as they could. The effort was laborious, and a white “driver” employed the lash to make slaves work as quickly as possible. Cotton planters projected the amount of cotton they could harvest based on the number of slaves under their control. In general, planters expected a good “hand,” or slave, to work ten acres of land and pick two hundred pounds of cotton a day. An overseer or master measured each individual slave’s daily yield. Great pressure existed to meet the expected daily amount, and some masters whipped slaves who picked less than expected. Cotton picking occurred as many as seven times a season as the plant grew and continued to produce bolls through the fall and early winter. During the picking season, slaves worked from sunrise to sunset with a ten-minute break at lunch; many slaveholders tended to give them little to eat, since spending on food would cut into their profits. Other slaveholders knew that feeding slaves could increase productivity and therefore provided what they thought would help ensure a profitable crop. The slaves’ day didn’t end after they picked the cotton; once they had brought it to the gin house to be weighed, they then had to care for the animals and perform other chores. Indeed, slaves often maintained their own gardens and livestock, which they tended after working the cotton fields, in order to supplement their supply of food. Sometimes the cotton was dried before it was ginned (put through the process of separating the seeds from the cotton fiber). The cotton gin allowed a slave to remove the seeds from fifty pounds of cotton a day, compared to one pound if done by hand. After the seeds had been removed, the cotton was pressed into bales. These bales, weighing about four hundred to five hundred pounds, were wrapped in burlap cloth and sent down the Mississippi River. Visit the Internet Archive to watch a 1937 WPA film showing cotton bales being loaded onto a steamboat. As the cotton industry boomed in the South, the Mississippi River quickly became the essential water highway in the United States. Steamboats, a crucial part of the transportation revolution thanks to their enormous freight-carrying capacity and ability to navigate shallow waterways, became a defining component of the cotton kingdom. Steamboats also illustrated the class and social distinctions of the antebellum age. While the decks carried precious cargo, ornate rooms graced the interior. In these spaces, whites socialized in the ship’s saloons and dining halls while black slaves served them (Figure). Investors poured huge sums into steamships. In 1817, only seventeen plied the waters of western rivers, but by 1837, there were over seven hundred steamships in operation. Major new ports developed at St. Louis, Missouri; Memphis, Tennessee; and other locations. By 1860, some thirty-five hundred vessels were steaming in and out of New Orleans, carrying an annual cargo made up primarily of cotton that amounted to $220 million worth of goods (approximately $6.5 billion in 2014 dollars). New Orleans had been part of the French empire before the United States purchased it, along with the rest of the Louisiana Territory, in 1803. In the first half of the nineteenth century, it rose in prominence and importance largely because of the cotton boom, steam-powered river traffic, and its strategic position near the mouth of the Mississippi River. Steamboats moved down the river transporting cotton grown on plantations along the river and throughout the South to the port at New Orleans. From there, the bulk of American cotton went to Liverpool, England, where it was sold to British manufacturers who ran the cotton mills in Manchester and elsewhere. This lucrative international trade brought new wealth and new residents to the city. By 1840, New Orleans alone had 12 percent of the nation’s total banking capital, and visitors often commented on the great cultural diversity of the city. In 1835, Joseph Holt Ingraham wrote: “Truly does New-Orleans represent every other city and nation upon earth. I know of none where is congregated so great a variety of the human species.” Slaves, cotton, and the steamship transformed the city from a relatively isolated corner of North America in the eighteenth century to a thriving metropolis that rivaled New York in importance (Figure). THE DOMESTIC SLAVE TRADE The South’s dependence on cotton was matched by its dependence on slaves to harvest the cotton. Despite the rhetoric of the Revolution that “all men are created equal,” slavery not only endured in the American republic but formed the very foundation of the country’s economic success. Cotton and slavery occupied a central—and intertwined—place in the nineteenth-century economy. In 1807, the U.S. Congress abolished the foreign slave trade, a ban that went into effect on January 1, 1808. After this date, importing slaves from Africa became illegal in the United States. While smuggling continued to occur, the end of the international slave trade meant that domestic slaves were in very high demand. Fortunately for Americans whose wealth depended upon the exploitation of slave labor, a fall in the price of tobacco had caused landowners in the Upper South to reduce their production of this crop and use more of their land to grow wheat, which was far more profitable. While tobacco was a labor-intensive crop that required many people to cultivate it, wheat was not. Former tobacco farmers in the older states of Virginia and Maryland found themselves with “surplus” slaves whom they were obligated to feed, clothe, and shelter. Some slaveholders responded to this situation by freeing slaves; far more decided to sell their excess bondsmen. Virginia and Maryland therefore took the lead in the domestic slave trade, the trading of slaves within the borders of the United States. The domestic slave trade offered many economic opportunities for white men. Those who sold their slaves could realize great profits, as could the slave brokers who served as middlemen between sellers and buyers. Other white men could benefit from the trade as owners of warehouses and pens in which slaves were held, or as suppliers of clothing and food for slaves on the move. Between 1790 and 1859, slaveholders in Virginia sold more than half a million slaves. In the early part of this period, many of these slaves were sold to people living in Kentucky, Tennessee, and North and South Carolina. By the 1820s, however, people in Kentucky and the Carolinas had begun to sell many of their slaves as well. Maryland slave dealers sold at least 185,000 slaves. Kentucky slaveholders sold some seventy-one thousand individuals. Most of the slave traders carried these slaves further south to Alabama, Louisiana, and Mississippi. New Orleans, the hub of commerce, boasted the largest slave market in the United States and grew to become the nation’s fourth-largest city as a result. Natchez, Mississippi, had the second-largest market. In Virginia, Maryland, the Carolinas, and elsewhere in the South, slave auctions happened every day. All told, the movement of slaves in the South made up one of the largest forced internal migrations in the United States. In each of the decades between 1820 and 1860, about 200,000 people were sold and relocated. The 1800 census recorded over one million African Americans, of which nearly 900,000 were slaves. By 1860, the total number of African Americans increased to 4.4 million, and of that number, 3.95 million were held in bondage. For many slaves, the domestic slave trade incited the terror of being sold away from family and friends. Solomon Northup Remembers the New Orleans Slave Market Solomon Northup was a free black man living in Saratoga, New York, when he was kidnapped and sold into slavery in 1841. He later escaped and wrote a book about his experiences: Twelve Years a Slave. Narrative of Solomon Northup, a Citizen of New-York, Kidnapped in Washington City in 1841 and Rescued in 1853 (the basis of a 2013 Academy Award–winning film). This excerpt derives from Northup’s description of being sold in New Orleans, along with fellow slave Eliza and her children Randall and Emily. One old gentleman, who said he wanted a coachman, appeared to take a fancy to me. . . . The same man also purchased Randall. The little fellow was made to jump, and run across the floor, and perform many other feats, exhibiting his activity and condition. All the time the trade was going on, Eliza was crying aloud, and wringing her hands. She besought the man not to buy him, unless he also bought her self and Emily. . . . Freeman turned round to her, savagely, with his whip in his uplifted hand, ordering her to stop her noise, or he would flog her. He would not have such work—such snivelling; and unless she ceased that minute, he would take her to the yard and give her a hundred lashes. . . . Eliza shrunk before him, and tried to wipe away her tears, but it was all in vain. She wanted to be with her children, she said, the little time she had to live. All the frowns and threats of Freeman, could not wholly silence the afflicted mother. What does Northup’s narrative tell you about the experience of being a slave? How does he characterize Freeman, the slave trader? How does he characterize Eliza? THE SOUTH IN THE AMERICAN AND WORLD MARKETS The first half of the nineteenth century saw a market revolution in the United States, one in which industrialization brought changes to both the production and the consumption of goods. Some southerners of the time believed that their region’s reliance on a single cash crop and its use of slaves to produce it gave the South economic independence and made it immune from the effects of these changes, but this was far from the truth. Indeed, the production of cotton brought the South more firmly into the larger American and Atlantic markets. Northern mills depended on the South for supplies of raw cotton that was then converted into textiles. But this domestic cotton market paled in comparison to the Atlantic market. About 75 percent of the cotton produced in the United States was eventually exported abroad. Exporting at such high volumes made the United States the undisputed world leader in cotton production. Between the years 1820 and 1860, approximately 80 percent of the global cotton supply was produced in the United States. Nearly all the exported cotton was shipped to Great Britain, fueling its burgeoning textile industry and making the powerful British Empire increasingly dependent on American cotton and southern slavery. The power of cotton on the world market may have brought wealth to the South, but it also increased its economic dependence on other countries and other parts of the United States. Much of the corn and pork that slaves consumed came from farms in the West. Some of the inexpensive clothing, called “slops,” and shoes worn by slaves were manufactured in the North. The North also supplied the furnishings found in the homes of both wealthy planters and members of the middle class. Many of the trappings of domestic life, such as carpets, lamps, dinnerware, upholstered furniture, books, and musical instruments—all the accoutrements of comfortable living for southern whites—were made in either the North or Europe. Southern planters also borrowed money from banks in northern cities, and in the southern summers, took advantage of the developments in transportation to travel to resorts at Saratoga, New York; Litchfield, Connecticut; and Newport, Rhode Island. Section Summary In the years before the Civil War, the South produced the bulk of the world’s supply of cotton. The Mississippi River Valley slave states became the epicenter of cotton production, an area of frantic economic activity where the landscape changed dramatically as land was transformed from pinewoods and swamps into cotton fields. Cotton’s profitability relied on the institution of slavery, which generated the product that fueled cotton mill profits in the North. When the international slave trade was outlawed in 1808, the domestic slave trade exploded, providing economic opportunities for whites involved in many aspects of the trade and increasing the possibility of slaves’ dislocation and separation from kin and friends. Although the larger American and Atlantic markets relied on southern cotton in this era, the South depended on these other markets for food, manufactured goods, and loans. Thus, the market revolution transformed the South just as it had other regions. Review Questions Which of the following was not one of the effects of the cotton boom? - U.S. trade increased with France and Spain. - Northern manufacturing expanded. - The need for slave labor grew. - Port cities like New Orleans expanded. Hint: A The abolition of the foreign slave trade in 1807 led to _______. - a dramatic decrease in the price and demand for slaves - the rise of a thriving domestic slave trade - a reform movement calling for the complete end to slavery in the United States - the decline of cotton production Hint: B Why did some southerners believe their region was immune to the effects of the market revolution? Why was this thinking misguided? Hint: Some southerners believed that their region’s monopoly over the lucrative cotton crop—on which both the larger American and Atlantic markets depended—and their possession of a slave labor force allowed the South to remain independent from the market revolution. However, the very cotton that provided the South with such economic potency also increased its reliance on the larger U.S. and world markets, which supplied—among other things—the food and clothes slaves needed, the furniture and other manufactured goods that defined the southern standard of comfortable living, and the banks from which southerners borrowed needed funds.	oercommons	2025-03-18T00:37:00.443048	null	{ "license": "Creative Commons - Attribution - https://creativecommons.org/licenses/by/4.0/", "url": "https://oercommons.org/courseware/lesson/15457/overview", "title": "U.S. History, Cotton is King: The Antebellum South, 1800–1860", "author": null }
https://oercommons.org/courseware/lesson/15458/overview	African Americans in the Antebellum United States Overview By the end of this section, you will be able to: - Discuss the similarities and differences in the lives of slaves and free blacks - Describe the independent culture and customs that slaves developed In addition to cotton, the great commodity of the antebellum South was human chattel. Slavery was the cornerstone of the southern economy. By 1850, about 3.2 million slaves labored in the United States, 1.8 million of whom worked in the cotton fields. Slaves faced arbitrary power abuses from whites; they coped by creating family and community networks. Storytelling, song, and Christianity also provided solace and allowed slaves to develop their own interpretations of their condition. LIFE AS A SLAVE Southern whites frequently relied upon the idea of paternalism—the premise that white slaveholders acted in the best interests of slaves, taking responsibility for their care, feeding, discipline, and even their Christian morality—to justify the existence of slavery. This grossly misrepresented the reality of slavery, which was, by any measure, a dehumanizing, traumatizing, and horrifying human disaster and crime against humanity. Nevertheless, slaves were hardly passive victims of their conditions; they sought and found myriad ways to resist their shackles and develop their own communities and cultures. Slaves often used the notion of paternalism to their advantage, finding opportunities within this system to engage in acts of resistance and win a degree of freedom and autonomy. For example, some slaves played into their masters’ racism by hiding their intelligence and feigning childishness and ignorance. The slaves could then slow down the workday and sabotage the system in small ways by “accidentally” breaking tools, for example; the master, seeing his slaves as unsophisticated and childlike, would believe these incidents were accidents rather than rebellions. Some slaves engaged in more dramatic forms of resistance, such as poisoning their masters slowly. Other slaves reported rebellious slaves to their masters, hoping to gain preferential treatment. Slaves who informed their masters about planned slave rebellions could often expect the slaveholder’s gratitude and, perhaps, more lenient treatment. Such expectations were always tempered by the individual personality and caprice of the master. Slaveholders used both psychological coercion and physical violence to prevent slaves from disobeying their wishes. Often, the most efficient way to discipline slaves was to threaten to sell them. The lash, while the most common form of punishment, was effective but not efficient; whippings sometimes left slaves incapacitated or even dead. Slave masters also used punishment gear like neck braces, balls and chains, leg irons, and paddles with holes to produce blood blisters. Slaves lived in constant terror of both physical violence and separation from family and friends (Figure). Under southern law, slaves could not marry. Nonetheless, some slaveholders allowed marriages to promote the birth of children and to foster harmony on plantations. Some masters even forced certain slaves to form unions, anticipating the birth of more children (and consequently greater profits) from them. Masters sometimes allowed slaves to choose their own partners, but they could also veto a match. Slave couples always faced the prospect of being sold away from each other, and, once they had children, the horrifying reality that their children could be sold and sent away at any time. Browse a collection of first-hand narratives of slaves and former slaves at the National Humanities Center to learn more about the experience of slavery. Slave parents had to show their children the best way to survive under slavery. This meant teaching them to be discreet, submissive, and guarded around whites. Parents also taught their children through the stories they told. Popular stories among slaves included tales of tricksters, sly slaves, or animals like Brer Rabbit, who outwitted their antagonists (Figure). Such stories provided comfort in humor and conveyed the slaves’ sense of the wrongs of slavery. Slaves’ work songs commented on the harshness of their life and often had double meanings—a literal meaning that whites would not find offensive and a deeper meaning for slaves. African beliefs, including ideas about the spiritual world and the importance of African healers, survived in the South as well. Whites who became aware of non-Christian rituals among slaves labeled such practices as witchcraft. Among Africans, however, the rituals and use of various plants by respected slave healers created connections between the African past and the American South while also providing a sense of community and identity for slaves. Other African customs, including traditional naming patterns, the making of baskets, and the cultivation of certain native African plants that had been brought to the New World, also endured. African Americans and Christian Spirituals Many slaves embraced Christianity. Their masters emphasized a scriptural message of obedience to whites and a better day awaiting slaves in heaven, but slaves focused on the uplifting message of being freed from bondage. The styles of worship in the Methodist and Baptist churches, which emphasized emotional responses to scripture, attracted slaves to those traditions and inspired some to become preachers. Spiritual songs that referenced the Exodus (the biblical account of the Hebrews’ escape from slavery in Egypt), such as “Roll, Jordan, Roll,” allowed slaves to freely express messages of hope, struggle, and overcoming adversity (Figure). What imagery might the Jordan River suggest to slaves working in the Deep South? What lyrics in this song suggest redemption and a better world ahead? Listen to a rendition of “Roll, Jordan, Roll” from the movie based on Solomon Northup’s memoir and life. THE FREE BLACK POPULATION Complicating the picture of the antebellum South was the existence of a large free black population. In fact, more free blacks lived in the South than in the North; roughly 261,000 lived in slave states, while 226,000 lived in northern states without slavery. Most free blacks did not live in the Lower, or Deep South: the states of Alabama, Arkansas, Florida, Georgia, Louisiana, Mississippi, South Carolina, and Texas. Instead, the largest number lived in the upper southern states of Delaware, Maryland, Virginia, North Carolina, and later Kentucky, Missouri, Tennessee, and the District of Columbia. Part of the reason for the large number of free blacks living in slave states were the many instances of manumission—the formal granting of freedom to slaves—that occurred as a result of the Revolution, when many slaveholders put into action the ideal that “all men are created equal” and freed their slaves. The transition in the Upper South to the staple crop of wheat, which did not require large numbers of slaves to produce, also spurred manumissions. Another large group of free blacks in the South had been free residents of Louisiana before the 1803 Louisiana Purchase, while still other free blacks came from Cuba and Haiti. Most free blacks in the South lived in cities, and a majority of free blacks were lighter-skinned women, a reflection of the interracial unions that formed between white men and black women. Everywhere in the United States blackness had come to be associated with slavery, the station at the bottom of the social ladder. Both whites and those with African ancestry tended to delineate varying degrees of lightness in skin color in a social hierarchy. In the slaveholding South, different names described one’s distance from blackness or whiteness: mulattos (those with one black and one white parent), quadroons (those with one black grandparent), and octoroons (those with one black great-grandparent) (Figure). Lighter-skinned blacks often looked down on their darker counterparts, an indication of the ways in which both whites and blacks internalized the racism of the age. Some free blacks in the South owned slaves of their own. Andrew Durnford, for example, was born in New Orleans in 1800, three years before the Louisiana Purchase. His father was white, and his mother was a free black. Durnford became an American citizen after the Louisiana Purchase, rising to prominence as a Louisiana sugar planter and slaveholder. William Ellison, another free black who amassed great wealth and power in the South, was born a slave in 1790 in South Carolina. After buying his freedom and that of his wife and daughter, he proceeded to purchase his own slaves, whom he then put to work manufacturing cotton gins. By the eve of the Civil War, Ellison had become one of the richest and largest slaveholders in the entire state. The phenomenon of free blacks amassing large fortunes within a slave society predicated on racial difference, however, was exceedingly rare. Most free blacks in the South lived under the specter of slavery and faced many obstacles. Beginning in the early nineteenth century, southern states increasingly made manumission of slaves illegal. They also devised laws that divested free blacks of their rights, such as the right to testify against whites in court or the right to seek employment where they pleased. Interestingly, it was in the upper southern states that such laws were the harshest. In Virginia, for example, legislators made efforts to require free blacks to leave the state. In parts of the Deep South, free blacks were able to maintain their rights more easily. The difference in treatment between free blacks in the Deep South and those in the Upper South, historians have surmised, came down to economics. In the Deep South, slavery as an institution was strong and profitable. In the Upper South, the opposite was true. The anxiety of this economic uncertainty manifested in the form of harsh laws that targeted free blacks. SLAVE REVOLTS Slaves resisted their enslavement in small ways every day, but this resistance did not usually translate into mass uprisings. Slaves understood that the chances of ending slavery through rebellion were slim and would likely result in massive retaliation; many also feared the risk that participating in such actions would pose to themselves and their families. White slaveholders, however, constantly feared uprisings and took drastic steps, including torture and mutilation, whenever they believed that rebellions might be simmering. Gripped by the fear of insurrection, whites often imagined revolts to be in the works even when no uprising actually happened. At least two major slave uprisings did occur in the antebellum South. In 1811, a major rebellion broke out in the sugar parishes of the booming territory of Louisiana. Inspired by the successful overthrow of the white planter class in Haiti, Louisiana slaves took up arms against planters. Perhaps as many five hundred slaves joined the rebellion, led by Charles Deslondes, a mixed-race slave driver on a sugar plantation owned by Manuel Andry. The revolt began in January 1811 on Andry’s plantation. Deslondes and other slaves attacked the Andry household, where they killed the slave master’s son (although Andry himself escaped). The rebels then began traveling toward New Orleans, armed with weapons gathered at Andry’s plantation. Whites mobilized to stop the rebellion, but not before Deslondes and the other rebelling slaves set fire to three plantations and killed numerous whites. A small white force led by Andry ultimately captured Deslondes, whose body was mutilated and burned following his execution. Other slave rebels were beheaded, and their heads placed on pikes along the Mississippi River. The second rebellion, led by the slave Nat Turner, occurred in 1831 in Southampton County, Virginia. Turner had suffered not only from personal enslavement, but also from the additional trauma of having his wife sold away from him. Bolstered by Christianity, Turner became convinced that like Christ, he should lay down his life to end slavery. Mustering his relatives and friends, he began the rebellion August 22, killing scores of whites in the county. Whites mobilized quickly and within forty-eight hours had brought the rebellion to an end. Shocked by Nat Turner’s Rebellion, Virginia’s state legislature considered ending slavery in the state in order to provide greater security. In the end, legislators decided slavery would remain and that their state would continue to play a key role in the domestic slave trade. SLAVE MARKETS As discussed above, after centuries of slave trade with West Africa, Congress banned the further importation of slaves beginning in 1808. The domestic slave trade then expanded rapidly. As the cotton trade grew in size and importance, so did the domestic slave trade; the cultivation of cotton gave new life and importance to slavery, increasing the value of slaves. To meet the South’s fierce demand for labor, American smugglers illegally transferred slaves through Florida and later through Texas. Many more slaves arrived illegally from Cuba; indeed, Cubans relied on the smuggling of slaves to prop up their finances. The largest number of slaves after 1808, however, came from the massive, legal internal slave market in which slave states in the Upper South sold enslaved men, women, and children to states in the Lower South. For slaves, the domestic trade presented the full horrors of slavery as children were ripped from their mothers and fathers and families destroyed, creating heartbreak and alienation. Some slaveholders sought to increase the number of slave children by placing male slaves with fertile female slaves, and slave masters routinely raped their female slaves. The resulting births played an important role in slavery’s expansion in the first half of the nineteenth century, as many slave children were born as a result of rape. One account written by a slave named William J. Anderson captures the horror of sexual exploitation in the antebellum South. Anderson wrote about how a Mississippi slaveholder divested a poor female slave of all wearing apparel, tied her down to stakes, and whipped her with a handsaw until he broke it over her naked body. In process of time he ravished [raped] her person, and became the father of a child by her. Besides, he always kept a colored Miss in the house with him. This is another curse of Slavery—concubinage and illegitimate connections—which is carried on to an alarming extent in the far South. A poor slave man who lives close by his wife, is permitted to visit her but very seldom, and other men, both white and colored, cohabit with her. It is undoubtedly the worst place of incest and bigamy in the world. A white man thinks nothing of putting a colored man out to carry the fore row [front row in field work], and carry on the same sport with the colored man’s wife at the same time. Anderson, a devout Christian, recognized and explains in his narrative that one of the evils of slavery is the way it undermines the family. Anderson was not the only critic of slavery to emphasize this point. Frederick Douglass, a Maryland slave who escaped to the North in 1838, elaborated on this dimension of slavery in his 1845 narrative. He recounted how slave masters had to sell their own children whom they had with slave women to appease the white wives who despised their offspring. The selling of slaves was a major business enterprise in the antebellum South, representing a key part of the economy. White men invested substantial sums in slaves, carefully calculating the annual returns they could expect from a slave as well as the possibility of greater profits through natural increase. The domestic slave trade was highly visible, and like the infamous Middle Passage that brought captive Africans to the Americas, it constituted an equally disruptive and horrifying journey now called the second middle passage. Between 1820 and 1860, white American traders sold a million or more slaves in the domestic slave market. Groups of slaves were transported by ship from places like Virginia, a state that specialized in raising slaves for sale, to New Orleans, where they were sold to planters in the Mississippi Valley. Other slaves made the overland trek from older states like North Carolina to new and booming Deep South states like Alabama. New Orleans had the largest slave market in the United States (Figure). Slaveholders brought their slaves there from the East (Virginia, Maryland, and the Carolinas) and the West (Tennessee and Kentucky) to be sold for work in the Mississippi Valley. The slave trade benefited whites in the Chesapeake and Carolinas, providing them with extra income: A healthy young male slave in the 1850s could be sold for $1,000 (approximately $30,000 in 2014 dollars), and a planter who could sell ten such slaves collected a windfall. In fact, by the 1850s, the demand for slaves reached an all-time high, and prices therefore doubled. A slave who would have sold for $400 in the 1820s could command a price of $800 in the 1850s. The high price of slaves in the 1850s and the inability of natural increase to satisfy demands led some southerners to demand the reopening of the international slave trade, a movement that caused a rift between the Upper South and the Lower South. Whites in the Upper South who sold slaves to their counterparts in the Lower South worried that reopening the trade would lower prices and therefore hurt their profits. John Brown on Slave Life in Georgia A slave named John Brown lived in Virginia, North Carolina, and Georgia before he escaped and moved to England. While there, he dictated his autobiography to someone at the British and Foreign Anti-Slavery Society, who published it in 1855. I really thought my mother would have died of grief at being obliged to leave her two children, her mother, and her relations behind. But it was of no use lamenting, the few things we had were put together that night, and we completed our preparations for being parted for life by kissing one another over and over again, and saying good bye till some of us little ones fell asleep. . . . And here I may as well tell what kind of man our new master was. He was of small stature, and thin, but very strong. He had sandy hair, a very red face, and chewed tobacco. His countenance had a very cruel expression, and his disposition was a match for it. He was, indeed, a very bad man, and used to flog us dreadfully. He would make his slaves work on one meal a day, until quite night, and after supper, set them to burn brush or spin cotton. We worked from four in the morning till twelve before we broke our fast, and from that time till eleven or twelve at night . . . we labored eighteen hours a day. —John Brown, Slave Life in Georgia: A Narrative of the Life, Sufferings, and Escape of John Brown, A Fugitive Slave, Now in England, 1855 What features of the domestic slave trade does Brown’s narrative illuminate? Why do you think he brought his story to an antislavery society? How do you think people responded to this narrative? Read through several narratives at “Born in Slavery,” part of the American Memory collection at the Library of Congress. Do these narratives have anything in common? What differences can you find between them? Section Summary Slave labor in the antebellum South generated great wealth for plantation owners. Slaves, in contrast, endured daily traumas as the human property of masters. Slaves resisted their condition in a variety of ways, and many found some solace in Christianity and the communities they created in the slave quarters. While some free blacks achieved economic prosperity and even became slaveholders themselves, the vast majority found themselves restricted by the same white-supremacist assumptions upon which the institution of slavery was based. Review Questions Under the law in the antebellum South, slaves were ________. - servants - animals - property - indentures Hint: C How did both slaveholders and slaves use the concept of paternalism to their advantage? Hint: Southern whites often used paternalism to justify the institution of slavery, arguing that slaves, like children, needed the care, feeding, discipline, and moral and religious education that they could provide. Slaves often used this misguided notion to their advantage: By feigning ignorance and playing into slaveholders’ paternalistic perceptions of them, slaves found opportunities to resist their condition and gain a degree of freedom and autonomy.	oercommons	2025-03-18T00:37:00.473937	null	{ "license": "Creative Commons - Attribution - https://creativecommons.org/licenses/by/4.0/", "url": "https://oercommons.org/courseware/lesson/15458/overview", "title": "U.S. History, Cotton is King: The Antebellum South, 1800–1860", "author": null }
https://oercommons.org/courseware/lesson/15459/overview	Wealth and Culture in the South Overview By the end of this section, you will be able to: - Assess the distribution of wealth in the antebellum South - Describe the southern culture of honor - Identify the main proslavery arguments in the years prior to the Civil War During the antebellum years, wealthy southern planters formed an elite master class that wielded most of the economic and political power of the region. They created their own standards of gentility and honor, defining ideals of southern white manhood and womanhood and shaping the culture of the South. To defend the system of forced labor on which their economic survival and genteel lifestyles depended, elite southerners developed several proslavery arguments that they levied at those who would see the institution dismantled. SLAVERY AND THE WHITE CLASS STRUCTURE The South prospered, but its wealth was very unequally distributed. Upward social mobility did not exist for the millions of slaves who produced a good portion of the nation’s wealth, while poor southern whites envisioned a day when they might rise enough in the world to own slaves of their own. Because of the cotton boom, there were more millionaires per capita in the Mississippi River Valley by 1860 than anywhere else in the United States. However, in that same year, only 3 percent of whites owned more than fifty slaves, and two-thirds of white households in the South did not own any slaves at all (Figure). Distribution of wealth in the South became less democratic over time; fewer whites owned slaves in 1860 than in 1840. At the top of southern white society stood the planter elite, which comprised two groups. In the Upper South, an aristocratic gentry, generation upon generation of whom had grown up with slavery, held a privileged place. In the Deep South, an elite group of slaveholders gained new wealth from cotton. Some members of this group hailed from established families in the eastern states (Virginia and the Carolinas), while others came from humbler backgrounds. South Carolinian Nathaniel Heyward, a wealthy rice planter and member of the aristocratic gentry, came from an established family and sat atop the pyramid of southern slaveholders. He amassed an enormous estate; in 1850, he owned more than eighteen hundred slaves. When he died in 1851, he left an estate worth more than $2 million (approximately $63 million in 2014 dollars). As cotton production increased, new wealth flowed to the cotton planters. These planters became the staunchest defenders of slavery, and as their wealth grew, they gained considerable political power. One member of the planter elite was Edward Lloyd V, who came from an established and wealthy family of Talbot County, Maryland. Lloyd had inherited his position rather than rising to it through his own labors. His hundreds of slaves formed a crucial part of his wealth. Like many of the planter elite, Lloyd’s plantation was a masterpiece of elegant architecture and gardens (Figure). One of the slaves on Lloyd’s plantation was Frederick Douglass, who escaped in 1838 and became an abolitionist leader, writer, statesman, and orator in the North. In his autobiography, Douglass described the plantation’s elaborate gardens and racehorses, but also its underfed and brutalized slave population. Lloyd provided employment opportunities to other whites in Talbot County, many of whom served as slave traders and the “slave breakers” entrusted with beating and overworking unruly slaves into submission. Like other members of the planter elite, Lloyd himself served in a variety of local and national political offices. He was governor of Maryland from 1809 to 1811, a member of the House of Representatives from 1807 to 1809, and a senator from 1819 to 1826. As a representative and a senator, Lloyd defended slavery as the foundation of the American economy. Wealthy plantation owners like Lloyd came close to forming an American ruling class in the years before the Civil War. They helped shape foreign and domestic policy with one goal in view: to expand the power and reach of the cotton kingdom of the South. Socially, they cultivated a refined manner and believed whites, especially members of their class, should not perform manual labor. Rather, they created an identity for themselves based on a world of leisure in which horse racing and entertainment mattered greatly, and where the enslavement of others was the bedrock of civilization. Below the wealthy planters were the yeoman farmers, or small landowners (Figure). Below yeomen were poor, landless whites, who made up the majority of whites in the South. These landless white men dreamed of owning land and slaves and served as slave overseers, drivers, and traders in the southern economy. In fact, owning land and slaves provided one of the only opportunities for upward social and economic mobility. In the South, living the American dream meant possessing slaves, producing cotton, and owning land. Despite this unequal distribution of wealth, non-slaveholding whites shared with white planters a common set of values, most notably a belief in white supremacy. Whites, whether rich or poor, were bound together by racism. Slavery defused class tensions among them, because no matter how poor they were, white southerners had race in common with the mighty plantation owners. Non-slaveholders accepted the rule of the planters as defenders of their shared interest in maintaining a racial hierarchy. Significantly, all whites were also bound together by the constant, prevailing fear of slave uprisings. D. R. Hundley on the Southern Yeoman D. R. Hundley was a well-educated planter, lawyer, and banker from Alabama. Something of an amateur sociologist, he argued against the common northern assumption that the South was made up exclusively of two tiers of white residents: the very wealthy planter class and the very poor landless whites. In his 1860 book, Social Relations in Our Southern States, Hundley describes what he calls the “Southern Yeomen,” a social group he insists is roughly equivalent to the middle-class farmers of the North. But you have no Yeomen in the South, my dear Sir? Beg your pardon, our dear Sir, but we have—hosts of them. I thought you had only poor White Trash? Yes, we dare say as much—and that the moon is made of green cheese! . . . Know, then, that the Poor Whites of the South constitute a separate class to themselves; the Southern Yeomen are as distinct from them as the Southern Gentleman is from the Cotton Snob. Certainly the Southern Yeomen are nearly always poor, at least so far as this world’s goods are to be taken into account. As a general thing they own no slaves; and even in case they do, the wealthiest of them rarely possess more than from ten to fifteen. . . . The Southern Yeoman much resembles in his speech, religious opinions, household arrangements, indoor sports, and family traditions, the middle class farmers of the Northern States. He is fully as intelligent as the latter, and is on the whole much better versed in the lore of politics and the provisions of our Federal and State Constitutions. . . . [A]lthough not as a class pecuniarily interested in slave property, the Southern Yeomanry are almost unanimously pro-slavery in sentiment. Nor do we see how any honest, thoughtful person can reasonably find fault with them on this account. —D. R. Hundley, Social Relations in Our Southern States, 1860 What elements of social relations in the South is Hundley attempting to emphasize for his readers? In what respects might his position as an educated and wealthy planter influence his understanding of social relations in the South? Because race bound all whites together as members of the master race, non-slaveholding whites took part in civil duties. They served on juries and voted. They also engaged in the daily rounds of maintaining slavery by serving on neighborhood patrols to ensure that slaves did not escape and that rebellions did not occur. The practical consequence of such activities was that the institution of slavery, and its perpetuation, became a source of commonality among different economic and social tiers that otherwise were separated by a gulf of difference. Southern planters exerted a powerful influence on the federal government. Seven of the first eleven presidents owned slaves, and more than half of the Supreme Court justices who served on the court from its inception to the Civil War came from slaveholding states. However, southern white yeoman farmers generally did not support an active federal government. They were suspicious of the state bank and supported President Jackson’s dismantling of the Second Bank of the United States. They also did not support taxes to create internal improvements such as canals and railroads; to them, government involvement in the economic life of the nation disrupted what they perceived as the natural workings of the economy. They also feared a strong national government might tamper with slavery. Planters operated within a larger capitalist society, but the labor system they used to produce goods—that is, slavery—was similar to systems that existed before capitalism, such as feudalism and serfdom. Under capitalism, free workers are paid for their labor (by owners of capital) to produce commodities; the money from the sale of the goods is used to pay for the work performed. As slaves did not reap any earnings from their forced labor, some economic historians consider the antebellum plantation system a “pre-capitalist” system. HONOR IN THE SOUTH A complicated code of honor among privileged white southerners, dictating the beliefs and behavior of “gentlemen” and “ladies,” developed in the antebellum years. Maintaining appearances and reputation was supremely important. It can be argued that, as in many societies, the concept of honor in the antebellum South had much to do with control over dependents, whether slaves, wives, or relatives. Defending their honor and ensuring that they received proper respect became preoccupations of whites in the slaveholding South. To question another man’s assertions was to call his honor and reputation into question. Insults in the form of words or behavior, such as calling someone a coward, could trigger a rupture that might well end on the dueling ground (Figure). Dueling had largely disappeared in the antebellum North by the early nineteenth century, but it remained an important part of the southern code of honor through the Civil War years. Southern white men, especially those of high social status, settled their differences with duels, before which antagonists usually attempted reconciliation, often through the exchange of letters addressing the alleged insult. If the challenger was not satisfied by the exchange, a duel would often result. The dispute between South Carolina’s James Hammond and his erstwhile friend (and brother-in-law) Wade Hampton II illustrates the southern culture of honor and the place of the duel in that culture. A strong friendship bound Hammond and Hampton together. Both stood at the top of South Carolina’s society as successful, married plantation owners involved in state politics. Prior to his election as governor of the state in 1842, Hammond became sexually involved with each of Hampton’s four teenage daughters, who were his nieces by marriage. “[A]ll of them rushing on every occasion into my arms,” Hammond confided in his private diary, “covering me with kisses, lolling on my lap, pressing their bodies almost into mine . . . and permitting my hands to stray unchecked.” Hampton found out about these dalliances, and in keeping with the code of honor, could have demanded a duel with Hammond. However, Hampton instead tried to use the liaisons to destroy his former friend politically. This effort proved disastrous for Hampton, because it represented a violation of the southern code of honor. “As matters now stand,” Hammond wrote, “he [Hampton] is a convicted dastard who, not having nerve to redress his own wrongs, put forward bullies to do it for him. . . . To challenge me [to a duel] would be to throw himself upon my mercy for he knows I am not bound to meet him [for a duel].” Because Hampton’s behavior marked him as a man who lacked honor, Hammond was no longer bound to meet Hampton in a duel even if Hampton were to demand one. Hammond’s reputation, though tarnished, remained high in the esteem of South Carolinians, and the governor went on to serve as a U.S. senator from 1857 to 1860. As for the four Hampton daughters, they never married; their names were disgraced, not only by the whispered-about scandal but by their father’s actions in response to it; and no man of honor in South Carolina would stoop so low as to marry them. GENDER AND THE SOUTHERN HOUSEHOLD The antebellum South was an especially male-dominated society. Far more than in the North, southern men, particularly wealthy planters, were patriarchs and sovereigns of their own household. Among the white members of the household, labor and daily ritual conformed to rigid gender delineations. Men represented their household in the larger world of politics, business, and war. Within the family, the patriarchal male was the ultimate authority. White women were relegated to the household and lived under the thumb and protection of the male patriarch. The ideal southern lady conformed to her prescribed gender role, a role that was largely domestic and subservient. While responsibilities and experiences varied across different social tiers, women’s subordinate state in relation to the male patriarch remained the same. Writers in the antebellum period were fond of celebrating the image of the ideal southern woman (Figure). One such writer, Thomas Roderick Dew, president of Virginia’s College of William and Mary in the mid-nineteenth century, wrote approvingly of the virtue of southern women, a virtue he concluded derived from their natural weakness, piety, grace, and modesty. In his Dissertation on the Characteristic Differences Between the Sexes, he writes that southern women derive their power not by leading armies to combat, or of enabling her to bring into more formidable action the physical power which nature has conferred on her. No! It is but the better to perfect all those feminine graces, all those fascinating attributes, which render her the center of attraction, and which delight and charm all those who breathe the atmosphere in which she moves; and, in the language of Mr. Burke, would make ten thousand swords leap from their scabbards to avenge the insult that might be offered to her. By her very meekness and beauty does she subdue all around her. Such popular idealizations of elite southern white women, however, are difficult to reconcile with their lived experience: in their own words, these women frequently described the trauma of childbirth, the loss of children, and the loneliness of the plantation. Louisa Cheves McCord’s “Woman’s Progress” Louisa Cheves McCord was born in Charleston, South Carolina, in 1810. A child of some privilege in the South, she received an excellent education and became a prolific writer. As the excerpt from her poem “Woman’s Progress” indicates, some southern women also contributed to the idealization of southern white womanhood. Sweet Sister! stoop not thou to be a man! Man has his place as woman hers; and she As made to comfort, minister and help; Moulded for gentler duties, ill fulfils His jarring destinies. Her mission is To labour and to pray; to help, to heal, To soothe, to bear; patient, with smiles, to suffer; And with self-abnegation noble lose Her private interest in the dearer weal Of those she loves and lives for. Call not this— (The all-fulfilling of her destiny; She the world’s soothing mother)—call it not, With scorn and mocking sneer, a drudgery. The ribald tongue profanes Heaven’s holiest things, But holy still they are. The lowliest tasks Are sanctified in nobly acting them. Christ washed the apostles’ feet, not thus cast shame Upon the God-like in him. Woman lives Man’s constant prophet. If her life be true And based upon the instincts of her being, She is a living sermon of that truth Which ever through her gentle actions speaks, That life is given to labour and to love. —Louisa Susanna Cheves McCord, “Woman’s Progress,” 1853 What womanly virtues does Louisa Cheves McCord emphasize? How might her social status, as an educated southern woman of great privilege, influence her understanding of gender relations in the South? For slaveholding whites, the male-dominated household operated to protect gendered divisions and prevalent gender norms; for slave women, however, the same system exposed them to brutality and frequent sexual domination. The demands on the labor of slave women made it impossible for them to perform the role of domestic caretaker that was so idealized by southern men. That slaveholders put them out into the fields, where they frequently performed work traditionally thought of as male, reflected little the ideal image of gentleness and delicacy reserved for white women. Nor did the slave woman’s role as daughter, wife, or mother garner any patriarchal protection. Each of these roles and the relationships they defined was subject to the prerogative of a master, who could freely violate enslaved women’s persons, sell off their children, or separate them from their families. DEFENDING SLAVERY With the rise of democracy during the Jacksonian era in the 1830s, slaveholders worried about the power of the majority. If political power went to a majority that was hostile to slavery, the South—and the honor of white southerners—would be imperiled. White southerners keen on preserving the institution of slavery bristled at what they perceived to be northern attempts to deprive them of their livelihood. Powerful southerners like South Carolinian John C. Calhoun (Figure) highlighted laws like the Tariff of 1828 as evidence of the North’s desire to destroy the southern economy and, by extension, its culture. Such a tariff, he and others concluded, would disproportionately harm the South, which relied heavily on imports, and benefit the North, which would receive protections for its manufacturing centers. The tariff appeared to open the door for other federal initiatives, including the abolition of slavery. Because of this perceived threat to southern society, Calhoun argued that states could nullify federal laws. This belief illustrated the importance of the states’ rights argument to the southern states. It also showed slaveholders’ willingness to unite against the federal government when they believed it acted unjustly against their interests. As the nation expanded in the 1830s and 1840s, the writings of abolitionists—a small but vocal group of northerners committed to ending slavery—reached a larger national audience. White southerners responded by putting forth arguments in defense of slavery, their way of life, and their honor. Calhoun became a leading political theorist defending slavery and the rights of the South, which he saw as containing an increasingly embattled minority. He advanced the idea of a concurrent majority, a majority of a separate region (that would otherwise be in the minority of the nation) with the power to veto or disallow legislation put forward by a hostile majority. Calhoun’s idea of the concurrent majority found full expression in his 1850 essay “Disquisition on Government.” In this treatise, he wrote about government as a necessary means to ensure the preservation of society, since society existed to “preserve and protect our race.” If government grew hostile to society, then a concurrent majority had to take action, including forming a new government. “Disquisition on Government” advanced a profoundly anti-democratic argument. It illustrates southern leaders’ intense suspicion of democratic majorities and their ability to effect legislation that would challenge southern interests. Go to the Internet Archive to read John C. Calhoun’s “Disquisition on Government.” Why do you think he proposed the creation of a concurrent majority? White southerners reacted strongly to abolitionists’ attacks on slavery. In making their defense of slavery, they critiqued wage labor in the North. They argued that the Industrial Revolution had brought about a new type of slavery—wage slavery—and that this form of “slavery” was far worse than the slave labor used on southern plantations. Defenders of the institution also lashed out directly at abolitionists such as William Lloyd Garrison for daring to call into question their way of life. Indeed, Virginians cited Garrison as the instigator of Nat Turner’s 1831 rebellion. The Virginian George Fitzhugh contributed to the defense of slavery with his book Sociology for the South, or the Failure of Free Society (1854). Fitzhugh argued that laissez-faire capitalism, as celebrated by Adam Smith, benefited only the quick-witted and intelligent, leaving the ignorant at a huge disadvantage. Slaveholders, he argued, took care of the ignorant—in Fitzhugh’s argument, the slaves of the South. Southerners provided slaves with care from birth to death, he asserted; this offered a stark contrast to the wage slavery of the North, where workers were at the mercy of economic forces beyond their control. Fitzhugh’s ideas exemplified southern notions of paternalism. George Fitzhugh’s Defense of Slavery George Fitzhugh, a southern writer of social treatises, was a staunch supporter of slavery, not as a necessary evil but as what he argued was a necessary good, a way to take care of slaves and keep them from being a burden on society. He published Sociology for the South, or the Failure of Free Society in 1854, in which he laid out what he believed to be the benefits of slavery to both the slaves and society as a whole. According to Fitzhugh: [I]t is clear the Athenian democracy would not suit a negro nation, nor will the government of mere law suffice for the individual negro. He is but a grown up child and must be governed as a child . . . The master occupies towards him the place of parent or guardian. . . . The negro is improvident; will not lay up in summer for the wants of winter; will not accumulate in youth for the exigencies of age. He would become an insufferable burden to society. Society has the right to prevent this, and can only do so by subjecting him to domestic slavery. In the last place, the negro race is inferior to the white race, and living in their midst, they would be far outstripped or outwitted in the chase of free competition. . . . Our negroes are not only better off as to physical comfort than free laborers, but their moral condition is better. What arguments does Fitzhugh use to promote slavery? What basic premise underlies his ideas? Can you think of a modern parallel to Fitzhugh’s argument? The North also produced defenders of slavery, including Louis Agassiz, a Harvard professor of zoology and geology. Agassiz helped to popularize polygenism, the idea that different human races came from separate origins. According to this formulation, no single human family origin existed, and blacks made up a race wholly separate from the white race. Agassiz’s notion gained widespread popularity in the 1850s with the 1854 publication of George Gliddon and Josiah Nott’s Types of Mankind and other books. The theory of polygenism codified racism, giving the notion of black inferiority the lofty mantle of science. One popular advocate of the idea posited that blacks occupied a place in evolution between the Greeks and chimpanzees (Figure). Section Summary Although a small white elite owned the vast majority of slaves in the South, and most other whites could only aspire to slaveholders’ wealth and status, slavery shaped the social life of all white southerners in profound ways. Southern culture valued a behavioral code in which men’s honor, based on the domination of others and the protection of southern white womanhood, stood as the highest good. Slavery also decreased class tensions, binding whites together on the basis of race despite their inequalities of wealth. Several defenses of slavery were prevalent in the antebellum era, including Calhoun’s argument that the South’s “concurrent majority” could overrule federal legislation deemed hostile to southern interests; the notion that slaveholders’ care of their chattel made slaves better off than wage workers in the North; and the profoundly racist ideas underlying polygenism. Review Questions The largest group of whites in the South _______. - owned no slaves - owned between one and nine slaves each - owned between ten and ninety-nine slaves each - owned over one hundred slaves each Hint: A John C. Calhoun argued for greater rights for southerners with which idea? - polygenism - nullification - concurrent majority - paternalism Hint: C How did defenders of slavery use the concept of paternalism to structure their ideas? Hint: Defenders of slavery, such as George Fitzhugh, argued that only the clever and the bright could truly benefit within a laissez-faire economy. Premising their argument on the notion that slaves were, by nature, intellectually inferior and less able to compete, such defenders maintained that slaves were better off in the care of paternalistic masters. While northern workers found themselves trapped in wage slavery, they argued, southern slaves’ needs—for food, clothing, and shelter, among other things—were met by their masters’ paternal benevolence.	oercommons	2025-03-18T00:37:00.509086	null	{ "license": "Creative Commons - Attribution - https://creativecommons.org/licenses/by/4.0/", "url": "https://oercommons.org/courseware/lesson/15459/overview", "title": "U.S. History, Cotton is King: The Antebellum South, 1800–1860", "author": null }
https://oercommons.org/courseware/lesson/15460/overview	The Filibuster and the Quest for New Slave States Overview By the end of this section, you will be able to: - Explain the expansionist goals of advocates of slavery - Describe the filibuster expeditions undertaken during the antebellum era Southern expansionists had spearheaded the drive to add more territory to the United States. They applauded the Louisiana Purchase and fervently supported Indian removal, the annexation of Texas, and the Mexican-American War. Drawing inspiration from the annexation of Texas, proslavery expansionists hoped to replicate that feat by bringing Cuba and other territories into the United States and thereby enlarging the American empire of slavery. In the 1850s, the expansionist drive among white southerners intensified. Among southern imperialists, one way to push for the creation of an American empire of slavery was through the actions of filibusters—men who led unofficial military operations intended to seize land from foreign countries or foment revolution there. These unsanctioned military adventures were not part of the official foreign policy of the United States; American citizens simply formed themselves into private armies to forcefully annex new land without the government’s approval. An 1818 federal law made it a crime to undertake such adventures, which was an indication of both the reality of efforts at expansion through these illegal expeditions and the government’s effort to create a U.S. foreign policy. Nonetheless, Americans continued to filibuster throughout the nineteenth century. In 1819, an expedition of two hundred Americans invaded Spanish Texas, intent on creating a republic modeled on the United States, only to be driven out by Spanish forces. Using force, taking action, and asserting white supremacy in these militaristic drives were seen by many as an ideal of American male vigor. President Jackson epitomized this military prowess as an officer in the Tennessee militia, where earlier in the century he had played a leading role in ending the Creek War and driving Indian peoples out of Alabama and Georgia. His reputation helped him to win the presidency in 1828 and again in 1832. Filibustering plots picked up pace in the 1850s as the drive for expansion continued. Slaveholders looked south to the Caribbean, Mexico, and Central America, hoping to add new slave states. Spanish Cuba became the objective of many American slaveholders in the 1850s, as debate over the island dominated the national conversation. Many who urged its annexation believed Cuba had to be made part of the United States to prevent it from going the route of Haiti, with black slaves overthrowing their masters and creating another black republic, a prospect horrifying to many in the United States. Americans also feared that the British, who had an interest in the sugar island, would make the first move and snatch Cuba from the United States. Since Britain had outlawed slavery in its colonies in 1833, blacks on the island of Cuba would then be free. Narisco López, a Cuban who wanted to end Spanish control of the island, gained American support. He tried five times to take the island, with his last effort occurring in the summer of 1851 when he led an armed group from New Orleans. Thousands came out to cheer his small force as they set off to wrest Cuba from the Spanish. Unfortunately for López and his supporters, however, the effort to take Cuba did not produce the hoped-for spontaneous uprising of the Cuban people. Spanish authorities in Cuba captured and executed López and the American filibusters. Efforts to take Cuba continued under President Franklin Pierce, who had announced at his inauguration in 1853 his intention to pursue expansion. In 1854, American diplomats met in Ostend, Belgium, to find a way to gain Cuba. They wrote a secret memo, known as the Ostend Manifesto (thought to be penned by James Buchanan, who was elected president two years later), stating that if Spain refused to sell Cuba to the United States, the United States was justified in taking the island as a national security measure. The contents of this memo were supposed to remain secret, but details were leaked to the public, leading the House of Representatives to demand a copy. Many in the North were outraged over what appeared to be a southern scheme, orchestrated by what they perceived as the Slave Power—a term they used to describe the disproportionate influence that elite slaveholders wielded—to expand slavery. European powers also reacted with anger. Southern annexationists, however, applauded the effort to take Cuba. The Louisiana legislature in 1854 asked the federal government to take decisive action, and John Quitman, a former Mississippi governor, raised money from slaveholders to fund efforts to take the island. Read an 1860 editorial titled Annexation of Cuba Made Easy from the online archives of The New York Times. Does the author support annexation? Why or why not? Controversy around the Ostend Manifesto caused President Pierce to step back from the plan to take Cuba. After his election, President Buchanan, despite his earlier expansionist efforts, denounced filibustering as the action of pirates. Filibustering caused an even wider gulf between the North and the South (Figure). Cuba was not the only territory in slaveholders’ expansionist sights: some focused on Mexico and Central America. In 1855, Tennessee-born William Walker, along with an army of no more than sixty mercenaries, gained control of the Central American nation of Nicaragua. Previously, Walker had launched a successful invasion of Mexico, dubbing his conquered land the Republic of Sonora. In a relatively short period of time, Walker was dislodged from Sonora by Mexican authorities and forced to retreat back to the United States. His conquest of Nicaragua garnered far more attention, catapulting him into national popularity as the heroic embodiment of white supremacy (Figure). Why Nicaragua? Nicaragua presented a tempting target because it provided a quick route from the Caribbean to the Pacific: Only twelve miles of land stood between the Pacific Ocean, the inland Lake Nicaragua, and the river that drained into the Atlantic. Shipping from the East Coast to the West Coast of the United States had to travel either by land across the continent, south around the entire continent of South America, or through Nicaragua. Previously, American tycoon Cornelius Vanderbilt (Figure) had recognized the strategic importance of Nicaragua and worked with the Nicaraguan government to control shipping there. The filibustering of William Walker may have excited expansionist-minded southerners, but it greatly upset Vanderbilt’s business interests in the region. Walker clung to the racist, expansionist philosophies of the proslavery South. In 1856, Walker made slavery legal in Nicaragua—it had been illegal there for thirty years—in a move to gain the support of the South. He also reopened the slave trade. In 1856, he was elected president of Nicaragua, but in 1857, he was chased from the country. When he returned to Central America in 1860, he was captured by the British and released to Honduran authorities, who executed him by firing squad. Section Summary The decade of the 1850s witnessed various schemes to expand the American empire of slavery. The Ostend Manifesto articulated the right of the United States to forcefully seize Cuba if Spain would not sell it, while filibuster expeditions attempted to annex new slave states without the benefit of governmental approval. Those who pursued the goal of expanding American slavery believed they embodied the true spirit of white racial superiority. Review Questions Why did southern expansionists conduct filibuster expeditions? - to gain political advantage - to annex new slave states - to prove they could raise an army - to map unknown territories Hint: B The controversy at the heart of the Ostend Manifesto centered on the fate of: - Ostend, Belgium - Nicaragua - Cuba - Louisiana Hint: C Why did expansionists set their sights on the annexation of Spanish Cuba? Hint: Many slaveholding expansionists believed that the events of the Haitian Revolution could repeat themselves in Cuba, leading to the overthrow of slavery on the island and the creation of an independent black republic. Americans also feared that the British would seize Cuba—which, since Britain had outlawed slavery in its colonies in 1833, would render all slaves on the island free. Critical Thinking Questions Compare and contrast the steamboats of the antebellum years with technologies today. In your estimation, what modern technology compares to steamboats in its transformative power? Does the history of the cotton kingdom support or undermine the Jeffersonian vision of white farmers on self-sufficient farms? Explain your answer. Based on your reading of William J. Anderson’s and John Brown’s accounts, what types of traumas did slaves experience? How were the experiences of black women and men similar and different? What strategies did slaves employ to resist, revolt, and sustain their own independent communities and cultures? How did slaves use white southerners’ own philosophies—paternalism and Christianity, for example—to their advantage in these efforts? What are the major arguments put forward by proslavery advocates? How would you argue against their statements? Consider filibustering from the point of view of the Cuban or Nicaraguan people. If you lived in Cuba or Nicaragua, would you support filibustering? Why or why not?	oercommons	2025-03-18T00:37:00.538059	null	{ "license": "Creative Commons - Attribution - https://creativecommons.org/licenses/by/4.0/", "url": "https://oercommons.org/courseware/lesson/15460/overview", "title": "U.S. History, Cotton is King: The Antebellum South, 1800–1860", "author": null }
https://oercommons.org/courseware/lesson/15287/overview	Declaration of Independence When in the Course of human events, it becomes necessary for one people to dissolve the political bands which have connected them with another, and to assume among the powers of the earth, the separate and equal station to which the Laws of Nature and of Nature's God entitle them, a decent respect to the opinions of mankind requires that they should declare the causes which impel them to the separation. We hold these truths to be self-evident, that all men are created equal, that they are endowed by their Creator with certain unalienable Rights, that among these are Life, Liberty and the pursuit of Happiness. —That to secure these rights, Governments are instituted among Men, deriving their just powers from the consent of the governed, —That whenever any Form of Government becomes destructive of these ends, it is the Right of the People to alter or to abolish it, and to institute new Government, laying its foundation on such principles and organizing its powers in such form, as to them shall seem most likely to effect their Safety and Happiness. Prudence, indeed, will dictate that Governments long established should not be changed for light and transient causes; and accordingly all experience hath shewn, that mankind are more disposed to suffer, while evils are sufferable, than to right themselves by abolishing the forms to which they are accustomed. But when a long train of abuses and usurpations, pursuing invariably the same Object evinces a design to reduce them under absolute Despotism, it is their right, it is their duty, to throw off such Government, and to provide new Guards for their future security. —Such has been the patient sufferance of these Colonies; and such is now the necessity which constrains them to alter their former Systems of Government. The history of the present King of Great Britain is a history of repeated injuries and usurpations, all having in direct object the establishment of an absolute Tyranny over these States. To prove this, let Facts be submitted to a candid world. He has refused his Assent to Laws, the most wholesome and necessary for the public good. He has forbidden his Governors to pass Laws of immediate and pressing importance, unless suspended in their operation till his Assent should be obtained; and when so suspended, he has utterly neglected to attend to them. He has refused to pass other Laws for the accommodation of large districts of people, unless those people would relinquish the right of Representation in the Legislature, a right inestimable to them and formidable to tyrants only. He has called together legislative bodies at places unusual, uncomfortable, and distant from the depository of their public Records, for the sole purpose of fatiguing them into compliance with his measures. He has dissolved Representative Houses repeatedly, for opposing with manly firmness his invasions on the rights of the people. He has refused for a long time, after such dissolutions, to cause others to be elected; whereby the Legislative powers, incapable of Annihilation, have returned to the People at large for their exercise; the State remaining in the mean time exposed to all the dangers of invasion from without, and convulsions within. He has endeavoured to prevent the population of these States; for that purpose obstructing the Laws for Naturalization of Foreigners; refusing to pass others to encourage their migrations hither, and raising the conditions of new Appropriations of Lands. He has obstructed the Administration of Justice, by refusing his Assent to Laws for establishing Judiciary powers. He has made Judges dependent on his Will alone, for the tenure of their offices, and the amount and payment of their salaries. He has erected a multitude of New Offices, and sent hither swarms of Officers to harrass our people, and eat out their substance. He has kept among us, in times of peace, Standing Armies without the Consent of our legislatures. He has affected to render the Military independent of and superior to the Civil power. He has combined with others to subject us to a jurisdiction foreign to our constitution, and unacknowledged by our laws; giving his Assent to their Acts of pretended Legislation: For Quartering large bodies of armed troops among us: For protecting them, by a mock Trial, from punishment for any Murders which they should commit on the Inhabitants of these States: For cutting off our Trade with all parts of the world: For imposing Taxes on us without our Consent: For depriving us in many cases, of the benefits of Trial by Jury: For transporting us beyond Seas to be tried for pretended offences For abolishing the free System of English Laws in a neighbouring Province, establishing therein an Arbitrary government, and enlarging its Boundaries so as to render it at once an example and fit instrument for introducing the same absolute rule into these Colonies: For taking away our Charters, abolishing our most valuable Laws, and altering fundamentally the Forms of our Governments: For suspending our own Legislatures, and declaring themselves invested with power to legislate for us in all cases whatsoever. He has abdicated Government here, by declaring us out of his Protection and waging War against us. He has plundered our seas, ravaged our Coasts, burnt our towns, and destroyed the lives of our people. He is at this time transporting large Armies of foreign Mercenaries to compleat the works of death, desolation and tyranny, already begun with circumstances of Cruelty & perfidy scarcely paralleled in the most barbarous ages, and totally unworthy the Head of a civilized nation. He has constrained our fellow Citizens taken Captive on the high Seas to bear Arms against their Country, to become the executioners of their friends and Brethren, or to fall themselves by their Hands. He has excited domestic insurrections amongst us, and has endeavoured to bring on the inhabitants of our frontiers, the merciless Indian Savages, whose known rule of warfare, is an undistinguished destruction of all ages, sexes and conditions. In every stage of these Oppressions We have Petitioned for Redress in the most humble terms: Our repeated Petitions have been answered only by repeated injury. A Prince whose character is thus marked by every act which may define a Tyrant, is unfit to be the ruler of a free people. Nor have We been wanting in attentions to our Brittish brethren. We have warned them from time to time of attempts by their legislature to extend an unwarrantable jurisdiction over us. We have reminded them of the circumstances of our emigration and settlement here. We have appealed to their native justice and magnanimity, and we have conjured them by the ties of our common kindred to disavow these usurpations, which, would inevitably interrupt our connections and correspondence. They too have been deaf to the voice of justice and of consanguinity. We must, therefore, acquiesce in the necessity, which denounces our Separation, and hold them, as we hold the rest of mankind, Enemies in War, in Peace Friends. We, therefore, the Representatives of the united States of America, in General Congress, Assembled, appealing to the Supreme Judge of the world for the rectitude of our intentions, do, in the Name, and by Authority of the good People of these Colonies, solemnly publish and declare, That these United Colonies are, and of Right ought to be Free and Independent States; that they are Absolved from all Allegiance to the British Crown, and that all political connection between them and the State of Great Britain, is and ought to be totally dissolved; and that as Free and Independent States, they have full Power to levy War, conclude Peace, contract Alliances, establish Commerce, and to do all other Acts and Things which Independent States may of right do. And for the support of this Declaration, with a firm reliance on the protection of divine Providence, we mutually pledge to each other our Lives, our Fortunes and our sacred Honor. The 56 signatures on the Declaration appear in the positions indicated: Column 1 Georgia: Button Gwinnett Lyman Hall George Walton Column 2 North Carolina: William Hooper Joseph Hewes John Penn South Carolina: Edward Rutledge Thomas Heyward, Jr. Thomas Lynch, Jr. Arthur Middleton Column 3 Massachusetts: John Hancock Maryland: Samuel Chase William Paca Thomas Stone Charles Carroll of Carrollton Virginia: George Wythe Richard Henry Lee Thomas Jefferson Benjamin Harrison Thomas Nelson, Jr. Francis Lightfoot Lee Carter Braxton Column 4 Pennsylvania: Robert Morris Benjamin Rush Benjamin Franklin John Morton George Clymer James Smith George Taylor James Wilson George Ross Delaware: Caesar Rodney George Read Thomas McKean Column 5 New York: William Floyd Philip Livingston Francis Lewis Lewis Morris New Jersey: Richard Stockton John Witherspoon Francis Hopkinson John Hart Abraham Clark Column 6 New Hampshire: Josiah Bartlett William Whipple Massachusetts: Samuel Adams John Adams Robert Treat Paine Elbridge Gerry Rhode Island: Stephen Hopkins William Ellery Connecticut: Roger Sherman Samuel Huntington William Williams Oliver Wolcott New Hampshire: Matthew Thornton	oercommons	2025-03-18T00:37:00.563037	null	{ "license": "Creative Commons - Attribution - https://creativecommons.org/licenses/by/4.0/", "url": "https://oercommons.org/courseware/lesson/15287/overview", "title": "American Government, Declaration of Independence", "author": null }
https://oercommons.org/courseware/lesson/66276/overview	Glossary Overview Glossary Glossary: The Texas Legislature biennial sessions: In Texas, legislative sessions meet once every odd-numbered years, for 140 days bill: a proposed law that has been sponsored by a member of the legislature and submitted to the clerk of the House or Senate cracking: occurs when a constituency is divided between several districts in order to prevent it from achieving a majority in any one district. gerrymandering: the process in which voting districts are redrawn in a way to favor one party during elections legislative budget: the state budget that is prepared and submitted by the Legislative Budget Board (LBB) and that is fully considered by the House and Senate packing: occurs when a constituency or voting group is placed within a single district, thereby minimizing its influence in other districts. redistricting: the process of redrawing election districts and redistributing legislative representatives in the Texas House, Texas Senate, and U.S. House. Redistricting typically occurs every 10 years to reflect shifts in population or in response to legal challenges in existing districts single-member district: a district in which one official is elected rather than multiple officials. special session: a legislative session called by the governor that addresses an agenda set by him or her; lasts no longer than 30 days Voting Rights Act of 1965: mandates that electoral district lines cannot be drawn in such a manner as to “improperly dilute minorities’ voting power” License and Attribution CC LICENSED CONTENT, ORIGINAL The Texas Legislature: Glossary. Authored by: John Osterman. License: CC BY: Attribution	oercommons	2025-03-18T00:37:00.580185	05/05/2020	{ "license": "Creative Commons - Attribution - https://creativecommons.org/licenses/by/4.0/", "url": "https://oercommons.org/courseware/lesson/66276/overview", "title": "Texas Government 2.0, The Texas Legislature, Glossary", "author": "Kris Seago" }
https://oercommons.org/courseware/lesson/106234/overview	Education Standards Plot Coaster Lesson for 6th Grade Overview This resource details plot for students in 6th grade. It uses the plot diagram, but focuses on making the students see it as a roller coaster instead of a moutain. Introduction \| Anticipatory Set \| 1. Using a pencil and paper, describe how it feels to ride on a roller coaster. If you have never ridden on one before, describe what happens on a roller coaster. Teacher Note: Give the students some time to describe. Ask for volunteers to read what they wrote down. Connect it to plot by saying that coasters have a starting point, middle, and end. They also are interesting because of all of the twists and turns involved just like a story that has a solid plot. \| \| Instructional Activities (may take a few class periods/blocks) \| Using the Plot Coaster resource provided, have student take notes. Ensure that exposition, confict, rising action, climax, falling action, and resolution are all defined the way you wish to describe it to your students. Teacher Note: For climax, make sure to mention that although it looks like it happens in the middle, that is not always the case. Once students have the notes, direct their attention to a YouTube video of your choosing. I usually stick to pixar shorts because they are easy to follow. Have the students watch it completely, then go back and pause it at the specific parts. Have students list what they think each part represents on the plot coaster and why. Group students together and provide a blank plot coaster. Put on another video and replay it a few times. Instruct the students to wrie down the parts of plot. Once done, make sure to go over it. Have students get into groups once again. Choose a short story to read. The students now will be tasked with plotting the story on their own, but they will create their own roller coasters. You can have the students create roller coasters out of recycled objects or simply on paper. The students must label the parts of plot with the examples from the story. \| \| Closure \| Have students share their creations to the class OR have them do a gallery walk and leave comments about what they like on a piece of paper by the students' work. \|	oercommons	2025-03-18T00:37:00.602186	07/03/2023	{ "license": "Creative Commons - Attribution - https://creativecommons.org/licenses/by/4.0/", "url": "https://oercommons.org/courseware/lesson/106234/overview", "title": "Plot Coaster Lesson for 6th Grade", "author": "Paige Krempasky" }
https://oercommons.org/courseware/lesson/87989/overview	Spanish Civil War Overview The Spanish Civil War The onset of the Great Depression destabilized the economy of Spain and resulted in the collapse of the Spanish monarchy in 1931. After the establishment of a Republic, civil war erupted between Communists and Socialists on the left and the Spanish army on the right under the leadership of Francisco Franco. By 1939 Franco defeated his enemies and established a military dictatorship. Learning Objectives - Examine the development of Franco’s Fascist Spain. Key Terms / Key Concepts Falangism: a Fascist movement founded in Spain in 1933; the one legal party in Spain under the regime of Franco Francisco Franco: a Spanish general who ruled over Spain as a dictator for 36 years from 1939 until his death (He took control of Spain from the government of the Second Spanish Republic after winning the Civil War, and was in power until 1978, when the Spanish Constitution of 1978 went into effect.) personality cult: when an individual uses mass media, propaganda, or other methods to create an idealized, heroic, and at times worshipful image, often through unquestioned flattery and praise Spanish Civil War: a war from 1936 to 1939 between the Republicans (loyalists to the democratic, left leaning and relatively urban Second Spanish Republic along with Anarchists and Communists) and forces loyal to General Francisco Franco (Nationalists, Falangists, and Carlists - a largely aristocratic conservative group) Francisco Franco: El Caudillo Francisco Franco (December 4, 1892 – November 20, 1975) was a Spanish general who ruled over Spain as a dictator for 36 years from 1939 until his death. As a conservative and a monarchist military officer, he opposed the abolition of the monarchy and the establishment of a republic in 1931. With the 1936 elections, the conservative Spanish Confederation of Autonomous Right-wing Groups lost by a narrow margin and the leftist Popular Front came to power. This Popular Front was an alliance between Spanish Liberals and Communists. Intending to overthrow the republic, Franco worked with other like-minded generals in attempting a failed coup that precipitated the Spanish Civil War (1936 – 1939). With the death of the other generals during this war, Franco quickly became his faction’s only leader. After securing his position as military dictator, Franco eventually in 1947, restored the Spanish monarchy in name only with himself as regent. During the Civil War, Franco gained military support from various regimes and groups, especially Nazi Germany and the Fascist Italy. The opposition—or the Republican side—was supported by Spanish communists and anarchists, as well as the Soviet Union, Mexico, and the International Brigades. These brigades included volunteers from around the world who supported the Republic. Leaving half a million people dead, the war was eventually won by Franco in 1939. He established a military dictatorship, which he defined as a totalitarian state. Franco proclaimed himself Head of State and Government under the title El Caudillo, a term similar to Il Duce (Italian) for Benito Mussolini and Der Führer (German) for Adolf Hitler. Under Franco, Spain became a one-party state, as the various conservative and royalist factions were merged into the fascist party and other political parties were outlawed. Franco’s regime committed a series of violent human rights abuses against the Spanish people, which included the establishment of concentration camps and the use of forced labor and executions, mostly against political and ideological enemies, causing an estimated 200,000 to 400,000 deaths in more than 190 concentration camps over the course of his 36 years as dictator (1939 – 1975). During the last several decades of his regime, the number of executions declined considerably During World War II, Spain sympathized with its fellow Fascist European states, the Axis powers, Germany and Italy. Spain’s entry into the war on the Axis side was prevented largely by British Secret Intelligence Service (MI-6) efforts that included up to $200 million in bribes for Spanish officials to keep the regime from getting involved. Franco was also able to take advantage of the resources of the Axis Powers, while choosing to avoid becoming heavily involved in the Second World War. Ideology of Francoist Spain The consistent points in Francoism included authoritarianism, nationalism, national Catholicism, militarism, conservatism, anti-communism, and anti-liberalism. The Spanish State was authoritarian. It suppressed non-government trade unions and all political opponents across the political spectrum often through police repression. Most country towns and rural areas were patrolled by pairs of Guardia Civil—a military police made up of civilians, which functioned as a chief means of social control. Larger cities and capitals were mostly under the heavily armed Policía Armada, commonly called grises due to their grey uniforms. The Spanish state also enjoyed the broad support of the Roman Catholic Church. Many traditional Spanish Roman Catholics were relieved that Franco’s forces had crushed the atheistic, anti-clerical (anti-priests), Communists. Franco was also the focus of a personality cult which taught that he had been sent by Divine Providence to save the country from chaos and poverty. Franco’s Spanish nationalism promoted a unitary national identity by repressing Spain’s cultural diversity. Bullfighting and flamenco were promoted as national traditions, while those traditions not considered Spanish were suppressed. Franco’s view of Spanish tradition was somewhat artificial and arbitrary: while some regional traditions were suppressed, Flamenco, an Andalusian tradition, was considered part of a larger, national identity. All cultural activities were subject to censorship, and many were forbidden entirely, often in an erratic manner. Francoism professed a strong devotion to militarism, hypermasculinity, and the traditional role of women in society. A woman was to be loving to her parents and brothers and faithful to her husband, as well as reside with her family. Official propaganda confined women’s roles to family care and motherhood. Most progressive laws passed by the Second Republic were declared void. Women could not become judges, testify in trial, or become university professors. The Civil War had ravaged the Spanish economy. Infrastructure had been damaged, workers killed, and daily business severely hampered. For more than a decade after Franco’s victory, the economy improved little. Franco initially pursued a policy of autarky, cutting off almost all international trade. The policy had devastating effects, and the economy stagnated. Only black marketeers could enjoy an evident affluence. Up to 200,000 people died of starvation during the early years of Francoism, a period known as Los Años de Hambre (the Years of Hunger). This period coincided with the ravages of World War II (1939 – 1945). Falangism: Spanish Fascism Falangism was the official fascist ideology of Franco’s military dictatorship. Falangism was the political ideology of the Falange Española de las JONS when this political party was formed in Spain in 1934. Afterwards in 1937, Franco reformed this party as the Falange Española Tradicionalista y de las Juntas de Ofensiva Nacional Sindicalista (both known simply as the “Falange”). This new party remained the official party of the Spanish state until the collapse of this fascist regime soon after Franco’s death in 1975, Under the leadership of Franco, many of the more radical elements of Falangism considered fascist were diluted, and the party largely became an authoritarian, conservative ideology connected with Francoist Spain. Opponents of Franco’s changes to the party’s ideology included former Falange leader Manuel Hedilla. Falangism placed a strong emphasis on Catholic religious identity, though it held some secular views on the Church’s direct influence in society, as it believed that the state should have the supreme authority over the nation. Falangism emphasized the need for authority, hierarchy, and order in society. Falangism was also anti-communist, anti-capitalist, anti-democratic, and anti-liberal. Under Franco’s leadership, however, the Falange abandoned its original anti-capitalist tendencies, declaring the ideology to be fully compatible with capitalism. The Falange’s original manifesto, the “Twenty-Seven Points,” declared that Falangism supported the unity of Spain and the elimination of regional separatism that existed among the Basques and Catalans of Northwestern and Northeastern Spain. This manifesto established a dictatorship led by the Falange and used violence to regenerate Spain. It also promoted the revival and development of the Spanish Empire overseas and championed a social revolution to create a national syndicalist economy. Syndicalists hoped to transfer the ownership and control of the means of production (i.e., factories) and distribution to state controlled workers' unions. This new economy was to mutually organize and control economic activity, agrarian reform, industrial expansion, while respecting private property except for nationalizing credit facilities (i.e., banks) to prevent capitalist usury (charging interest on loans). It criminalized strikes by employees and lockouts by employers as illegal acts. Falangism supported the state to have jurisdiction of setting wages. The Franco-era Falange supported the development of workers cooperatives (employee-owned businesses) such as the Mondragon Corporation in 1956, because it bolstered the Francoist claim of the nonexistence of an oppressed working class in Spain during his rule. The Mondragon Corporation still operates in Spain today, but the Falange Española Tradicionalista y de las Juntas de Ofensiva Nacional Sindicalista dissolved in 1977 soon after Franco’s death in 1975. Attributions Title Image https://commons.wikimedia.org/wiki/File:Condor_Legion_marching_during_the_Spanish_Civil_War.jpg Photo of a victory parade of Spanish national troops and the German Condor Legion in honor of General Francisco Franco in the festively decorated streets of Ciudad de Leon, Castile and Leon on May 22, 1939 - Unknown authorUnknown author, Public domain, via Wikimedia Commons Adapted from: https://courses.lumenlearning.com/boundless-worldhistory/chapter/the-rise-of-fascism/	oercommons	2025-03-18T00:37:00.632434	Neil Greenwood	{ "license": "Creative Commons - Attribution - https://creativecommons.org/licenses/by/4.0/", "url": "https://oercommons.org/courseware/lesson/87989/overview", "title": "Statewide Dual Credit World History, The Catastrophe of the Modern Era: 1919-Present CE, Chapter 13: Post WWI, Spanish Civil War", "author": "Anna McCollum" }
https://oercommons.org/courseware/lesson/58764/overview	The Cardiovascular System: Blood Overview The Cardiovascular System: Blood Introduction Figure 18.1 Blood Cells A single drop of blood contains millions of red blood cells, white blood cells, and platelets. One of each type is shown here, isolated from a scanning electron micrograph. CHAPTER OBJECTIVES After studying this chapter, you will be able to: - Identify the primary functions of blood, its fluid and cellular components, and its physical characteristics - Identify the most important proteins and other solutes present in blood plasma - Describe the formation of the formed element components of blood - Discuss the structure and function of red blood cells and hemoglobin - Classify and characterize white blood cells - Describe the structure of platelets and explain the process of hemostasis - Explain the significance of AB and Rh blood groups in blood transfusions - Discuss a variety of blood disorders Single-celled organisms do not need blood. They obtain nutrients directly from and excrete wastes directly into their environment. The human organism cannot do that. Our large, complex bodies need blood to deliver nutrients to and remove wastes from our trillions of cells. The heart pumps blood throughout the body in a network of blood vessels. Together, these three components—blood, heart, and vessels—makes up the cardiovascular system. This chapter focuses on the medium of transport: blood. An Overview of Blood - Identify the primary functions of blood in transportation, defense, and maintenance of homeostasis - Name the fluid component of blood and the three major types of formed elements, and identify their relative proportions in a blood sample - Discuss the unique physical characteristics of blood - Identify the composition of blood plasma, including its most important solutes and plasma proteins Recall that blood is a connective tissue. Like all connective tissues, it is made up of cellular elements and an extracellular matrix. The cellular elements—referred to as the formed elements—include red blood cells (RBCs), white blood cells (WBCs), and cell fragments called platelets. The extracellular matrix, called plasma, makes blood unique among connective tissues because it is fluid. This fluid, which is mostly water, perpetually suspends the formed elements and enables them to circulate throughout the body within the cardiovascular system. Functions of Blood The primary function of blood is to deliver oxygen and nutrients to and remove wastes from body cells, but that is only the beginning of the story. The specific functions of blood also include defense, distribution of heat, and maintenance of homeostasis. Transportation Nutrients from the foods you eat are absorbed in the digestive tract. Most of these travel in the bloodstream directly to the liver, where they are processed and released back into the bloodstream for delivery to body cells. Oxygen from the air you breathe diffuses into the blood, which moves from the lungs to the heart, which then pumps it out to the rest of the body. Moreover, endocrine glands scattered throughout the body release their products, called hormones, into the bloodstream, which carries them to distant target cells. Blood also picks up cellular wastes and byproducts, and transports them to various organs for removal. For instance, blood moves carbon dioxide to the lungs for exhalation from the body, and various waste products are transported to the kidneys and liver for excretion from the body in the form of urine or bile. Defense Many types of WBCs protect the body from external threats, such as disease-causing bacteria that have entered the bloodstream in a wound. Other WBCs seek out and destroy internal threats, such as cells with mutated DNA that could multiply to become cancerous, or body cells infected with viruses. When damage to the vessels results in bleeding, blood platelets and certain proteins dissolved in the plasma, the fluid portion of the blood, interact to block the ruptured areas of the blood vessels involved. This protects the body from further blood loss. Maintenance of Homeostasis Recall that body temperature is regulated via a classic negative-feedback loop. If you were exercising on a warm day, your rising core body temperature would trigger several homeostatic mechanisms, including increased transport of blood from your core to your body periphery, which is typically cooler. As blood passes through the vessels of the skin, heat would be dissipated to the environment, and the blood returning to your body core would be cooler. In contrast, on a cold day, blood is diverted away from the skin to maintain a warmer body core. In extreme cases, this may result in frostbite. Blood also helps to maintain the chemical balance of the body. Proteins and other compounds in blood act as buffers, which thereby help to regulate the pH of body tissues. Blood also helps to regulate the water content of body cells. Composition of Blood You have probably had blood drawn from a superficial vein in your arm, which was then sent to a lab for analysis. Some of the most common blood tests—for instance, those measuring lipid or glucose levels in plasma—determine which substances are present within blood and in what quantities. Other blood tests check for the composition of the blood itself, including the quantities and types of formed elements. One such test, called a hematocrit, measures the percentage of RBCs, clinically known as erythrocytes, in a blood sample. It is performed by spinning the blood sample in a specialized centrifuge, a process that causes the heavier elements suspended within the blood sample to separate from the lightweight, liquid plasma (Figure 18.2). Because the heaviest elements in blood are the erythrocytes, these settle at the very bottom of the hematocrit tube. Located above the erythrocytes is a pale, thin layer composed of the remaining formed elements of blood. These are the WBCs, clinically known as leukocytes, and the platelets, cell fragments also called thrombocytes. This layer is referred to as the buffy coat because of its color; it normally constitutes less than 1 percent of a blood sample. Above the buffy coat is the blood plasma, normally a pale, straw-colored fluid, which constitutes the remainder of the sample. The volume of erythrocytes after centrifugation is also commonly referred to as packed cell volume (PCV). In normal blood, about 45 percent of a sample is erythrocytes. The hematocrit of any one sample can vary significantly, however, about 36–50 percent, according to gender and other factors. Normal hematocrit values for females range from 37 to 47, with a mean value of 41; for males, hematocrit ranges from 42 to 52, with a mean of 47. The percentage of other formed elements, the WBCs and platelets, is extremely small so it is not normally considered with the hematocrit. So the mean plasma percentage is the percent of blood that is not erythrocytes: for females, it is approximately 59 (or 100 minus 41), and for males, it is approximately 53 (or 100 minus 47). Figure 18.2 Composition of Blood The cellular elements of blood include a vast number of erythrocytes and comparatively fewer leukocytes and platelets. Plasma is the fluid in which the formed elements are suspended. A sample of blood spun in a centrifuge reveals that plasma is the lightest component. It floats at the top of the tube separated from the heaviest elements, the erythrocytes, by a buffy coat of leukocytes and platelets. Hematocrit is the percentage of the total sample that is comprised of erythrocytes. Depressed and elevated hematocrit levels are shown for comparison. Characteristics of Blood When you think about blood, the first characteristic that probably comes to mind is its color. Blood that has just taken up oxygen in the lungs is bright red, and blood that has released oxygen in the tissues is a more dusky red. This is because hemoglobin is a pigment that changes color, depending upon the degree of oxygen saturation. Blood is viscous and somewhat sticky to the touch. It has a viscosity approximately five times greater than water. Viscosity is a measure of a fluid’s thickness or resistance to flow, and is influenced by the presence of the plasma proteins and formed elements within the blood. The viscosity of blood has a dramatic impact on blood pressure and flow. Consider the difference in flow between water and honey. The more viscous honey would demonstrate a greater resistance to flow than the less viscous water. The same principle applies to blood. The normal temperature of blood is slightly higher than normal body temperature—about 38 °C (or 100.4 °F), compared to 37 °C (or 98.6 °F) for an internal body temperature reading, although daily variations of 0.5 °C are normal. Although the surface of blood vessels is relatively smooth, as blood flows through them, it experiences some friction and resistance, especially as vessels age and lose their elasticity, thereby producing heat. This accounts for its slightly higher temperature. The pH of blood averages about 7.4; however, it can range from 7.35 to 7.45 in a healthy person. Blood is therefore somewhat more basic (alkaline) on a chemical scale than pure water, which has a pH of 7.0. Blood contains numerous buffers that actually help to regulate pH. Blood constitutes approximately 8 percent of adult body weight. Adult males typically average about 5 to 6 liters of blood. Females average 4–5 liters. Blood Plasma Like other fluids in the body, plasma is composed primarily of water: In fact, it is about 92 percent water. Dissolved or suspended within this water is a mixture of substances, most of which are proteins. There are literally hundreds of substances dissolved or suspended in the plasma, although many of them are found only in very small quantities. INTERACTIVE LINK Visit this site for a list of normal levels established for many of the substances found in a sample of blood. Serum, one of the specimen types included, refers to a sample of plasma after clotting factors have been removed. What types of measurements are given for levels of glucose in the blood? Plasma Proteins About 7 percent of the volume of plasma—nearly all that is not water—is made of proteins. These include several plasma proteins (proteins that are unique to the plasma), plus a much smaller number of regulatory proteins, including enzymes and some hormones. The major components of plasma are summarized in Figure 18.3. The three major groups of plasma proteins are as follows: - Albumin is the most abundant of the plasma proteins. Manufactured by the liver, albumin molecules serve as binding proteins—transport vehicles for fatty acids and steroid hormones. Recall that lipids are hydrophobic; however, their binding to albumin enables their transport in the watery plasma. Albumin is also the most significant contributor to the osmotic pressure of blood; that is, its presence holds water inside the blood vessels and draws water from the tissues, across blood vessel walls, and into the bloodstream. This in turn helps to maintain both blood volume and blood pressure. Albumin normally accounts for approximately 54 percent of the total plasma protein content, in clinical levels of 3.5–5.0 g/dL blood. - The second most common plasma proteins are the globulins. A heterogeneous group, there are three main subgroups known as alpha, beta, and gamma globulins. The alpha and beta globulins transport iron, lipids, and the fat-soluble vitamins A, D, E, and K to the cells; like albumin, they also contribute to osmotic pressure. The gamma globulins are proteins involved in immunity and are better known as an antibodies or immunoglobulins. Although other plasma proteins are produced by the liver, immunoglobulins are produced by specialized leukocytes known as plasma cells. (Seek additional content for more information about immunoglobulins.) Globulins make up approximately 38 percent of the total plasma protein volume, in clinical levels of 1.0–1.5 g/dL blood. - The least abundant plasma protein is fibrinogen. Like albumin and the alpha and beta globulins, fibrinogen is produced by the liver. It is essential for blood clotting, a process described later in this chapter. Fibrinogen accounts for about 7 percent of the total plasma protein volume, in clinical levels of 0.2–0.45 g/dL blood. Other Plasma Solutes In addition to proteins, plasma contains a wide variety of other substances. These include various electrolytes, such as sodium, potassium, and calcium ions; dissolved gases, such as oxygen, carbon dioxide, and nitrogen; various organic nutrients, such as vitamins, lipids, glucose, and amino acids; and metabolic wastes. All of these nonprotein solutes combined contribute approximately 1 percent to the total volume of plasma. Figure 18.3 Major Blood Components CAREER CONNECTION Phlebotomy and Medical Lab Technology Phlebotomists are professionals trained to draw blood (phleb- = “a blood vessel”; -tomy = “to cut”). When more than a few drops of blood are required, phlebotomists perform a venipuncture, typically of a surface vein in the arm. They perform a capillary stick on a finger, an earlobe, or the heel of an infant when only a small quantity of blood is required. An arterial stick is collected from an artery and used to analyze blood gases. After collection, the blood may be analyzed by medical laboratories or perhaps used for transfusions, donations, or research. While many allied health professionals practice phlebotomy, the American Society of Phlebotomy Technicians issues certificates to individuals passing a national examination, and some large labs and hospitals hire individuals expressly for their skill in phlebotomy. Medical or clinical laboratories employ a variety of individuals in technical positions: - Medical technologists (MT), also known as clinical laboratory technologists (CLT), typically hold a bachelor’s degree and certification from an accredited training program. They perform a wide variety of tests on various body fluids, including blood. The information they provide is essential to the primary care providers in determining a diagnosis and in monitoring the course of a disease and response to treatment. - Medical laboratory technicians (MLT) typically have an associate’s degree but may perform duties similar to those of an MT. - Medical laboratory assistants (MLA) spend the majority of their time processing samples and carrying out routine assignments within the lab. Clinical training is required, but a degree may not be essential to obtaining a position. Production of the Formed Elements - Trace the generation of the formed elements of blood from bone marrow stem cells - Discuss the role of hemopoietic growth factors in promoting the production of the formed elements The lifespan of the formed elements is very brief. Although one type of leukocyte called memory cells can survive for years, most erythrocytes, leukocytes, and platelets normally live only a few hours to a few weeks. Thus, the body must form new blood cells and platelets quickly and continuously. When you donate a unit of blood during a blood drive (approximately 475 mL, or about 1 pint), your body typically replaces the donated plasma within 24 hours, but it takes about 4 to 6 weeks to replace the blood cells. This restricts the frequency with which donors can contribute their blood. The process by which this replacement occurs is called hemopoiesis, or hematopoiesis (from the Greek root haima- = “blood”; -poiesis = “production”). Sites of Hemopoiesis Prior to birth, hemopoiesis occurs in a number of tissues, beginning with the yolk sac of the developing embryo, and continuing in the fetal liver, spleen, lymphatic tissue, and eventually the red bone marrow. Following birth, most hemopoiesis occurs in the red marrow, a connective tissue within the spaces of spongy (cancellous) bone tissue. In children, hemopoiesis can occur in the medullary cavity of long bones; in adults, the process is largely restricted to the cranial and pelvic bones, the vertebrae, the sternum, and the proximal epiphyses of the femur and humerus. Throughout adulthood, the liver and spleen maintain their ability to generate the formed elements. This process is referred to as extramedullary hemopoiesis (meaning hemopoiesis outside the medullary cavity of adult bones). When a disease such as bone cancer destroys the bone marrow, causing hemopoiesis to fail, extramedullary hemopoiesis may be initiated. Differentiation of Formed Elements from Stem Cells All formed elements arise from stem cells of the red bone marrow. Recall that stem cells undergo mitosis plus cytokinesis (cellular division) to give rise to new daughter cells: One of these remains a stem cell and the other differentiates into one of any number of diverse cell types. Stem cells may be viewed as occupying a hierarchal system, with some loss of the ability to diversify at each step. The totipotent stem cell is the zygote, or fertilized egg. The totipotent (toti- = “all”) stem cell gives rise to all cells of the human body. The next level is the pluripotent stem cell, which gives rise to multiple types of cells of the body and some of the supporting fetal membranes. Beneath this level, the mesenchymal cell is a stem cell that develops only into types of connective tissue, including fibrous connective tissue, bone, cartilage, and blood, but not epithelium, muscle, and nervous tissue. One step lower on the hierarchy of stem cells is the hemopoietic stem cell, or hemocytoblast. All of the formed elements of blood originate from this specific type of cell. Hemopoiesis begins when the hemopoietic stem cell is exposed to appropriate chemical stimuli collectively called hemopoietic growth factors, which prompt it to divide and differentiate. One daughter cell remains a hemopoietic stem cell, allowing hemopoiesis to continue. The other daughter cell becomes either of two types of more specialized stem cells (Figure 18.4): - Lymphoid stem cells give rise to a class of leukocytes known as lymphocytes, which include the various T cells, B cells, and natural killer (NK) cells, all of which function in immunity. However, hemopoiesis of lymphocytes progresses somewhat differently from the process for the other formed elements. In brief, lymphoid stem cells quickly migrate from the bone marrow to lymphatic tissues, including the lymph nodes, spleen, and thymus, where their production and differentiation continues. B cells are so named since they mature in the bone marrow, while T cells mature in the thymus. - Myeloid stem cells give rise to all the other formed elements, including the erythrocytes; megakaryocytes that produce platelets; and a myeloblast lineage that gives rise to monocytes and three forms of granular leukocytes: neutrophils, eosinophils, and basophils. Figure 18.4 Hematopoietic System of Bone Marrow Hemopoiesis is the proliferation and differentiation of the formed elements of blood. Lymphoid and myeloid stem cells do not immediately divide and differentiate into mature formed elements. As you can see in Figure 18.4, there are several intermediate stages of precursor cells (literally, forerunner cells), many of which can be recognized by their names, which have the suffix -blast. For instance, megakaryoblasts are the precursors of megakaryocytes, and proerythroblasts become reticulocytes, which eject their nucleus and most other organelles before maturing into erythrocytes. Hemopoietic Growth Factors Development from stem cells to precursor cells to mature cells is again initiated by hemopoietic growth factors. These include the following: - Erythropoietin (EPO) is a glycoprotein hormone secreted by the interstitial fibroblast cells of the kidneys in response to low oxygen levels. It prompts the production of erythrocytes. Some athletes use synthetic EPO as a performance-enhancing drug (called blood doping) to increase RBC counts and subsequently increase oxygen delivery to tissues throughout the body. EPO is a banned substance in most organized sports, but it is also used medically in the treatment of certain anemia, specifically those triggered by certain types of cancer, and other disorders in which increased erythrocyte counts and oxygen levels are desirable. - Thrombopoietin, another glycoprotein hormone, is produced by the liver and kidneys. It triggers the development of megakaryocytes into platelets. - Cytokines are glycoproteins secreted by a wide variety of cells, including red bone marrow, leukocytes, macrophages, fibroblasts, and endothelial cells. They act locally as autocrine or paracrine factors, stimulating the proliferation of progenitor cells and helping to stimulate both nonspecific and specific resistance to disease. There are two major subtypes of cytokines known as colony-stimulating factors and interleukins. - Colony-stimulating factors (CSFs) are glycoproteins that act locally, as autocrine or paracrine factors. Some trigger the differentiation of myeloblasts into granular leukocytes, namely, neutrophils, eosinophils, and basophils. These are referred to as granulocyte CSFs. A different CSF induces the production of monocytes, called monocyte CSFs. Both granulocytes and monocytes are stimulated by GM-CSF; granulocytes, monocytes, platelets, and erythrocytes are stimulated by multi-CSF. Synthetic forms of these hormones are often administered to patients with various forms of cancer who are receiving chemotherapy to revive their WBC counts. - Interleukins are another class of cytokine signaling molecules important in hemopoiesis. They were initially thought to be secreted uniquely by leukocytes and to communicate only with other leukocytes, and were named accordingly, but are now known to be produced by a variety of cells including bone marrow and endothelium. Researchers now suspect that interleukins may play other roles in body functioning, including differentiation and maturation of cells, producing immunity and inflammation. To date, more than a dozen interleukins have been identified, with others likely to follow. They are generally numbered IL-1, IL-2, IL-3, etc. EVERYDAY CONNECTION Blood Doping In its original intent, the term blood doping was used to describe the practice of injecting by transfusion supplemental RBCs into an individual, typically to enhance performance in a sport. Additional RBCs would deliver more oxygen to the tissues, providing extra aerobic capacity, clinically referred to as VO2 max. The source of the cells was either from the recipient (autologous) or from a donor with compatible blood (homologous). This practice was aided by the well-developed techniques of harvesting, concentrating, and freezing of the RBCs that could be later thawed and injected, yet still retain their functionality. These practices are considered illegal in virtually all sports and run the risk of infection, significantly increasing the viscosity of the blood and the potential for transmission of blood-borne pathogens if the blood was collected from another individual. With the development of synthetic EPO in the 1980s, it became possible to provide additional RBCs by artificially stimulating RBC production in the bone marrow. Originally developed to treat patients suffering from anemia, renal failure, or cancer treatment, large quantities of EPO can be generated by recombinant DNA technology. Synthetic EPO is injected under the skin and can increase hematocrit for many weeks. It may also induce polycythemia and raise hematocrit to 70 or greater. This increased viscosity raises the resistance of the blood and forces the heart to pump more powerfully; in extreme cases, it has resulted in death. Other drugs such as cobalt II chloride have been shown to increase natural EPO gene expression. Blood doping has become problematic in many sports, especially cycling. Lance Armstrong, winner of seven Tour de France and many other cycling titles, was stripped of his victories and admitted to blood doping in 2013. INTERACTIVE LINK Watch this video to see doctors discuss the dangers of blood doping in sports. What are the some potential side effects of blood doping? Bone Marrow Sampling and Transplants Sometimes, a healthcare provider will order a bone marrow biopsy, a diagnostic test of a sample of red bone marrow, or a bone marrow transplant, a treatment in which a donor’s healthy bone marrow—and its stem cells—replaces the faulty bone marrow of a patient. These tests and procedures are often used to assist in the diagnosis and treatment of various severe forms of anemia, such as thalassemia major and sickle cell anemia, as well as some types of cancer, specifically leukemia. In the past, when a bone marrow sample or transplant was necessary, the procedure would have required inserting a large-bore needle into the region near the iliac crest of the pelvic bones (os coxae). This location was preferred, since its location close to the body surface makes it more accessible, and it is relatively isolated from most vital organs. Unfortunately, the procedure is quite painful. Now, direct sampling of bone marrow can often be avoided. In many cases, stem cells can be isolated in just a few hours from a sample of a patient’s blood. The isolated stem cells are then grown in culture using the appropriate hemopoietic growth factors, and analyzed or sometimes frozen for later use. For an individual requiring a transplant, a matching donor is essential to prevent the immune system from destroying the donor cells—a phenomenon known as tissue rejection. To treat patients with bone marrow transplants, it is first necessary to destroy the patient’s own diseased marrow through radiation and/or chemotherapy. Donor bone marrow stem cells are then intravenously infused. From the bloodstream, they establish themselves in the recipient’s bone marrow. Erythrocytes - Describe the anatomy of erythrocytes - Discuss the various steps in the lifecycle of an erythrocyte - Explain the composition and function of hemoglobin The erythrocyte, commonly known as a red blood cell (or RBC), is by far the most common formed element: A single drop of blood contains millions of erythrocytes and just thousands of leukocytes. Specifically, males have about 5.4 million erythrocytes per microliter (µL) of blood, and females have approximately 4.8 million per µL. In fact, erythrocytes are estimated to make up about 25 percent of the total cells in the body. As you can imagine, they are quite small cells, with a mean diameter of only about 7–8 micrometers (µm) (Figure 18.5). The primary functions of erythrocytes are to pick up inhaled oxygen from the lungs and transport it to the body’s tissues, and to pick up some (about 24 percent) carbon dioxide waste at the tissues and transport it to the lungs for exhalation. Erythrocytes remain within the vascular network. Although leukocytes typically leave the blood vessels to perform their defensive functions, movement of erythrocytes from the blood vessels is abnormal. Figure 18.5 Summary of Formed Elements in Blood Shape and Structure of Erythrocytes As an erythrocyte matures in the red bone marrow, it extrudes its nucleus and most of its other organelles. During the first day or two that it is in the circulation, an immature erythrocyte, known as a reticulocyte, will still typically contain remnants of organelles. Reticulocytes should comprise approximately 1–2 percent of the erythrocyte count and provide a rough estimate of the rate of RBC production, with abnormally low or high rates indicating deviations in the production of these cells. These remnants, primarily of networks (reticulum) of ribosomes, are quickly shed, however, and mature, circulating erythrocytes have few internal cellular structural components. Lacking mitochondria, for example, they rely on anaerobic respiration. This means that they do not utilize any of the oxygen they are transporting, so they can deliver it all to the tissues. They also lack endoplasmic reticula and do not synthesize proteins. Erythrocytes do, however, contain some structural proteins that help the blood cells maintain their unique structure and enable them to change their shape to squeeze through capillaries. This includes the protein spectrin, a cytoskeletal protein element. Erythrocytes are biconcave disks; that is, they are plump at their periphery and very thin in the center (Figure 18.6). Since they lack most organelles, there is more interior space for the presence of the hemoglobin molecules that, as you will see shortly, transport gases. The biconcave shape also provides a greater surface area across which gas exchange can occur, relative to its volume; a sphere of a similar diameter would have a lower surface area-to-volume ratio. In the capillaries, the oxygen carried by the erythrocytes can diffuse into the plasma and then through the capillary walls to reach the cells, whereas some of the carbon dioxide produced by the cells as a waste product diffuses into the capillaries to be picked up by the erythrocytes. Capillary beds are extremely narrow, slowing the passage of the erythrocytes and providing an extended opportunity for gas exchange to occur. However, the space within capillaries can be so minute that, despite their own small size, erythrocytes may have to fold in on themselves if they are to make their way through. Fortunately, their structural proteins like spectrin are flexible, allowing them to bend over themselves to a surprising degree, then spring back again when they enter a wider vessel. In wider vessels, erythrocytes may stack up much like a roll of coins, forming a rouleaux, from the French word for “roll.” Figure 18.6 Shape of Red Blood Cells Erythrocytes are biconcave discs with very shallow centers. This shape optimizes the ratio of surface area to volume, facilitating gas exchange. It also enables them to fold up as they move through narrow blood vessels. Hemoglobin Hemoglobin is a large molecule made up of proteins and iron. It consists of four folded chains of a protein called globin, designated alpha 1 and 2, and beta 1 and 2 (Figure 18.7a). Each of these globin molecules is bound to a red pigment molecule called heme, which contains an ion of iron (Fe2+) (Figure 18.7b). Figure 18.7 Hemoglobin (a) A molecule of hemoglobin contains four globin proteins, each of which is bound to one molecule of the iron-containing pigment heme. (b) A single erythrocyte can contain 300 million hemoglobin molecules, and thus more than 1 billion oxygen molecules. Each iron ion in the heme can bind to one oxygen molecule; therefore, each hemoglobin molecule can transport four oxygen molecules. An individual erythrocyte may contain about 300 million hemoglobin molecules, and therefore can bind to and transport up to 1.2 billion oxygen molecules (see Figure 18.7b). In the lungs, hemoglobin picks up oxygen, which binds to the iron ions, forming oxyhemoglobin. The bright red, oxygenated hemoglobin travels to the body tissues, where it releases some of the oxygen molecules, becoming darker red deoxyhemoglobin, sometimes referred to as reduced hemoglobin. Oxygen release depends on the need for oxygen in the surrounding tissues, so hemoglobin rarely if ever leaves all of its oxygen behind. In the capillaries, carbon dioxide enters the bloodstream. About 76 percent dissolves in the plasma, some of it remaining as dissolved CO2, and the remainder forming bicarbonate ion. About 23–24 percent of it binds to the amino acids in hemoglobin, forming a molecule known as carbaminohemoglobin. From the capillaries, the hemoglobin carries carbon dioxide back to the lungs, where it releases it for exchange of oxygen. Changes in the levels of RBCs can have significant effects on the body’s ability to effectively deliver oxygen to the tissues. Ineffective hematopoiesis results in insufficient numbers of RBCs and results in one of several forms of anemia. An overproduction of RBCs produces a condition called polycythemia. The primary drawback with polycythemia is not a failure to directly deliver enough oxygen to the tissues, but rather the increased viscosity of the blood, which makes it more difficult for the heart to circulate the blood. In patients with insufficient hemoglobin, the tissues may not receive sufficient oxygen, resulting in another form of anemia. In determining oxygenation of tissues, the value of greatest interest in healthcare is the percent saturation; that is, the percentage of hemoglobin sites occupied by oxygen in a patient’s blood. Clinically this value is commonly referred to simply as “percent sat.” Percent saturation is normally monitored using a device known as a pulse oximeter, which is applied to a thin part of the body, typically the tip of the patient’s finger. The device works by sending two different wavelengths of light (one red, the other infrared) through the finger and measuring the light with a photodetector as it exits. Hemoglobin absorbs light differentially depending upon its saturation with oxygen. The machine calibrates the amount of light received by the photodetector against the amount absorbed by the partially oxygenated hemoglobin and presents the data as percent saturation. Normal pulse oximeter readings range from 95–100 percent. Lower percentages reflect hypoxemia, or low blood oxygen. The term hypoxia is more generic and simply refers to low oxygen levels. Oxygen levels are also directly monitored from free oxygen in the plasma typically following an arterial stick. When this method is applied, the amount of oxygen present is expressed in terms of partial pressure of oxygen or simply pO2 and is typically recorded in units of millimeters of mercury, mm Hg. The kidneys filter about 180 liters (~380 pints) of blood in an average adult each day, or about 20 percent of the total resting volume, and thus serve as ideal sites for receptors that determine oxygen saturation. In response to hypoxemia, less oxygen will exit the vessels supplying the kidney, resulting in hypoxia (low oxygen concentration) in the tissue fluid of the kidney where oxygen concentration is actually monitored. Interstitial fibroblasts within the kidney secrete EPO, thereby increasing erythrocyte production and restoring oxygen levels. In a classic negative-feedback loop, as oxygen saturation rises, EPO secretion falls, and vice versa, thereby maintaining homeostasis. Populations dwelling at high elevations, with inherently lower levels of oxygen in the atmosphere, naturally maintain a hematocrit higher than people living at sea level. Consequently, people traveling to high elevations may experience symptoms of hypoxemia, such as fatigue, headache, and shortness of breath, for a few days after their arrival. In response to the hypoxemia, the kidneys secrete EPO to step up the production of erythrocytes until homeostasis is achieved once again. To avoid the symptoms of hypoxemia, or altitude sickness, mountain climbers typically rest for several days to a week or more at a series of camps situated at increasing elevations to allow EPO levels and, consequently, erythrocyte counts to rise. When climbing the tallest peaks, such as Mt. Everest and K2 in the Himalayas, many mountain climbers rely upon bottled oxygen as they near the summit. Lifecycle of Erythrocytes Production of erythrocytes in the marrow occurs at the staggering rate of more than 2 million cells per second. For this production to occur, a number of raw materials must be present in adequate amounts. These include the same nutrients that are essential to the production and maintenance of any cell, such as glucose, lipids, and amino acids. However, erythrocyte production also requires several trace elements: - Iron. We have said that each heme group in a hemoglobin molecule contains an ion of the trace mineral iron. On average, less than 20 percent of the iron we consume is absorbed. Heme iron, from animal foods such as meat, poultry, and fish, is absorbed more efficiently than non-heme iron from plant foods. Upon absorption, iron becomes part of the body’s total iron pool. The bone marrow, liver, and spleen can store iron in the protein compounds ferritin and hemosiderin. Ferroportin transports the iron across the intestinal cell plasma membranes and from its storage sites into tissue fluid where it enters the blood. When EPO stimulates the production of erythrocytes, iron is released from storage, bound to transferrin, and carried to the red marrow where it attaches to erythrocyte precursors. - Copper. A trace mineral, copper is a component of two plasma proteins, hephaestin and ceruloplasmin. Without these, hemoglobin could not be adequately produced. Located in intestinal villi, hephaestin enables iron to be absorbed by intestinal cells. Ceruloplasmin transports copper. Both enable the oxidation of iron from Fe2+ to Fe3+, a form in which it can be bound to its transport protein, transferrin, for transport to body cells. In a state of copper deficiency, the transport of iron for heme synthesis decreases, and iron can accumulate in tissues, where it can eventually lead to organ damage. - Zinc. The trace mineral zinc functions as a co-enzyme that facilitates the synthesis of the heme portion of hemoglobin. - B vitamins. The B vitamins folate and vitamin B12 function as co-enzymes that facilitate DNA synthesis. Thus, both are critical for the synthesis of new cells, including erythrocytes. Erythrocytes live up to 120 days in the circulation, after which the worn-out cells are removed by a type of myeloid phagocytic cell called a macrophage, located primarily within the bone marrow, liver, and spleen. The components of the degraded erythrocytes’ hemoglobin are further processed as follows: - Globin, the protein portion of hemoglobin, is broken down into amino acids, which can be sent back to the bone marrow to be used in the production of new erythrocytes. Hemoglobin that is not phagocytized is broken down in the circulation, releasing alpha and beta chains that are removed from circulation by the kidneys. - The iron contained in the heme portion of hemoglobin may be stored in the liver or spleen, primarily in the form of ferritin or hemosiderin, or carried through the bloodstream by transferrin to the red bone marrow for recycling into new erythrocytes. - The non-iron portion of heme is degraded into the waste product biliverdin, a green pigment, and then into another waste product, bilirubin, a yellow pigment. Bilirubin binds to albumin and travels in the blood to the liver, which uses it in the manufacture of bile, a compound released into the intestines to help emulsify dietary fats. In the large intestine, bacteria breaks the bilirubin apart from the bile and converts it to urobilinogen and then into stercobilin. It is then eliminated from the body in the feces. Broad-spectrum antibiotics typically eliminate these bacteria as well and may alter the color of feces. The kidneys also remove any circulating bilirubin and other related metabolic byproducts such as urobilins and secrete them into the urine. The breakdown pigments formed from the destruction of hemoglobin can be seen in a variety of situations. At the site of an injury, biliverdin from damaged RBCs produces some of the dramatic colors associated with bruising. With a failing liver, bilirubin cannot be removed effectively from circulation and causes the body to assume a yellowish tinge associated with jaundice. Stercobilins within the feces produce the typical brown color associated with this waste. And the yellow of urine is associated with the urobilins. The erythrocyte lifecycle is summarized in Figure 18.8. Figure 18.8 Erythrocyte Lifecycle Erythrocytes are produced in the bone marrow and sent into the circulation. At the end of their lifecycle, they are destroyed by macrophages, and their components are recycled. Disorders of Erythrocytes The size, shape, and number of erythrocytes, and the number of hemoglobin molecules can have a major impact on a person’s health. When the number of RBCs or hemoglobin is deficient, the general condition is called anemia. There are more than 400 types of anemia and more than 3.5 million Americans suffer from this condition. Anemia can be broken down into three major groups: those caused by blood loss, those caused by faulty or decreased RBC production, and those caused by excessive destruction of RBCs. Clinicians often use two groupings in diagnosis: The kinetic approach focuses on evaluating the production, destruction, and removal of RBCs, whereas the morphological approach examines the RBCs themselves, paying particular emphasis to their size. A common test is the mean corpuscle volume (MCV), which measures size. Normal-sized cells are referred to as normocytic, smaller-than-normal cells are referred to as microcytic, and larger-than-normal cells are referred to as macrocytic. Reticulocyte counts are also important and may reveal inadequate production of RBCs. The effects of the various anemias are widespread, because reduced numbers of RBCs or hemoglobin will result in lower levels of oxygen being delivered to body tissues. Since oxygen is required for tissue functioning, anemia produces fatigue, lethargy, and an increased risk for infection. An oxygen deficit in the brain impairs the ability to think clearly, and may prompt headaches and irritability. Lack of oxygen leaves the patient short of breath, even as the heart and lungs work harder in response to the deficit. Blood loss anemias are fairly straightforward. In addition to bleeding from wounds or other lesions, these forms of anemia may be due to ulcers, hemorrhoids, inflammation of the stomach (gastritis), and some cancers of the gastrointestinal tract. The excessive use of aspirin or other nonsteroidal anti-inflammatory drugs such as ibuprofen can trigger ulceration and gastritis. Excessive menstruation and loss of blood during childbirth are also potential causes. Anemias caused by faulty or decreased RBC production include sickle cell anemia, iron deficiency anemia, vitamin deficiency anemia, and diseases of the bone marrow and stem cells. - A characteristic change in the shape of erythrocytes is seen in sickle cell disease (also referred to as sickle cell anemia). A genetic disorder, it is caused by production of an abnormal type of hemoglobin, called hemoglobin S, which delivers less oxygen to tissues and causes erythrocytes to assume a sickle (or crescent) shape, especially at low oxygen concentrations (Figure 18.9). These abnormally shaped cells can then become lodged in narrow capillaries because they are unable to fold in on themselves to squeeze through, blocking blood flow to tissues and causing a variety of serious problems from painful joints to delayed growth and even blindness and cerebrovascular accidents (strokes). Sickle cell anemia is a genetic condition particularly found in individuals of African descent. Figure 18.9 Sickle Cells Sickle cell anemia is caused by a mutation in one of the hemoglobin genes. Erythrocytes produce an abnormal type of hemoglobin, which causes the cell to take on a sickle or crescent shape. (credit: Janice Haney Carr) - Iron deficiency anemia is the most common type and results when the amount of available iron is insufficient to allow production of sufficient heme. This condition can occur in individuals with a deficiency of iron in the diet and is especially common in teens and children as well as in vegans and vegetarians. Additionally, iron deficiency anemia may be caused by either an inability to absorb and transport iron or slow, chronic bleeding. - Vitamin-deficient anemias generally involve insufficient vitamin B12 and folate. - Megaloblastic anemia involves a deficiency of vitamin B12 and/or folate, and often involves diets deficient in these essential nutrients. Lack of meat or a viable alternate source, and overcooking or eating insufficient amounts of vegetables may lead to a lack of folate. - Pernicious anemia is caused by poor absorption of vitamin B12 and is often seen in patients with Crohn’s disease (a severe intestinal disorder often treated by surgery), surgical removal of the intestines or stomach (common in some weight loss surgeries), intestinal parasites, and AIDS. - Pregnancies, some medications, excessive alcohol consumption, and some diseases such as celiac disease are also associated with vitamin deficiencies. It is essential to provide sufficient folic acid during the early stages of pregnancy to reduce the risk of neurological defects, including spina bifida, a failure of the neural tube to close. - Assorted disease processes can also interfere with the production and formation of RBCs and hemoglobin. If myeloid stem cells are defective or replaced by cancer cells, there will be insufficient quantities of RBCs produced. - Aplastic anemia is the condition in which there are deficient numbers of RBC stem cells. Aplastic anemia is often inherited, or it may be triggered by radiation, medication, chemotherapy, or infection. - Thalassemia is an inherited condition typically occurring in individuals from the Middle East, the Mediterranean, African, and Southeast Asia, in which maturation of the RBCs does not proceed normally. The most severe form is called Cooley’s anemia. - Lead exposure from industrial sources or even dust from paint chips of iron-containing paints or pottery that has not been properly glazed may also lead to destruction of the red marrow. - Various disease processes also can lead to anemias. These include chronic kidney diseases often associated with a decreased production of EPO, hypothyroidism, some forms of cancer, lupus, and rheumatoid arthritis. In contrast to anemia, an elevated RBC count is called polycythemia and is detected in a patient’s elevated hematocrit. It can occur transiently in a person who is dehydrated; when water intake is inadequate or water losses are excessive, the plasma volume falls. As a result, the hematocrit rises. For reasons mentioned earlier, a mild form of polycythemia is chronic but normal in people living at high altitudes. Some elite athletes train at high elevations specifically to induce this phenomenon. Finally, a type of bone marrow disease called polycythemia vera (from the Greek vera = “true”) causes an excessive production of immature erythrocytes. Polycythemia vera can dangerously elevate the viscosity of blood, raising blood pressure and making it more difficult for the heart to pump blood throughout the body. It is a relatively rare disease that occurs more often in men than women, and is more likely to be present in elderly patients those over 60 years of age. Leukocytes and Platelets - Describe the general characteristics of leukocytes - Classify leukocytes according to their lineage, their main structural features, and their primary functions - Discuss the most common malignancies involving leukocytes - Identify the lineage, basic structure, and function of platelets The leukocyte, commonly known as a white blood cell (or WBC), is a major component of the body’s defenses against disease. Leukocytes protect the body against invading microorganisms and body cells with mutated DNA, and they clean up debris. Platelets are essential for the repair of blood vessels when damage to them has occurred; they also provide growth factors for healing and repair. See Figure 18.5 for a summary of leukocytes and platelets. Characteristics of Leukocytes Although leukocytes and erythrocytes both originate from hematopoietic stem cells in the bone marrow, they are very different from each other in many significant ways. For instance, leukocytes are far less numerous than erythrocytes: Typically there are only 5000 to 10,000 per µL. They are also larger than erythrocytes and are the only formed elements that are complete cells, possessing a nucleus and organelles. And although there is just one type of erythrocyte, there are many types of leukocytes. Most of these types have a much shorter lifespan than that of erythrocytes, some as short as a few hours or even a few minutes in the case of acute infection. One of the most distinctive characteristics of leukocytes is their movement. Whereas erythrocytes spend their days circulating within the blood vessels, leukocytes routinely leave the bloodstream to perform their defensive functions in the body’s tissues. For leukocytes, the vascular network is simply a highway they travel and soon exit to reach their true destination. When they arrive, they are often given distinct names, such as macrophage or microglia, depending on their function. As shown in Figure 18.10, they leave the capillaries—the smallest blood vessels—or other small vessels through a process known as emigration(from the Latin for “removal”) or diapedesis (dia- = “through”; -pedan = “to leap”) in which they squeeze through adjacent cells in a blood vessel wall. Once they have exited the capillaries, some leukocytes will take up fixed positions in lymphatic tissue, bone marrow, the spleen, the thymus, or other organs. Others will move about through the tissue spaces very much like amoebas, continuously extending their plasma membranes, sometimes wandering freely, and sometimes moving toward the direction in which they are drawn by chemical signals. This attracting of leukocytes occurs because of positive chemotaxis (literally “movement in response to chemicals”), a phenomenon in which injured or infected cells and nearby leukocytes emit the equivalent of a chemical “911” call, attracting more leukocytes to the site. In clinical medicine, the differential counts of the types and percentages of leukocytes present are often key indicators in making a diagnosis and selecting a treatment. Figure 18.10 Emigration Leukocytes exit the blood vessel and then move through the connective tissue of the dermis toward the site of a wound. Some leukocytes, such as the eosinophil and neutrophil, are characterized as granular leukocytes. They release chemicals from their granules that destroy pathogens; they are also capable of phagocytosis. The monocyte, an agranular leukocyte, differentiates into a macrophage that then phagocytizes the pathogens. Classification of Leukocytes When scientists first began to observe stained blood slides, it quickly became evident that leukocytes could be divided into two groups, according to whether their cytoplasm contained highly visible granules: - Granular leukocytes contain abundant granules within the cytoplasm. They include neutrophils, eosinophils, and basophils (you can view their lineage from myeloid stem cells in Figure 18.4). - While granules are not totally lacking in agranular leukocytes, they are far fewer and less obvious. Agranular leukocytes include monocytes, which mature into macrophages that are phagocytic, and lymphocytes, which arise from the lymphoid stem cell line. Granular Leukocytes We will consider the granular leukocytes in order from most common to least common. All of these are produced in the red bone marrow and have a short lifespan of hours to days. They typically have a lobed nucleus and are classified according to which type of stain best highlights their granules (Figure 18.11). Figure 18.11 Granular Leukocytes A neutrophil has small granules that stain light lilac and a nucleus with two to five lobes. An eosinophil’s granules are slightly larger and stain reddish-orange, and its nucleus has two to three lobes. A basophil has large granules that stain dark blue to purple and a two-lobed nucleus. The most common of all the leukocytes, neutrophils will normally comprise 50–70 percent of total leukocyte count. They are 10–12 µm in diameter, significantly larger than erythrocytes. They are called neutrophils because their granules show up most clearly with stains that are chemically neutral (neither acidic nor basic). The granules are numerous but quite fine and normally appear light lilac. The nucleus has a distinct lobed appearance and may have two to five lobes, the number increasing with the age of the cell. Older neutrophils have increasing numbers of lobes and are often referred to as polymorphonuclear (a nucleus with many forms), or simply “polys.” Younger and immature neutrophils begin to develop lobes and are known as “bands.” Neutrophils are rapid responders to the site of infection and are efficient phagocytes with a preference for bacteria. Their granules include lysozyme, an enzyme capable of lysing, or breaking down, bacterial cell walls; oxidants such as hydrogen peroxide; and defensins, proteins that bind to and puncture bacterial and fungal plasma membranes, so that the cell contents leak out. Abnormally high counts of neutrophils indicate infection and/or inflammation, particularly triggered by bacteria, but are also found in burn patients and others experiencing unusual stress. A burn injury increases the proliferation of neutrophils in order to fight off infection that can result from the destruction of the barrier of the skin. Low counts may be caused by drug toxicity and other disorders, and may increase an individual’s susceptibility to infection. Eosinophils typically represent 2–4 percent of total leukocyte count. They are also 10–12 µm in diameter. The granules of eosinophils stain best with an acidic stain known as eosin. The nucleus of the eosinophil will typically have two to three lobes and, if stained properly, the granules will have a distinct red to orange color. The granules of eosinophils include antihistamine molecules, which counteract the activities of histamines, inflammatory chemicals produced by basophils and mast cells. Some eosinophil granules contain molecules toxic to parasitic worms, which can enter the body through the integument, or when an individual consumes raw or undercooked fish or meat. Eosinophils are also capable of phagocytosis and are particularly effective when antibodies bind to the target and form an antigen-antibody complex. High counts of eosinophils are typical of patients experiencing allergies, parasitic worm infestations, and some autoimmune diseases. Low counts may be due to drug toxicity and stress. Basophils are the least common leukocytes, typically comprising less than one percent of the total leukocyte count. They are slightly smaller than neutrophils and eosinophils at 8–10 µm in diameter. The granules of basophils stain best with basic (alkaline) stains. Basophils contain large granules that pick up a dark blue stain and are so common they may make it difficult to see the two-lobed nucleus. In general, basophils intensify the inflammatory response. They share this trait with mast cells. In the past, mast cells were considered to be basophils that left the circulation. However, this appears not to be the case, as the two cell types develop from different lineages. The granules of basophils release histamines, which contribute to inflammation, and heparin, which opposes blood clotting. High counts of basophils are associated with allergies, parasitic infections, and hypothyroidism. Low counts are associated with pregnancy, stress, and hyperthyroidism. Agranular Leukocytes Agranular leukocytes contain smaller, less-visible granules in their cytoplasm than do granular leukocytes. The nucleus is simple in shape, sometimes with an indentation but without distinct lobes. There are two major types of agranulocytes: lymphocytes and monocytes (see Figure 18.4). Lymphocytes are the only formed element of blood that arises from lymphoid stem cells. Although they form initially in the bone marrow, much of their subsequent development and reproduction occurs in the lymphatic tissues. Lymphocytes are the second most common type of leukocyte, accounting for about 20–30 percent of all leukocytes, and are essential for the immune response. The size range of lymphocytes is quite extensive, with some authorities recognizing two size classes and others three. Typically, the large cells are 10–14 µm and have a smaller nucleus-to-cytoplasm ratio and more granules. The smaller cells are typically 6–9 µm with a larger volume of nucleus to cytoplasm, creating a “halo” effect. A few cells may fall outside these ranges, at 14–17 µm. This finding has led to the three size range classification. The three major groups of lymphocytes include natural killer cells, B cells, and T cells. Natural killer (NK) cells are capable of recognizing cells that do not express “self” proteins on their plasma membrane or that contain foreign or abnormal markers. These “nonself” cells include cancer cells, cells infected with a virus, and other cells with atypical surface proteins. Thus, they provide generalized, nonspecific immunity. The larger lymphocytes are typically NK cells. B cells and T cells, also called B lymphocytes and T lymphocytes, play prominent roles in defending the body against specific pathogens (disease-causing microorganisms) and are involved in specific immunity. One form of B cells (plasma cells) produces the antibodies or immunoglobulins that bind to specific foreign or abnormal components of plasma membranes. This is also referred to as humoral (body fluid) immunity. T cells provide cellular-level immunity by physically attacking foreign or diseased cells. A memory cell is a variety of both B and T cells that forms after exposure to a pathogen and mounts rapid responses upon subsequent exposures. Unlike other leukocytes, memory cells live for many years. B cells undergo a maturation process in the bone marrow, whereas T cells undergo maturation in the thymus. This site of the maturation process gives rise to the name B and T cells. The functions of lymphocytes are complex and will be covered in detail in the chapter covering the lymphatic system and immunity. Smaller lymphocytes are either B or T cells, although they cannot be differentiated in a normal blood smear. Abnormally high lymphocyte counts are characteristic of viral infections as well as some types of cancer. Abnormally low lymphocyte counts are characteristic of prolonged (chronic) illness or immunosuppression, including that caused by HIV infection and drug therapies that often involve steroids. Monocytes originate from myeloid stem cells. They normally represent 2–8 percent of the total leukocyte count. They are typically easily recognized by their large size of 12–20 µm and indented or horseshoe-shaped nuclei. Macrophages are monocytes that have left the circulation and phagocytize debris, foreign pathogens, worn-out erythrocytes, and many other dead, worn out, or damaged cells. Macrophages also release antimicrobial defensins and chemotactic chemicals that attract other leukocytes to the site of an infection. Some macrophages occupy fixed locations, whereas others wander through the tissue fluid. Abnormally high counts of monocytes are associated with viral or fungal infections, tuberculosis, and some forms of leukemia and other chronic diseases. Abnormally low counts are typically caused by suppression of the bone marrow. Lifecycle of Leukocytes Most leukocytes have a relatively short lifespan, typically measured in hours or days. Production of all leukocytes begins in the bone marrow under the influence of CSFs and interleukins. Secondary production and maturation of lymphocytes occurs in specific regions of lymphatic tissue known as germinal centers. Lymphocytes are fully capable of mitosis and may produce clones of cells with identical properties. This capacity enables an individual to maintain immunity throughout life to many threats that have been encountered in the past. Disorders of Leukocytes Leukopenia is a condition in which too few leukocytes are produced. If this condition is pronounced, the individual may be unable to ward off disease. Excessive leukocyte proliferation is known as leukocytosis. Although leukocyte counts are high, the cells themselves are often nonfunctional, leaving the individual at increased risk for disease. Leukemia is a cancer involving an abundance of leukocytes. It may involve only one specific type of leukocyte from either the myeloid line (myelocytic leukemia) or the lymphoid line (lymphocytic leukemia). In chronic leukemia, mature leukocytes accumulate and fail to die. In acute leukemia, there is an overproduction of young, immature leukocytes. In both conditions the cells do not function properly. Lymphoma is a form of cancer in which masses of malignant T and/or B lymphocytes collect in lymph nodes, the spleen, the liver, and other tissues. As in leukemia, the malignant leukocytes do not function properly, and the patient is vulnerable to infection. Some forms of lymphoma tend to progress slowly and respond well to treatment. Others tend to progress quickly and require aggressive treatment, without which they are rapidly fatal. Platelets You may occasionally see platelets referred to as thrombocytes, but because this name suggests they are a type of cell, it is not accurate. A platelet is not a cell but rather a fragment of the cytoplasm of a cell called a megakaryocyte that is surrounded by a plasma membrane. Megakaryocytes are descended from myeloid stem cells (see Figure 18.4) and are large, typically 50–100 µm in diameter, and contain an enlarged, lobed nucleus. As noted earlier, thrombopoietin, a glycoprotein secreted by the kidneys and liver, stimulates the proliferation of megakaryoblasts, which mature into megakaryocytes. These remain within bone marrow tissue (Figure 18.12) and ultimately form platelet-precursor extensions that extend through the walls of bone marrow capillaries to release into the circulation thousands of cytoplasmic fragments, each enclosed by a bit of plasma membrane. These enclosed fragments are platelets. Each megakarocyte releases 2000–3000 platelets during its lifespan. Following platelet release, megakaryocyte remnants, which are little more than a cell nucleus, are consumed by macrophages. Platelets are relatively small, 2–4 µm in diameter, but numerous, with typically 150,000–160,000 per µL of blood. After entering the circulation, approximately one-third migrate to the spleen for storage for later release in response to any rupture in a blood vessel. They then become activated to perform their primary function, which is to limit blood loss. Platelets remain only about 10 days, then are phagocytized by macrophages. Platelets are critical to hemostasis, the stoppage of blood flow following damage to a vessel. They also secrete a variety of growth factors essential for growth and repair of tissue, particularly connective tissue. Infusions of concentrated platelets are now being used in some therapies to stimulate healing. Disorders of Platelets Thrombocytosis is a condition in which there are too many platelets. This may trigger formation of unwanted blood clots (thrombosis), a potentially fatal disorder. If there is an insufficient number of platelets, called thrombocytopenia, blood may not clot properly, and excessive bleeding may result. Figure 18.12 Platelets Platelets are derived from cells called megakaryocytes. INTERACTIVE LINK Figure 18.13 Leukocytes (Micrographs provided by the Regents of University of Michigan Medical School © 2012) View University of Michigan Webscopes at http://virtualslides.med.umich.edu/Histology/Cardiovascular%20System/081-2_HISTO_40X.svs/view.apml?cwidth=860&cheight=733&chost=virtualslides.med.umich.edu&listview=1&title=&csis=1 and explore the blood slides in greater detail. The Webscope feature allows you to move the slides as you would with a mechanical stage. You can increase and decrease the magnification. There is a chance to review each of the leukocytes individually after you have attempted to identify them from the first two blood smears. In addition, there are a few multiple choice questions. Are you able to recognize and identify the various formed elements? You will need to do this is a systematic manner, scanning along the image. The standard method is to use a grid, but this is not possible with this resource. Try constructing a simple table with each leukocyte type and then making a mark for each cell type you identify. Attempt to classify at least 50 and perhaps as many as 100 different cells. Based on the percentage of cells that you count, do the numbers represent a normal blood smear or does something appear to be abnormal? Hemostasis - Describe the three mechanisms involved in hemostasis - Explain how the extrinsic and intrinsic coagulation pathways lead to the common pathway, and the coagulation factors involved in each - Discuss disorders affecting hemostasis Platelets are key players in hemostasis, the process by which the body seals a ruptured blood vessel and prevents further loss of blood. Although rupture of larger vessels usually requires medical intervention, hemostasis is quite effective in dealing with small, simple wounds. There are three steps to the process: vascular spasm, the formation of a platelet plug, and coagulation (blood clotting). Failure of any of these steps will result in hemorrhage—excessive bleeding. Vascular Spasm When a vessel is severed or punctured, or when the wall of a vessel is damaged, vascular spasm occurs. In vascular spasm, the smooth muscle in the walls of the vessel contracts dramatically. This smooth muscle has both circular layers; larger vessels also have longitudinal layers. The circular layers tend to constrict the flow of blood, whereas the longitudinal layers, when present, draw the vessel back into the surrounding tissue, often making it more difficult for a surgeon to locate, clamp, and tie off a severed vessel. The vascular spasm response is believed to be triggered by several chemicals called endothelins that are released by vessel-lining cells and by pain receptors in response to vessel injury. This phenomenon typically lasts for up to 30 minutes, although it can last for hours. Formation of the Platelet Plug In the second step, platelets, which normally float free in the plasma, encounter the area of vessel rupture with the exposed underlying connective tissue and collagenous fibers. The platelets begin to clump together, become spiked and sticky, and bind to the exposed collagen and endothelial lining. This process is assisted by a glycoprotein in the blood plasma called von Willebrand factor, which helps stabilize the growing platelet plug. As platelets collect, they simultaneously release chemicals from their granules into the plasma that further contribute to hemostasis. Among the substances released by the platelets are: - adenosine diphosphate (ADP), which helps additional platelets to adhere to the injury site, reinforcing and expanding the platelet plug - serotonin, which maintains vasoconstriction - prostaglandins and phospholipids, which also maintain vasoconstriction and help to activate further clotting chemicals, as discussed next A platelet plug can temporarily seal a small opening in a blood vessel. Plug formation, in essence, buys the body time while more sophisticated and durable repairs are being made. In a similar manner, even modern naval warships still carry an assortment of wooden plugs to temporarily repair small breaches in their hulls until permanent repairs can be made. Coagulation Those more sophisticated and more durable repairs are collectively called coagulation, the formation of a blood clot. The process is sometimes characterized as a cascade, because one event prompts the next as in a multi-level waterfall. The result is the production of a gelatinous but robust clot made up of a mesh of fibrin—an insoluble filamentous protein derived from fibrinogen, the plasma protein introduced earlier—in which platelets and blood cells are trapped. Figure 18.14 summarizes the three steps of hemostasis. Figure 18.14 Hemostasis (a) An injury to a blood vessel initiates the process of hemostasis. Blood clotting involves three steps. First, vascular spasm constricts the flow of blood. Next, a platelet plug forms to temporarily seal small openings in the vessel. Coagulation then enables the repair of the vessel wall once the leakage of blood has stopped. (b) The synthesis of fibrin in blood clots involves either an intrinsic pathway or an extrinsic pathway, both of which lead to a common pathway. (credit a: Kevin MacKenzie) Clotting Factors Involved in Coagulation In the coagulation cascade, chemicals called clotting factors (or coagulation factors) prompt reactions that activate still more coagulation factors. The process is complex, but is initiated along two basic pathways: - The extrinsic pathway, which normally is triggered by trauma. - The intrinsic pathway, which begins in the bloodstream and is triggered by internal damage to the wall of the vessel. Both of these merge into a third pathway, referred to as the common pathway (see Figure 18.14b). All three pathways are dependent upon the 12 known clotting factors, including Ca2+ and vitamin K (Table 18.1). Clotting factors are secreted primarily by the liver and the platelets. The liver requires the fat-soluble vitamin K to produce many of them. Vitamin K (along with biotin and folate) is somewhat unusual among vitamins in that it is not only consumed in the diet but is also synthesized by bacteria residing in the large intestine. The calcium ion, considered factor IV, is derived from the diet and from the breakdown of bone. Some recent evidence indicates that activation of various clotting factors occurs on specific receptor sites on the surfaces of platelets. The 12 clotting factors are numbered I through XIII according to the order of their discovery. Factor VI was once believed to be a distinct clotting factor, but is now thought to be identical to factor V. Rather than renumber the other factors, factor VI was allowed to remain as a placeholder and also a reminder that knowledge changes over time. Clotting Factors \| Factor number \| Name \| Type of molecule \| Source \| Pathway(s) \| \|---\|---\|---\|---\|---\| \| I \| Fibrinogen \| Plasma protein \| Liver \| Common; converted into fibrin \| \| II \| Prothrombin \| Plasma protein \| Liver* \| Common; converted into thrombin \| \| III \| Tissue thromboplastin or tissue factor \| Lipoprotein mixture \| Damaged cells and platelets \| Extrinsic \| \| IV \| Calcium ions \| Inorganic ions in plasma \| Diet, platelets, bone matrix \| Entire process \| \| V \| Proaccelerin \| Plasma protein \| Liver, platelets \| Extrinsic and intrinsic \| \| VI \| Not used \| Not used \| Not used \| Not used \| \| VII \| Proconvertin \| Plasma protein \| Liver * \| Extrinsic \| \| VIII \| Antihemolytic factor A \| Plasma protein factor \| Platelets and endothelial cells \| Intrinsic; deficiency results in hemophilia A \| \| IX \| Antihemolytic factor B (plasma thromboplastin component) \| Plasma protein \| Liver* \| Intrinsic; deficiency results in hemophilia B \| \| X \| Stuart–Prower factor (thrombokinase) \| Protein \| Liver* \| Extrinsic and intrinsic \| \| XI \| Antihemolytic factor C (plasma thromboplastin antecedent) \| Plasma protein \| Liver \| Intrinsic; deficiency results in hemophilia C \| \| XII \| Hageman factor \| Plasma protein \| Liver \| Intrinsic; initiates clotting in vitro also activates plasmin \| \| XIII \| Fibrin-stabilizing factor \| Plasma protein \| Liver, platelets \| Stabilizes fibrin; slows fibrinolysis \| Table 18.1 *Vitamin K required. Extrinsic Pathway The quicker responding and more direct extrinsic pathway (also known as the tissue factor pathway) begins when damage occurs to the surrounding tissues, such as in a traumatic injury. Upon contact with blood plasma, the damaged extravascular cells, which are extrinsic to the bloodstream, release factor III (thromboplastin). Sequentially, Ca2+ then factor VII (proconvertin), which is activated by factor III, are added, forming an enzyme complex. This enzyme complex leads to activation of factor X (Stuart–Prower factor), which activates the common pathway discussed below. The events in the extrinsic pathway are completed in a matter of seconds. Intrinsic Pathway The intrinsic pathway (also known as the contact activation pathway) is longer and more complex. In this case, the factors involved are intrinsic to (present within) the bloodstream. The pathway can be prompted by damage to the tissues, resulting from internal factors such as arterial disease; however, it is most often initiated when factor XII (Hageman factor) comes into contact with foreign materials, such as when a blood sample is put into a glass test tube. Within the body, factor XII is typically activated when it encounters negatively charged molecules, such as inorganic polymers and phosphate produced earlier in the series of intrinsic pathway reactions. Factor XII sets off a series of reactions that in turn activates factor XI (antihemolytic factor C or plasma thromboplastin antecedent) then factor IX (antihemolytic factor B or plasma thromboplasmin). In the meantime, chemicals released by the platelets increase the rate of these activation reactions. Finally, factor VIII (antihemolytic factor A) from the platelets and endothelial cells combines with factor IX (antihemolytic factor B or plasma thromboplasmin) to form an enzyme complex that activates factor X (Stuart–Prower factor or thrombokinase), leading to the common pathway. The events in the intrinsic pathway are completed in a few minutes. Common Pathway Both the intrinsic and extrinsic pathways lead to the common pathway, in which fibrin is produced to seal off the vessel. Once factor X has been activated by either the intrinsic or extrinsic pathway, the enzyme prothrombinase converts factor II, the inactive enzyme prothrombin, into the active enzyme thrombin. (Note that if the enzyme thrombin were not normally in an inactive form, clots would form spontaneously, a condition not consistent with life.) Then, thrombin converts factor I, the soluble fibrinogen, into the insoluble fibrin protein strands. Factor XIII then stabilizes the fibrin clot. Fibrinolysis The stabilized clot is acted upon by contractile proteins within the platelets. As these proteins contract, they pull on the fibrin threads, bringing the edges of the clot more tightly together, somewhat as we do when tightening loose shoelaces (see Figure 18.14a). This process also wrings out of the clot a small amount of fluid called serum, which is blood plasma without its clotting factors. To restore normal blood flow as the vessel heals, the clot must eventually be removed. Fibrinolysis is the gradual degradation of the clot. Again, there is a fairly complicated series of reactions that involves factor XII and protein-catabolizing enzymes. During this process, the inactive protein plasminogen is converted into the active plasmin, which gradually breaks down the fibrin of the clot. Additionally, bradykinin, a vasodilator, is released, reversing the effects of the serotonin and prostaglandins from the platelets. This allows the smooth muscle in the walls of the vessels to relax and helps to restore the circulation. Plasma Anticoagulants An anticoagulant is any substance that opposes coagulation. Several circulating plasma anticoagulants play a role in limiting the coagulation process to the region of injury and restoring a normal, clot-free condition of blood. For instance, a cluster of proteins collectively referred to as the protein C system inactivates clotting factors involved in the intrinsic pathway. TFPI (tissue factor pathway inhibitor) inhibits the conversion of the inactive factor VII to the active form in the extrinsic pathway. Antithrombin inactivates factor X and opposes the conversion of prothrombin (factor II) to thrombin in the common pathway. And as noted earlier, basophils release heparin, a short-acting anticoagulant that also opposes prothrombin. Heparin is also found on the surfaces of cells lining the blood vessels. A pharmaceutical form of heparin is often administered therapeutically, for example, in surgical patients at risk for blood clots. INTERACTIVE LINK View these animations to explore the intrinsic, extrinsic, and common pathways that are involved the process of coagulation. The coagulation cascade restores hemostasis by activating coagulation factors in the presence of an injury. How does the endothelium of the blood vessel walls prevent the blood from coagulating as it flows through the blood vessels? Disorders of Clotting Either an insufficient or an excessive production of platelets can lead to severe disease or death. As discussed earlier, an insufficient number of platelets, called thrombocytopenia, typically results in the inability of blood to form clots. This can lead to excessive bleeding, even from minor wounds. Another reason for failure of the blood to clot is the inadequate production of functional amounts of one or more clotting factors. This is the case in the genetic disorder hemophilia, which is actually a group of related disorders, the most common of which is hemophilia A, accounting for approximately 80 percent of cases. This disorder results in the inability to synthesize sufficient quantities of factor VIII. Hemophilia B is the second most common form, accounting for approximately 20 percent of cases. In this case, there is a deficiency of factor IX. Both of these defects are linked to the X chromosome and are typically passed from a healthy (carrier) mother to her male offspring, since males are XY. Females would need to inherit a defective gene from each parent to manifest the disease, since they are XX. Patients with hemophilia bleed from even minor internal and external wounds, and leak blood into joint spaces after exercise and into urine and stool. Hemophilia C is a rare condition that is triggered by an autosomal (not sex) chromosome that renders factor XI nonfunctional. It is not a true recessive condition, since even individuals with a single copy of the mutant gene show a tendency to bleed. Regular infusions of clotting factors isolated from healthy donors can help prevent bleeding in hemophiliac patients. At some point, genetic therapy will become a viable option. In contrast to the disorders characterized by coagulation failure is thrombocytosis, also mentioned earlier, a condition characterized by excessive numbers of platelets that increases the risk for excessive clot formation, a condition known as thrombosis. A thrombus (plural = thrombi) is an aggregation of platelets, erythrocytes, and even WBCs typically trapped within a mass of fibrin strands. While the formation of a clot is normal following the hemostatic mechanism just described, thrombi can form within an intact or only slightly damaged blood vessel. In a large vessel, a thrombus will adhere to the vessel wall and decrease the flow of blood, and is referred to as a mural thrombus. In a small vessel, it may actually totally block the flow of blood and is termed an occlusive thrombus. Thrombi are most commonly caused by vessel damage to the endothelial lining, which activates the clotting mechanism. These may include venous stasis, when blood in the veins, particularly in the legs, remains stationary for long periods. This is one of the dangers of long airplane flights in crowded conditions and may lead to deep vein thrombosis or atherosclerosis, an accumulation of debris in arteries. Thrombophilia, also called hypercoagulation, is a condition in which there is a tendency to form thrombosis. This may be familial (genetic) or acquired. Acquired forms include the autoimmune disease lupus, immune reactions to heparin, polycythemia vera, thrombocytosis, sickle cell disease, pregnancy, and even obesity. A thrombus can seriously impede blood flow to or from a region and will cause a local increase in blood pressure. If flow is to be maintained, the heart will need to generate a greater pressure to overcome the resistance. When a portion of a thrombus breaks free from the vessel wall and enters the circulation, it is referred to as an embolus. An embolus that is carried through the bloodstream can be large enough to block a vessel critical to a major organ. When it becomes trapped, an embolus is called an embolism. In the heart, brain, or lungs, an embolism may accordingly cause a heart attack, a stroke, or a pulmonary embolism. These are medical emergencies. Among the many known biochemical activities of aspirin is its role as an anticoagulant. Aspirin (acetylsalicylic acid) is very effective at inhibiting the aggregation of platelets. It is routinely administered during a heart attack or stroke to reduce the adverse effects. Physicians sometimes recommend that patients at risk for cardiovascular disease take a low dose of aspirin on a daily basis as a preventive measure. However, aspirin can also lead to serious side effects, including increasing the risk of ulcers. A patient is well advised to consult a physician before beginning any aspirin regimen. A class of drugs collectively known as thrombolytic agents can help speed up the degradation of an abnormal clot. If a thrombolytic agent is administered to a patient within 3 hours following a thrombotic stroke, the patient’s prognosis improves significantly. However, some strokes are not caused by thrombi, but by hemorrhage. Thus, the cause must be determined before treatment begins. Tissue plasminogen activator is an enzyme that catalyzes the conversion of plasminogen to plasmin, the primary enzyme that breaks down clots. It is released naturally by endothelial cells but is also used in clinical medicine. New research is progressing using compounds isolated from the venom of some species of snakes, particularly vipers and cobras, which may eventually have therapeutic value as thrombolytic agents. Blood Typing - Describe the two basic physiological consequences of transfusion of incompatible blood - Compare and contrast ABO and Rh blood groups - Identify which blood groups may be safely transfused into patients with different ABO types - Discuss the pathophysiology of hemolytic disease of the newborn Blood transfusions in humans were risky procedures until the discovery of the major human blood groups by Karl Landsteiner, an Austrian biologist and physician, in 1900. Until that point, physicians did not understand that death sometimes followed blood transfusions, when the type of donor blood infused into the patient was incompatible with the patient’s own blood. Blood groups are determined by the presence or absence of specific marker molecules on the plasma membranes of erythrocytes. With their discovery, it became possible for the first time to match patient-donor blood types and prevent transfusion reactions and deaths. Antigens, Antibodies, and Transfusion Reactions Antigens are substances that the body does not recognize as belonging to the “self” and that therefore trigger a defensive response from the leukocytes of the immune system. (Seek more content for additional information on immunity.) Here, we will focus on the role of immunity in blood transfusion reactions. With RBCs in particular, you may see the antigens referred to as isoantigens or agglutinogens (surface antigens) and the antibodies referred to as isoantibodies or agglutinins. In this chapter, we will use the more common terms antigens and antibodies. Antigens are generally large proteins, but may include other classes of organic molecules, including carbohydrates, lipids, and nucleic acids. Following an infusion of incompatible blood, erythrocytes with foreign antigens appear in the bloodstream and trigger an immune response. Proteins called antibodies (immunoglobulins), which are produced by certain B lymphocytes called plasma cells, attach to the antigens on the plasma membranes of the infused erythrocytes and cause them to adhere to one another. - Because the arms of the Y-shaped antibodies attach randomly to more than one nonself erythrocyte surface, they form clumps of erythrocytes. This process is called agglutination. - The clumps of erythrocytes block small blood vessels throughout the body, depriving tissues of oxygen and nutrients. - As the erythrocyte clumps are degraded, in a process called hemolysis, their hemoglobin is released into the bloodstream. This hemoglobin travels to the kidneys, which are responsible for filtration of the blood. However, the load of hemoglobin released can easily overwhelm the kidney’s capacity to clear it, and the patient can quickly develop kidney failure. More than 50 antigens have been identified on erythrocyte membranes, but the most significant in terms of their potential harm to patients are classified in two groups: the ABO blood group and the Rh blood group. The ABO Blood Group Although the ABO blood group name consists of three letters, ABO blood typing designates the presence or absence of just two antigens, A and B. Both are glycoproteins. People whose erythrocytes have A antigens on their erythrocyte membrane surfaces are designated blood type A, and those whose erythrocytes have B antigens are blood type B. People can also have both A and B antigens on their erythrocytes, in which case they are blood type AB. People with neither A nor B antigens are designated blood type O. ABO blood types are genetically determined. Normally the body must be exposed to a foreign antigen before an antibody can be produced. This is not the case for the ABO blood group. Individuals with type A blood—without any prior exposure to incompatible blood—have preformed antibodies to the B antigen circulating in their blood plasma. These antibodies, referred to as anti-B antibodies, will cause agglutination and hemolysis if they ever encounter erythrocytes with B antigens. Similarly, an individual with type B blood has pre-formed anti-A antibodies. Individuals with type AB blood, which has both antigens, do not have preformed antibodies to either of these. People with type O blood lack antigens A and B on their erythrocytes, but both anti-A and anti-B antibodies circulate in their blood plasma. Rh Blood Groups The Rh blood group is classified according to the presence or absence of a second erythrocyte antigen identified as Rh. (It was first discovered in a type of primate known as a rhesus macaque, which is often used in research, because its blood is similar to that of humans.) Although dozens of Rh antigens have been identified, only one, designated D, is clinically important. Those who have the Rh D antigen present on their erythrocytes—about 85 percent of Americans—are described as Rh positive (Rh+) and those who lack it are Rh negative (Rh−). Note that the Rh group is distinct from the ABO group, so any individual, no matter their ABO blood type, may have or lack this Rh antigen. When identifying a patient’s blood type, the Rh group is designated by adding the word positive or negative to the ABO type. For example, A positive (A+) means ABO group A blood with the Rh antigen present, and AB negative (AB−) means ABO group AB blood without the Rh antigen. Table 18.2 summarizes the distribution of the ABO and Rh blood types within the United States. Summary of ABO and Rh Blood Types within the United States \| Blood Type \| African-Americans \| Asian-Americans \| Caucasian-Americans \| Latino/Latina-Americans \| \|---\|---\|---\|---\|---\| \| A+ \| 24 \| 27 \| 33 \| 29 \| \| A− \| 2 \| 0.5 \| 7 \| 2 \| \| B+ \| 18 \| 25 \| 9 \| 9 \| \| B− \| 1 \| 0.4 \| 2 \| 1 \| \| AB+ \| 4 \| 7 \| 3 \| 2 \| \| AB− \| 0.3 \| 0.1 \| 1 \| 0.2 \| \| O+ \| 47 \| 39 \| 37 \| 53 \| \| O− \| 4 \| 1 \| 8 \| 4 \| Table 18.2 n contrast to the ABO group antibodies, which are preformed, antibodies to the Rh antigen are produced only in Rh− individuals after exposure to the antigen. This process, called sensitization, occurs following a transfusion with Rh-incompatible blood or, more commonly, with the birth of an Rh+ baby to an Rh− mother. Problems are rare in a first pregnancy, since the baby’s Rh+cells rarely cross the placenta (the organ of gas and nutrient exchange between the baby and the mother). However, during or immediately after birth, the Rh− mother can be exposed to the baby’s Rh+ cells (Figure 18.15). Research has shown that this occurs in about 13−14 percent of such pregnancies. After exposure, the mother’s immune system begins to generate anti-Rh antibodies. If the mother should then conceive another Rh+ baby, the Rh antibodies she has produced can cross the placenta into the fetal bloodstream and destroy the fetal RBCs. This condition, known as hemolytic disease of the newborn (HDN) or erythroblastosis fetalis, may cause anemia in mild cases, but the agglutination and hemolysis can be so severe that without treatment the fetus may die in the womb or shortly after birth. Figure 18.15 Erythroblastosis Fetalis The first exposure of an Rh− mother to Rh+ erythrocytes during pregnancy induces sensitization. Anti-Rh antibodies begin to circulate in the mother’s bloodstream. A second exposure occurs with a subsequent pregnancy with an Rh+ fetus in the uterus. Maternal anti-Rh antibodies may cross the placenta and enter the fetal bloodstream, causing agglutination and hemolysis of fetal erythrocytes. A drug known as RhoGAM, short for Rh immune globulin, can temporarily prevent the development of Rh antibodies in the Rh−mother, thereby averting this potentially serious disease for the fetus. RhoGAM antibodies destroy any fetal Rh+ erythrocytes that may cross the placental barrier. RhoGAM is normally administered to Rh− mothers during weeks 26−28 of pregnancy and within 72 hours following birth. It has proven remarkably effective in decreasing the incidence of HDN. Earlier we noted that the incidence of HDN in an Rh+ subsequent pregnancy to an Rh− mother is about 13–14 percent without preventive treatment. Since the introduction of RhoGAM in 1968, the incidence has dropped to about 0.1 percent in the United States. Determining ABO Blood Types Clinicians are able to determine a patient’s blood type quickly and easily using commercially prepared antibodies. An unknown blood sample is allocated into separate wells. Into one well a small amount of anti-A antibody is added, and to another a small amount of anti-B antibody. If the antigen is present, the antibodies will cause visible agglutination of the cells (Figure 18.16). The blood should also be tested for Rh antibodies. Figure 18.16 Cross Matching Blood Types This sample of a commercially produced “bedside” card enables quick typing of both a recipient’s and donor’s blood before transfusion. The card contains three reaction sites or wells. One is coated with an anti-A antibody, one with an anti-B antibody, and one with an anti-D antibody (tests for the presence of Rh factor D). Mixing a drop of blood and saline into each well enables the blood to interact with a preparation of type-specific antibodies, also called anti-seras. Agglutination of RBCs in a given site indicates a positive identification of the blood antigens, in this case A and Rh antigens for blood type A+. For the purpose of transfusion, the donor’s and recipient’s blood types must match. ABO Transfusion Protocols To avoid transfusion reactions, it is best to transfuse only matching blood types; that is, a type B+ recipient should ideally receive blood only from a type B+ donor and so on. That said, in emergency situations, when acute hemorrhage threatens the patient’s life, there may not be time for cross matching to identify blood type. In these cases, blood from a universal donor—an individual with type O− blood—may be transfused. Recall that type O erythrocytes do not display A or B antigens. Thus, anti-A or anti-B antibodies that might be circulating in the patient’s blood plasma will not encounter any erythrocyte surface antigens on the donated blood and therefore will not be provoked into a response. One problem with this designation of universal donor is if the O− individual had prior exposure to Rh antigen, Rh antibodies may be present in the donated blood. Also, introducing type O blood into an individual with type A, B, or AB blood will nevertheless introduce antibodies against both A and B antigens, as these are always circulating in the type O blood plasma. This may cause problems for the recipient, but because the volume of blood transfused is much lower than the volume of the patient’s own blood, the adverse effects of the relatively few infused plasma antibodies are typically limited. Rh factor also plays a role. If Rh− individuals receiving blood have had prior exposure to Rh antigen, antibodies for this antigen may be present in the blood and trigger agglutination to some degree. Although it is always preferable to cross match a patient’s blood before transfusing, in a true life-threatening emergency situation, this is not always possible, and these procedures may be implemented. A patient with blood type AB+ is known as the universal recipient. This patient can theoretically receive any type of blood, because the patient’s own blood—having both A and B antigens on the erythrocyte surface—does not produce anti-A or anti-B antibodies. In addition, an Rh+ patient can receive both Rh+ and Rh− blood. However, keep in mind that the donor’s blood will contain circulating antibodies, again with possible negative implications. Figure 18.17 summarizes the blood types and compatibilities. At the scene of multiple-vehicle accidents, military engagements, and natural or human-caused disasters, many victims may suffer simultaneously from acute hemorrhage, yet type O blood may not be immediately available. In these circumstances, medics may at least try to replace some of the volume of blood that has been lost. This is done by intravenous administration of a saline solution that provides fluids and electrolytes in proportions equivalent to those of normal blood plasma. Research is ongoing to develop a safe and effective artificial blood that would carry out the oxygen-carrying function of blood without the RBCs, enabling transfusions in the field without concern for incompatibility. These blood substitutes normally contain hemoglobin- as well as perfluorocarbon-based oxygen carriers. Figure 18.17 ABO Blood Group This chart summarizes the characteristics of the blood types in the ABO blood group. See the text for more on the concept of a universal donor or recipient. Key Terms - ABO blood group - blood-type classification based on the presence or absence of A and B glycoproteins on the erythrocyte membrane surface - agglutination - clustering of cells into masses linked by antibodies - agranular leukocytes - leukocytes with few granules in their cytoplasm; specifically, monocytes, lymphocytes, and NK cells - albumin - most abundant plasma protein, accounting for most of the osmotic pressure of plasma - anemia - deficiency of red blood cells or hemoglobin - antibodies - (also, immunoglobulins or gamma globulins) antigen-specific proteins produced by specialized B lymphocytes that protect the body by binding to foreign objects such as bacteria and viruses - anticoagulant - substance such as heparin that opposes coagulation - antithrombin - anticoagulant that inactivates factor X and opposes the conversion of prothrombin (factor II) into thrombin in the common pathway - B lymphocytes - (also, B cells) lymphocytes that defend the body against specific pathogens and thereby provide specific immunity - basophils - granulocytes that stain with a basic (alkaline) stain and store histamine and heparin - bilirubin - yellowish bile pigment produced when iron is removed from heme and is further broken down into waste products - biliverdin - green bile pigment produced when the non-iron portion of heme is degraded into a waste product; converted to bilirubin in the liver - blood - liquid connective tissue composed of formed elements—erythrocytes, leukocytes, and platelets—and a fluid extracellular matrix called plasma; component of the cardiovascular system - bone marrow biopsy - diagnostic test of a sample of red bone marrow - bone marrow transplant - treatment in which a donor’s healthy bone marrow with its stem cells replaces diseased or damaged bone marrow of a patient - buffy coat - thin, pale layer of leukocytes and platelets that separates the erythrocytes from the plasma in a sample of centrifuged blood - carbaminohemoglobin - compound of carbon dioxide and hemoglobin, and one of the ways in which carbon dioxide is carried in the blood - clotting factors - group of 12 identified substances active in coagulation - coagulation - formation of a blood clot; part of the process of hemostasis - colony-stimulating factors (CSFs) - glycoproteins that trigger the proliferation and differentiation of myeloblasts into granular leukocytes (basophils, neutrophils, and eosinophils) - common pathway - final coagulation pathway activated either by the intrinsic or the extrinsic pathway, and ending in the formation of a blood clot - cross matching - blood test for identification of blood type using antibodies and small samples of blood - cytokines - class of proteins that act as autocrine or paracrine signaling molecules; in the cardiovascular system, they stimulate the proliferation of progenitor cells and help to stimulate both nonspecific and specific resistance to disease - defensins - antimicrobial proteins released from neutrophils and macrophages that create openings in the plasma membranes to kill cells - deoxyhemoglobin - molecule of hemoglobin without an oxygen molecule bound to it - diapedesis - (also, emigration) process by which leukocytes squeeze through adjacent cells in a blood vessel wall to enter tissues - embolus - thrombus that has broken free from the blood vessel wall and entered the circulation - emigration - (also, diapedesis) process by which leukocytes squeeze through adjacent cells in a blood vessel wall to enter tissues - eosinophils - granulocytes that stain with eosin; they release antihistamines and are especially active against parasitic worms - erythrocyte - (also, red blood cell) mature myeloid blood cell that is composed mostly of hemoglobin and functions primarily in the transportation of oxygen and carbon dioxide - erythropoietin (EPO) - glycoprotein that triggers the bone marrow to produce RBCs; secreted by the kidney in response to low oxygen levels - extrinsic pathway - initial coagulation pathway that begins with tissue damage and results in the activation of the common pathway - ferritin - protein-containing storage form of iron found in the bone marrow, liver, and spleen - fibrin - insoluble, filamentous protein that forms the structure of a blood clot - fibrinogen - plasma protein produced in the liver and involved in blood clotting - fibrinolysis - gradual degradation of a blood clot - formed elements - cellular components of blood; that is, erythrocytes, leukocytes, and platelets - globin - heme-containing globular protein that is a constituent of hemoglobin - globulins - heterogeneous group of plasma proteins that includes transport proteins, clotting factors, immune proteins, and others - granular leukocytes - leukocytes with abundant granules in their cytoplasm; specifically, neutrophils, eosinophils, and basophils - hematocrit - (also, packed cell volume) volume percentage of erythrocytes in a sample of centrifuged blood - heme - red, iron-containing pigment to which oxygen binds in hemoglobin - hemocytoblast - hemopoietic stem cell that gives rise to the formed elements of blood - hemoglobin - oxygen-carrying compound in erythrocytes - hemolysis - destruction (lysis) of erythrocytes and the release of their hemoglobin into circulation - hemolytic disease of the newborn (HDN) - (also, erythroblastosis fetalis) disorder causing agglutination and hemolysis in an Rh+ fetus or newborn of an Rh− mother - hemophilia - genetic disorder characterized by inadequate synthesis of clotting factors - hemopoiesis - production of the formed elements of blood - hemopoietic growth factors - chemical signals including erythropoietin, thrombopoietin, colony-stimulating factors, and interleukins that regulate the differentiation and proliferation of particular blood progenitor cells - hemopoietic stem cell - type of pluripotent stem cell that gives rise to the formed elements of blood (hemocytoblast) - hemorrhage - excessive bleeding - hemosiderin - protein-containing storage form of iron found in the bone marrow, liver, and spleen - hemostasis - physiological process by which bleeding ceases - heparin - short-acting anticoagulant stored in mast cells and released when tissues are injured, opposes prothrombin - hypoxemia - below-normal level of oxygen saturation of blood (typically <95 percent) - immunoglobulins - (also, antibodies or gamma globulins) antigen-specific proteins produced by specialized B lymphocytes that protect the body by binding to foreign objects such as bacteria and viruses - interleukins - signaling molecules that may function in hemopoiesis, inflammation, and specific immune responses - intrinsic pathway - initial coagulation pathway that begins with vascular damage or contact with foreign substances, and results in the activation of the common pathway - leukemia - cancer involving leukocytes - leukocyte - (also, white blood cell) colorless, nucleated blood cell, the chief function of which is to protect the body from disease - leukocytosis - excessive leukocyte proliferation - leukopenia - below-normal production of leukocytes - lymphocytes - agranular leukocytes of the lymphoid stem cell line, many of which function in specific immunity - lymphoid stem cells - type of hemopoietic stem cells that gives rise to lymphocytes, including various T cells, B cells, and NK cells, all of which function in immunity - lymphoma - form of cancer in which masses of malignant T and/or B lymphocytes collect in lymph nodes, the spleen, the liver, and other tissues - lysozyme - digestive enzyme with bactericidal properties - macrophage - phagocytic cell of the myeloid lineage; a matured monocyte - megakaryocyte - bone marrow cell that produces platelets - memory cell - type of B or T lymphocyte that forms after exposure to a pathogen - monocytes - agranular leukocytes of the myeloid stem cell line that circulate in the bloodstream; tissue monocytes are macrophages - myeloid stem cells - type of hemopoietic stem cell that gives rise to some formed elements, including erythrocytes, megakaryocytes that produce platelets, and a myeloblast lineage that gives rise to monocytes and three forms of granular leukocytes (neutrophils, eosinophils, and basophils) - natural killer (NK) cells - cytotoxic lymphocytes capable of recognizing cells that do not express “self” proteins on their plasma membrane or that contain foreign or abnormal markers; provide generalized, nonspecific immunity - neutrophils - granulocytes that stain with a neutral dye and are the most numerous of the leukocytes; especially active against bacteria - oxyhemoglobin - molecule of hemoglobin to which oxygen is bound - packed cell volume (PCV) - (also, hematocrit) volume percentage of erythrocytes present in a sample of centrifuged blood - plasma - in blood, the liquid extracellular matrix composed mostly of water that circulates the formed elements and dissolved materials throughout the cardiovascular system - plasmin - blood protein active in fibrinolysis - platelet plug - accumulation and adhesion of platelets at the site of blood vessel injury - platelets - (also, thrombocytes) one of the formed elements of blood that consists of cell fragments broken off from megakaryocytes - pluripotent stem cell - stem cell that derives from totipotent stem cells and is capable of differentiating into many, but not all, cell types - polycythemia - elevated level of hemoglobin, whether adaptive or pathological - polymorphonuclear - having a lobed nucleus, as seen in some leukocytes - positive chemotaxis - process in which a cell is attracted to move in the direction of chemical stimuli - red blood cells (RBCs) - (also, erythrocytes) one of the formed elements of blood that transports oxygen - reticulocyte - immature erythrocyte that may still contain fragments of organelles - Rh blood group - blood-type classification based on the presence or absence of the antigen Rh on the erythrocyte membrane surface - serum - blood plasma that does not contain clotting factors - sickle cell disease - (also, sickle cell anemia) inherited blood disorder in which hemoglobin molecules are malformed, leading to the breakdown of RBCs that take on a characteristic sickle shape - T lymphocytes - (also, T cells) lymphocytes that provide cellular-level immunity by physically attacking foreign or diseased cells - thalassemia - inherited blood disorder in which maturation of RBCs does not proceed normally, leading to abnormal formation of hemoglobin and the destruction of RBCs - thrombin - enzyme essential for the final steps in formation of a fibrin clot - thrombocytes - platelets, one of the formed elements of blood that consists of cell fragments broken off from megakaryocytes - thrombocytopenia - condition in which there are too few platelets, resulting in abnormal bleeding (hemophilia) - thrombocytosis - condition in which there are too many platelets, resulting in abnormal clotting (thrombosis) - thrombopoietin - hormone secreted by the liver and kidneys that prompts the development of megakaryocytes into thrombocytes (platelets) - thrombosis - excessive clot formation - thrombus - aggregation of fibrin, platelets, and erythrocytes in an intact artery or vein - tissue factor - protein thromboplastin, which initiates the extrinsic pathway when released in response to tissue damage - totipotent stem cell - embryonic stem cell that is capable of differentiating into any and all cells of the body; enabling the full development of an organism - transferrin - plasma protein that binds reversibly to iron and distributes it throughout the body - universal donor - individual with type O− blood - universal recipient - individual with type AB+ blood - vascular spasm - initial step in hemostasis, in which the smooth muscle in the walls of the ruptured or damaged blood vessel contracts - white blood cells (WBCs) - (also, leukocytes) one of the formed elements of blood that provides defense against disease agents and foreign materials Chapter Review 18.1 An Overview of Blood Blood is a fluid connective tissue critical to the transportation of nutrients, gases, and wastes throughout the body; to defend the body against infection and other threats; and to the homeostatic regulation of pH, temperature, and other internal conditions. Blood is composed of formed elements—erythrocytes, leukocytes, and cell fragments called platelets—and a fluid extracellular matrix called plasma. More than 90 percent of plasma is water. The remainder is mostly plasma proteins—mainly albumin, globulins, and fibrinogen—and other dissolved solutes such as glucose, lipids, electrolytes, and dissolved gases. Because of the formed elements and the plasma proteins and other solutes, blood is sticky and more viscous than water. It is also slightly alkaline, and its temperature is slightly higher than normal body temperature. 18.2 Production of the Formed Elements Through the process of hemopoiesis, the formed elements of blood are continually produced, replacing the relatively short-lived erythrocytes, leukocytes, and platelets. Hemopoiesis begins in the red bone marrow, with hemopoietic stem cells that differentiate into myeloid and lymphoid lineages. Myeloid stem cells give rise to most of the formed elements. Lymphoid stem cells give rise only to the various lymphocytes designated as B and T cells, and NK cells. Hemopoietic growth factors, including erythropoietin, thrombopoietin, colony-stimulating factors, and interleukins, promote the proliferation and differentiation of formed elements. 18.3 Erythrocytes The most abundant formed elements in blood, erythrocytes are red, biconcave disks packed with an oxygen-carrying compound called hemoglobin. The hemoglobin molecule contains four globin proteins bound to a pigment molecule called heme, which contains an ion of iron. In the bloodstream, iron picks up oxygen in the lungs and drops it off in the tissues; the amino acids in hemoglobin then transport carbon dioxide from the tissues back to the lungs. Erythrocytes live only 120 days on average, and thus must be continually replaced. Worn-out erythrocytes are phagocytized by macrophages and their hemoglobin is broken down. The breakdown products are recycled or removed as wastes: Globin is broken down into amino acids for synthesis of new proteins; iron is stored in the liver or spleen or used by the bone marrow for production of new erythrocytes; and the remnants of heme are converted into bilirubin, or other waste products that are taken up by the liver and excreted in the bile or removed by the kidneys. Anemia is a deficiency of RBCs or hemoglobin, whereas polycythemia is an excess of RBCs. 18.4 Leukocytes and Platelets Leukocytes function in body defenses. They squeeze out of the walls of blood vessels through emigration or diapedesis, then may move through tissue fluid or become attached to various organs where they fight against pathogenic organisms, diseased cells, or other threats to health. Granular leukocytes, which include neutrophils, eosinophils, and basophils, originate with myeloid stem cells, as do the agranular monocytes. The other agranular leukocytes, NK cells, B cells, and T cells, arise from the lymphoid stem cell line. The most abundant leukocytes are the neutrophils, which are first responders to infections, especially with bacteria. About 20–30 percent of all leukocytes are lymphocytes, which are critical to the body’s defense against specific threats. Leukemia and lymphoma are malignancies involving leukocytes. Platelets are fragments of cells known as megakaryocytes that dwell within the bone marrow. While many platelets are stored in the spleen, others enter the circulation and are essential for hemostasis; they also produce several growth factors important for repair and healing. 18.5 Hemostasis Hemostasis is the physiological process by which bleeding ceases. Hemostasis involves three basic steps: vascular spasm, the formation of a platelet plug, and coagulation, in which clotting factors promote the formation of a fibrin clot. Fibrinolysis is the process in which a clot is degraded in a healing vessel. Anticoagulants are substances that oppose coagulation. They are important in limiting the extent and duration of clotting. Inadequate clotting can result from too few platelets, or inadequate production of clotting factors, for instance, in the genetic disorder hemophilia. Excessive clotting, called thrombosis, can be caused by excessive numbers of platelets. A thrombus is a collection of fibrin, platelets, and erythrocytes that has accumulated along the lining of a blood vessel, whereas an embolus is a thrombus that has broken free from the vessel wall and is circulating in the bloodstream. 18.6 Blood Typing Antigens are nonself molecules, usually large proteins, which provoke an immune response. In transfusion reactions, antibodies attach to antigens on the surfaces of erythrocytes and cause agglutination and hemolysis. ABO blood group antigens are designated A and B. People with type A blood have A antigens on their erythrocytes, whereas those with type B blood have B antigens. Those with AB blood have both A and B antigens, and those with type O blood have neither A nor B antigens. The blood plasma contains preformed antibodies against the antigens not present on a person’s erythrocytes. A second group of blood antigens is the Rh group, the most important of which is Rh D. People with Rh− blood do not have this antigen on their erythrocytes, whereas those who are Rh+ do. About 85 percent of Americans are Rh+. When a woman who is Rh− becomes pregnant with an Rh+ fetus, her body may begin to produce anti-Rh antibodies. If she subsequently becomes pregnant with a second Rh+ fetus and is not treated preventively with RhoGAM, the fetus will be at risk for an antigen-antibody reaction, including agglutination and hemolysis. This is known as hemolytic disease of the newborn. Cross matching to determine blood type is necessary before transfusing blood, unless the patient is experiencing hemorrhage that is an immediate threat to life, in which case type O− blood may be transfused. Interactive Link Questions Visit this site for a list of normal levels established for many of the substances found in a sample of blood. Serum, one of the specimen types included, refers to a sample of plasma after clotting factors have been removed. What types of measurements are given for levels of glucose in the blood? 2.Watch this video to see doctors discuss the dangers of blood doping in sports. What are the some potential side effects of blood doping? 3.Figure 18.13 Are you able to recognize and identify the various formed elements? You will need to do this is a systematic manner, scanning along the image. The standard method is to use a grid, but this is not possible with this resource. Try constructing a simple table with each leukocyte type and then making a mark for each cell type you identify. Attempt to classify at least 50 and perhaps as many as 100 different cells. Based on the percentage of cells that you count, do the numbers represent a normal blood smear or does something appear to be abnormal? 4.View these animations to explore the intrinsic, extrinsic, and common pathways that are involved the process of coagulation. The coagulation cascade restores hemostasis by activating coagulation factors in the presence of an injury. How does the endothelium of the blood vessel walls prevent the blood from coagulating as it flows through the blood vessels? Review Questions Which of the following statements about blood is true? - Blood is about 92 percent water. - Blood is slightly more acidic than water. - Blood is slightly more viscous than water. - Blood is slightly more salty than seawater. Which of the following statements about albumin is true? - It draws water out of the blood vessels and into the body’s tissues. - It is the most abundant plasma protein. - It is produced by specialized leukocytes called plasma cells. - All of the above are true. Which of the following plasma proteins is not produced by the liver? - fibrinogen - alpha globulin - beta globulin - immunoglobulin Which of the formed elements arise from myeloid stem cells? - B cells - natural killer cells - platelets - all of the above Which of the following statements about erythropoietin is true? - It facilitates the proliferation and differentiation of the erythrocyte lineage. - It is a hormone produced by the thyroid gland. - It is a hemopoietic growth factor that prompts lymphoid stem cells to leave the bone marrow. - Both a and b are true. Interleukins are associated primarily with which of the following? - production of various lymphocytes - immune responses - inflammation - all of the above Which of the following statements about mature, circulating erythrocytes is true? - They have no nucleus. - They are packed with mitochondria. - They survive for an average of 4 days. - All of the above A molecule of hemoglobin ________. - is shaped like a biconcave disk packed almost entirely with iron - contains four glycoprotein units studded with oxygen - consists of four globin proteins, each bound to a molecule of heme - can carry up to 120 molecules of oxygen The production of healthy erythrocytes depends upon the availability of ________. - copper - zinc - vitamin B12 - copper, zinc, and vitamin B12 Aging and damaged erythrocytes are removed from the circulation by ________. - myeoblasts - monocytes - macrophages - mast cells A patient has been suffering for 2 months with a chronic, watery diarrhea. A blood test is likely to reveal ________. - a hematocrit below 30 percent - hypoxemia - anemia - polycythemia The process by which leukocytes squeeze through adjacent cells in a blood vessel wall is called ________. - leukocytosis - positive chemotaxis - emigration - cytoplasmic extending Which of the following describes a neutrophil? - abundant, agranular, especially effective against cancer cells - abundant, granular, especially effective against bacteria - rare, agranular, releases antimicrobial defensins - rare, granular, contains multiple granules packed with histamine T and B lymphocytes ________. - are polymorphonuclear - are involved with specific immune function - proliferate excessively in leukopenia - are most active against parasitic worms A patient has been experiencing severe, persistent allergy symptoms that are reduced when she takes an antihistamine. Before the treatment, this patient was likely to have had increased activity of which leukocyte? - basophils - neutrophils - monocytes - natural killer cells Thrombocytes are more accurately called ________. - clotting factors - megakaryoblasts - megakaryocytes - platelets The first step in hemostasis is ________. - vascular spasm - conversion of fibrinogen to fibrin - activation of the intrinsic pathway - activation of the common pathway Prothrombin is converted to thrombin during the ________. - intrinsic pathway - extrinsic pathway - common pathway - formation of the platelet plug Hemophilia is characterized by ________. - inadequate production of heparin - inadequate production of clotting factors - excessive production of fibrinogen - excessive production of platelets The process in which antibodies attach to antigens, causing the formation of masses of linked cells, is called ________. - sensitization - coagulation - agglutination - hemolysis People with ABO blood type O ________. - have both antigens A and B on their erythrocytes - lack both antigens A and B on their erythrocytes - have neither anti-A nor anti-B antibodies circulating in their blood plasma - are considered universal recipients Hemolytic disease of the newborn is a risk during a subsequent pregnancy in which ________. - a type AB mother is carrying a type O fetus - a type O mother is carrying a type AB fetus - an Rh+ mother is carrying an Rh− fetus - an Rh− mother is carrying a second Rh+ fetus Critical Thinking Questions A patient’s hematocrit is 42 percent. Approximately what percentage of the patient’s blood is plasma? 28.Why would it be incorrect to refer to the formed elements as cells? 29.True or false: The buffy coat is the portion of a blood sample that is made up of its proteins. 30.Myelofibrosis is a disorder in which inflammation and scar tissue formation in the bone marrow impair hemopoiesis. One sign is an enlarged spleen. Why? 31.Would you expect a patient with a form of cancer called acute myelogenous leukemia to experience impaired production of erythrocytes, or impaired production of lymphocytes? Explain your choice. 32.A young woman has been experiencing unusually heavy menstrual bleeding for several years. She follows a strict vegan diet (no animal foods). She is at risk for what disorder, and why? 33.A patient has thalassemia, a genetic disorder characterized by abnormal synthesis of globin proteins and excessive destruction of erythrocytes. This patient is jaundiced and is found to have an excessive level of bilirubin in his blood. Explain the connection. 34.One of the more common adverse effects of cancer chemotherapy is the destruction of leukocytes. Before his next scheduled chemotherapy treatment, a patient undergoes a blood test called an absolute neutrophil count (ANC), which reveals that his neutrophil count is 1900 cells per microliter. Would his healthcare team be likely to proceed with his chemotherapy treatment? Why? 35.A patient was admitted to the burn unit the previous evening suffering from a severe burn involving his left upper extremity and shoulder. A blood test reveals that he is experiencing leukocytosis. Why is this an expected finding? 36.A lab technician collects a blood sample in a glass tube. After about an hour, she harvests serum to continue her blood analysis. Explain what has happened during the hour that the sample was in the glass tube. 37.Explain why administration of a thrombolytic agent is a first intervention for someone who has suffered a thrombotic stroke. 38.Following a motor vehicle accident, a patient is rushed to the emergency department with multiple traumatic injuries, causing severe bleeding. The patient’s condition is critical, and there is no time for determining his blood type. What type of blood is transfused, and why? 39.In preparation for a scheduled surgery, a patient visits the hospital lab for a blood draw. The technician collects a blood sample and performs a test to determine its type. She places a sample of the patient’s blood in two wells. To the first well she adds anti-A antibody. To the second she adds anti-B antibody. Both samples visibly agglutinate. Has the technician made an error, or is this a normal response? If normal, what blood type does this indicate?	oercommons	2025-03-18T00:37:00.751671	null	{ "license": "Creative Commons - Attribution - https://creativecommons.org/licenses/by/4.0/", "url": "https://oercommons.org/courseware/lesson/58764/overview", "title": "Anatomy and Physiology, Fluids and Transport", "author": null }
https://oercommons.org/courseware/lesson/58765/overview	The Cardiovascular System: The Heart Overview The Cardiovascular System: The Heart Introduction Figure 19.1 Human Heart This artist’s conception of the human heart suggests a powerful engine—not inappropriate for a muscular pump that keeps the body continually supplied with blood. (credit: Patrick J. Lynch) CHAPTER OBJECTIVES After studying this chapter, you will be able to: - Identify and describe the interior and exterior parts of the human heart - Describe the path of blood through the cardiac circuits - Describe the size, shape, and location of the heart - Compare cardiac muscle to skeletal and smooth muscle - Explain the cardiac conduction system - Describe the process and purpose of an electrocardiogram - Explain the cardiac cycle - Calculate cardiac output - Describe the effects of exercise on cardiac output and heart rate - Name the centers of the brain that control heart rate and describe their function - Identify other factors affecting heart rate - Describe fetal heart development In this chapter, you will explore the remarkable pump that propels the blood into the vessels. There is no single better word to describe the function of the heart other than “pump,” since its contraction develops the pressure that ejects blood into the major vessels: the aorta and pulmonary trunk. From these vessels, the blood is distributed to the remainder of the body. Although the connotation of the term “pump” suggests a mechanical device made of steel and plastic, the anatomical structure is a living, sophisticated muscle. As you read this chapter, try to keep these twin concepts in mind: pump and muscle. Although the term “heart” is an English word, cardiac (heart-related) terminology can be traced back to the Latin term, “kardia.” Cardiology is the study of the heart, and cardiologists are the physicians who deal primarily with the heart. Heart Anatomy - Describe the location and position of the heart within the body cavity - Describe the internal and external anatomy of the heart - Identify the tissue layers of the heart - Relate the structure of the heart to its function as a pump - Compare systemic circulation to pulmonary circulation - Identify the veins and arteries of the coronary circulation system - Trace the pathway of oxygenated and deoxygenated blood thorough the chambers of the heart The vital importance of the heart is obvious. If one assumes an average rate of contraction of 75 contractions per minute, a human heart would contract approximately 108,000 times in one day, more than 39 million times in one year, and nearly 3 billion times during a 75-year lifespan. Each of the major pumping chambers of the heart ejects approximately 70 mL blood per contraction in a resting adult. This would be equal to 5.25 liters of fluid per minute and approximately 14,000 liters per day. Over one year, that would equal 10,000,000 liters or 2.6 million gallons of blood sent through roughly 60,000 miles of vessels. In order to understand how that happens, it is necessary to understand the anatomy and physiology of the heart. Location of the Heart The human heart is located within the thoracic cavity, medially between the lungs in the space known as the mediastinum. Figure 19.2 shows the position of the heart within the thoracic cavity. Within the mediastinum, the heart is separated from the other mediastinal structures by a tough membrane known as the pericardium, or pericardial sac, and sits in its own space called the pericardial cavity. The dorsal surface of the heart lies near the bodies of the vertebrae, and its anterior surface sits deep to the sternum and costal cartilages. The great veins, the superior and inferior venae cavae, and the great arteries, the aorta and pulmonary trunk, are attached to the superior surface of the heart, called the base. The base of the heart is located at the level of the third costal cartilage, as seen in Figure 19.2. The inferior tip of the heart, the apex, lies just to the left of the sternum between the junction of the fourth and fifth ribs near their articulation with the costal cartilages. The right side of the heart is deflected anteriorly, and the left side is deflected posteriorly. It is important to remember the position and orientation of the heart when placing a stethoscope on the chest of a patient and listening for heart sounds, and also when looking at images taken from a midsagittal perspective. The slight deviation of the apex to the left is reflected in a depression in the medial surface of the inferior lobe of the left lung, called the cardiac notch. Figure 19.2 Position of the Heart in the Thorax The heart is located within the thoracic cavity, medially between the lungs in the mediastinum. It is about the size of a fist, is broad at the top, and tapers toward the base. EVERYDAY CONNECTION CPR The position of the heart in the torso between the vertebrae and sternum (see Figure 19.2 for the position of the heart within the thorax) allows for individuals to apply an emergency technique known as cardiopulmonary resuscitation (CPR) if the heart of a patient should stop. By applying pressure with the flat portion of one hand on the sternum in the area between the line at T4 and T9 (Figure 19.3), it is possible to manually compress the blood within the heart enough to push some of the blood within it into the pulmonary and systemic circuits. This is particularly critical for the brain, as irreversible damage and death of neurons occur within minutes of loss of blood flow. Current standards call for compression of the chest at least 5 cm deep and at a rate of 100 compressions per minute, a rate equal to the beat in “Staying Alive,” recorded in 1977 by the Bee Gees. If you are unfamiliar with this song, a version is available on www.youtube.com. At this stage, the emphasis is on performing high-quality chest compressions, rather than providing artificial respiration. CPR is generally performed until the patient regains spontaneous contraction or is declared dead by an experienced healthcare professional. When performed by untrained or overzealous individuals, CPR can result in broken ribs or a broken sternum, and can inflict additional severe damage on the patient. It is also possible, if the hands are placed too low on the sternum, to manually drive the xiphoid process into the liver, a consequence that may prove fatal for the patient. Proper training is essential. This proven life-sustaining technique is so valuable that virtually all medical personnel as well as concerned members of the public should be certified and routinely recertified in its application. CPR courses are offered at a variety of locations, including colleges, hospitals, the American Red Cross, and some commercial companies. They normally include practice of the compression technique on a mannequin. Figure 19.3 CPR Technique If the heart should stop, CPR can maintain the flow of blood until the heart resumes beating. By applying pressure to the sternum, the blood within the heart will be squeezed out of the heart and into the circulation. Proper positioning of the hands on the sternum to perform CPR would be between the lines at T4 and T9. INTERACTIVE LINK Visit the American Heart Association website to help locate a course near your home in the United States. There are also many other national and regional heart associations that offer the same service, depending upon the location. Shape and Size of the Heart The shape of the heart is similar to a pinecone, rather broad at the superior surface and tapering to the apex (see Figure 19.2). A typical heart is approximately the size of your fist: 12 cm (5 in) in length, 8 cm (3.5 in) wide, and 6 cm (2.5 in) in thickness. Given the size difference between most members of the sexes, the weight of a female heart is approximately 250–300 grams (9 to 11 ounces), and the weight of a male heart is approximately 300–350 grams (11 to 12 ounces). The heart of a well-trained athlete, especially one specializing in aerobic sports, can be considerably larger than this. Cardiac muscle responds to exercise in a manner similar to that of skeletal muscle. That is, exercise results in the addition of protein myofilaments that increase the size of the individual cells without increasing their numbers, a concept called hypertrophy. Hearts of athletes can pump blood more effectively at lower rates than those of nonathletes. Enlarged hearts are not always a result of exercise; they can result from pathologies, such as hypertrophic cardiomyopathy. The cause of an abnormally enlarged heart muscle is unknown, but the condition is often undiagnosed and can cause sudden death in apparently otherwise healthy young people. Chambers and Circulation through the Heart The human heart consists of four chambers: The left side and the right side each have one atrium and one ventricle. Each of the upper chambers, the right atrium (plural = atria) and the left atrium, acts as a receiving chamber and contracts to push blood into the lower chambers, the right ventricle and the left ventricle. The ventricles serve as the primary pumping chambers of the heart, propelling blood to the lungs or to the rest of the body. There are two distinct but linked circuits in the human circulation called the pulmonary and systemic circuits. Although both circuits transport blood and everything it carries, we can initially view the circuits from the point of view of gases. The pulmonary circuit transports blood to and from the lungs, where it picks up oxygen and delivers carbon dioxide for exhalation. The systemic circuit transports oxygenated blood to virtually all of the tissues of the body and returns relatively deoxygenated blood and carbon dioxide to the heart to be sent back to the pulmonary circulation. The right ventricle pumps deoxygenated blood into the pulmonary trunk, which leads toward the lungs and bifurcates into the left and right pulmonary arteries. These vessels in turn branch many times before reaching the pulmonary capillaries, where gas exchange occurs: Carbon dioxide exits the blood and oxygen enters. The pulmonary trunk arteries and their branches are the only arteries in the post-natal body that carry relatively deoxygenated blood. Highly oxygenated blood returning from the pulmonary capillaries in the lungs passes through a series of vessels that join together to form the pulmonary veins—the only post-natal veins in the body that carry highly oxygenated blood. The pulmonary veins conduct blood into the left atrium, which pumps the blood into the left ventricle, which in turn pumps oxygenated blood into the aorta and on to the many branches of the systemic circuit. Eventually, these vessels will lead to the systemic capillaries, where exchange with the tissue fluid and cells of the body occurs. In this case, oxygen and nutrients exit the systemic capillaries to be used by the cells in their metabolic processes, and carbon dioxide and waste products will enter the blood. The blood exiting the systemic capillaries is lower in oxygen concentration than when it entered. The capillaries will ultimately unite to form venules, joining to form ever-larger veins, eventually flowing into the two major systemic veins, the superior vena cava and the inferior vena cava, which return blood to the right atrium. The blood in the superior and inferior venae cavae flows into the right atrium, which pumps blood into the right ventricle. This process of blood circulation continues as long as the individual remains alive. Understanding the flow of blood through the pulmonary and systemic circuits is critical to all health professions (Figure 19.4). Figure 19.4 Dual System of the Human Blood Circulation Blood flows from the right atrium to the right ventricle, where it is pumped into the pulmonary circuit. The blood in the pulmonary artery branches is low in oxygen but relatively high in carbon dioxide. Gas exchange occurs in the pulmonary capillaries (oxygen into the blood, carbon dioxide out), and blood high in oxygen and low in carbon dioxide is returned to the left atrium. From here, blood enters the left ventricle, which pumps it into the systemic circuit. Following exchange in the systemic capillaries (oxygen and nutrients out of the capillaries and carbon dioxide and wastes in), blood returns to the right atrium and the cycle is repeated. Membranes, Surface Features, and Layers Our exploration of more in-depth heart structures begins by examining the membrane that surrounds the heart, the prominent surface features of the heart, and the layers that form the wall of the heart. Each of these components plays its own unique role in terms of function. Membranes The membrane that directly surrounds the heart and defines the pericardial cavity is called the pericardium or pericardial sac. It also surrounds the “roots” of the major vessels, or the areas of closest proximity to the heart. The pericardium, which literally translates as “around the heart,” consists of two distinct sublayers: the sturdy outer fibrous pericardium and the inner serous pericardium. The fibrous pericardium is made of tough, dense connective tissue that protects the heart and maintains its position in the thorax. The more delicate serous pericardium consists of two layers: the parietal pericardium, which is fused to the fibrous pericardium, and an inner visceral pericardium, or epicardium, which is fused to the heart and is part of the heart wall. The pericardial cavity, filled with lubricating serous fluid, lies between the epicardium and the pericardium. In most organs within the body, visceral serous membranes such as the epicardium are microscopic. However, in the case of the heart, it is not a microscopic layer but rather a macroscopic layer, consisting of a simple squamous epithelium called a mesothelium, reinforced with loose, irregular, or areolar connective tissue that attaches to the pericardium. This mesothelium secretes the lubricating serous fluid that fills the pericardial cavity and reduces friction as the heart contracts. Figure 19.5illustrates the pericardial membrane and the layers of the heart. Figure 19.5 Pericardial Membranes and Layers of the Heart Wall The pericardial membrane that surrounds the heart consists of three layers and the pericardial cavity. The heart wall also consists of three layers. The pericardial membrane and the heart wall share the epicardium. DISORDERS OF THE... Heart: Cardiac Tamponade If excess fluid builds within the pericardial space, it can lead to a condition called cardiac tamponade, or pericardial tamponade. With each contraction of the heart, more fluid—in most instances, blood—accumulates within the pericardial cavity. In order to fill with blood for the next contraction, the heart must relax. However, the excess fluid in the pericardial cavity puts pressure on the heart and prevents full relaxation, so the chambers within the heart contain slightly less blood as they begin each heart cycle. Over time, less and less blood is ejected from the heart. If the fluid builds up slowly, as in hypothyroidism, the pericardial cavity may be able to expand gradually to accommodate this extra volume. Some cases of fluid in excess of one liter within the pericardial cavity have been reported. Rapid accumulation of as little as 100 mL of fluid following trauma may trigger cardiac tamponade. Other common causes include myocardial rupture, pericarditis, cancer, or even cardiac surgery. Removal of this excess fluid requires insertion of drainage tubes into the pericardial cavity. Premature removal of these drainage tubes, for example, following cardiac surgery, or clot formation within these tubes are causes of this condition. Untreated, cardiac tamponade can lead to death. Surface Features of the Heart Inside the pericardium, the surface features of the heart are visible, including the four chambers. There is a superficial leaf-like extension of the atria near the superior surface of the heart, one on each side, called an auricle—a name that means “ear like”—because its shape resembles the external ear of a human (Figure 19.6). Auricles are relatively thin-walled structures that can fill with blood and empty into the atria or upper chambers of the heart. You may also hear them referred to as atrial appendages. Also prominent is a series of fat-filled grooves, each of which is known as a sulcus (plural = sulci), along the superior surfaces of the heart. Major coronary blood vessels are located in these sulci. The deep coronary sulcus is located between the atria and ventricles. Located between the left and right ventricles are two additional sulci that are not as deep as the coronary sulcus. The anterior interventricular sulcus is visible on the anterior surface of the heart, whereas the posterior interventricular sulcus is visible on the posterior surface of the heart. Figure 19.6 illustrates anterior and posterior views of the surface of the heart. Figure 19.6 External Anatomy of the Heart Inside the pericardium, the surface features of the heart are visible. Layers The wall of the heart is composed of three layers of unequal thickness. From superficial to deep, these are the epicardium, the myocardium, and the endocardium (see Figure 19.5). The outermost layer of the wall of the heart is also the innermost layer of the pericardium, the epicardium, or the visceral pericardium discussed earlier. The middle and thickest layer is the myocardium, made largely of cardiac muscle cells. It is built upon a framework of collagenous fibers, plus the blood vessels that supply the myocardium and the nerve fibers that help regulate the heart. It is the contraction of the myocardium that pumps blood through the heart and into the major arteries. The muscle pattern is elegant and complex, as the muscle cells swirl and spiral around the chambers of the heart. They form a figure 8 pattern around the atria and around the bases of the great vessels. Deeper ventricular muscles also form a figure 8 around the two ventricles and proceed toward the apex. More superficial layers of ventricular muscle wrap around both ventricles. This complex swirling pattern allows the heart to pump blood more effectively than a simple linear pattern would. Figure 19.7 illustrates the arrangement of muscle cells. Figure 19.7 Heart Musculature The swirling pattern of cardiac muscle tissue contributes significantly to the heart’s ability to pump blood effectively. Although the ventricles on the right and left sides pump the same amount of blood per contraction, the muscle of the left ventricle is much thicker and better developed than that of the right ventricle. In order to overcome the high resistance required to pump blood into the long systemic circuit, the left ventricle must generate a great amount of pressure. The right ventricle does not need to generate as much pressure, since the pulmonary circuit is shorter and provides less resistance. Figure 19.8illustrates the differences in muscular thickness needed for each of the ventricles. Figure 19.8 Differences in Ventricular Muscle Thickness The myocardium in the left ventricle is significantly thicker than that of the right ventricle. Both ventricles pump the same amount of blood, but the left ventricle must generate a much greater pressure to overcome greater resistance in the systemic circuit. The ventricles are shown in both relaxed and contracting states. Note the differences in the relative size of the lumens, the region inside each ventricle where the blood is contained. The innermost layer of the heart wall, the endocardium, is joined to the myocardium with a thin layer of connective tissue. The endocardium lines the chambers where the blood circulates and covers the heart valves. It is made of simple squamous epithelium called endothelium, which is continuous with the endothelial lining of the blood vessels (see Figure 19.5). Once regarded as a simple lining layer, recent evidence indicates that the endothelium of the endocardium and the coronary capillaries may play active roles in regulating the contraction of the muscle within the myocardium. The endothelium may also regulate the growth patterns of the cardiac muscle cells throughout life, and the endothelins it secretes create an environment in the surrounding tissue fluids that regulates ionic concentrations and states of contractility. Endothelins are potent vasoconstrictors and, in a normal individual, establish a homeostatic balance with other vasoconstrictors and vasodilators. Internal Structure of the Heart Recall that the heart’s contraction cycle follows a dual pattern of circulation—the pulmonary and systemic circuits—because of the pairs of chambers that pump blood into the circulation. In order to develop a more precise understanding of cardiac function, it is first necessary to explore the internal anatomical structures in more detail. Septa of the Heart The word septum is derived from the Latin for “something that encloses;” in this case, a septum (plural = septa) refers to a wall or partition that divides the heart into chambers. The septa are physical extensions of the myocardium lined with endocardium. Located between the two atria is the interatrial septum. Normally in an adult heart, the interatrial septum bears an oval-shaped depression known as the fossa ovalis, a remnant of an opening in the fetal heart known as the foramen ovale. The foramen ovale allowed blood in the fetal heart to pass directly from the right atrium to the left atrium, allowing some blood to bypass the pulmonary circuit. Within seconds after birth, a flap of tissue known as the septum primum that previously acted as a valve closes the foramen ovale and establishes the typical cardiac circulation pattern. Between the two ventricles is a second septum known as the interventricular septum. Unlike the interatrial septum, the interventricular septum is normally intact after its formation during fetal development. It is substantially thicker than the interatrial septum, since the ventricles generate far greater pressure when they contract. The septum between the atria and ventricles is known as the atrioventricular septum. It is marked by the presence of four openings that allow blood to move from the atria into the ventricles and from the ventricles into the pulmonary trunk and aorta. Located in each of these openings between the atria and ventricles is a valve, a specialized structure that ensures one-way flow of blood. The valves between the atria and ventricles are known generically as atrioventricular valves. The valves at the openings that lead to the pulmonary trunk and aorta are known generically as semilunar valves. The interventricular septum is visible in Figure 19.9. In this figure, the atrioventricular septum has been removed to better show the bicupid and tricuspid valves; the interatrial septum is not visible, since its location is covered by the aorta and pulmonary trunk. Since these openings and valves structurally weaken the atrioventricular septum, the remaining tissue is heavily reinforced with dense connective tissue called the cardiac skeleton, or skeleton of the heart. It includes four rings that surround the openings between the atria and ventricles, and the openings to the pulmonary trunk and aorta, and serve as the point of attachment for the heart valves. The cardiac skeleton also provides an important boundary in the heart electrical conduction system. Figure 19.9 Internal Structures of the Heart This anterior view of the heart shows the four chambers, the major vessels and their early branches, as well as the valves. The presence of the pulmonary trunk and aorta covers the interatrial septum, and the atrioventricular septum is cut away to show the atrioventricular valves. DISORDERS OF THE... Heart: Heart Defects One very common form of interatrial septum pathology is patent foramen ovale, which occurs when the septum primum does not close at birth, and the fossa ovalis is unable to fuse. The word patent is from the Latin root patens for “open.” It may be benign or asymptomatic, perhaps never being diagnosed, or in extreme cases, it may require surgical repair to close the opening permanently. As much as 20–25 percent of the general population may have a patent foramen ovale, but fortunately, most have the benign, asymptomatic version. Patent foramen ovale is normally detected by auscultation of a heart murmur (an abnormal heart sound) and confirmed by imaging with an echocardiogram. Despite its prevalence in the general population, the causes of patent ovale are unknown, and there are no known risk factors. In nonlife-threatening cases, it is better to monitor the condition than to risk heart surgery to repair and seal the opening. Coarctation of the aorta is a congenital abnormal narrowing of the aorta that is normally located at the insertion of the ligamentum arteriosum, the remnant of the fetal shunt called the ductus arteriosus. If severe, this condition drastically restricts blood flow through the primary systemic artery, which is life threatening. In some individuals, the condition may be fairly benign and not detected until later in life. Detectable symptoms in an infant include difficulty breathing, poor appetite, trouble feeding, or failure to thrive. In older individuals, symptoms include dizziness, fainting, shortness of breath, chest pain, fatigue, headache, and nosebleeds. Treatment involves surgery to resect (remove) the affected region or angioplasty to open the abnormally narrow passageway. Studies have shown that the earlier the surgery is performed, the better the chance of survival. A patent ductus arteriosus is a congenital condition in which the ductus arteriosus fails to close. The condition may range from severe to benign. Failure of the ductus arteriosus to close results in blood flowing from the higher pressure aorta into the lower pressure pulmonary trunk. This additional fluid moving toward the lungs increases pulmonary pressure and makes respiration difficult. Symptoms include shortness of breath (dyspnea), tachycardia, enlarged heart, a widened pulse pressure, and poor weight gain in infants. Treatments include surgical closure (ligation), manual closure using platinum coils or specialized mesh inserted via the femoral artery or vein, or nonsteroidal anti-inflammatory drugs to block the synthesis of prostaglandin E2, which maintains the vessel in an open position. If untreated, the condition can result in congestive heart failure. Septal defects are not uncommon in individuals and may be congenital or caused by various disease processes. Tetralogy of Fallot is a congenital condition that may also occur from exposure to unknown environmental factors; it occurs when there is an opening in the interventricular septum caused by blockage of the pulmonary trunk, normally at the pulmonary semilunar valve. This allows blood that is relatively low in oxygen from the right ventricle to flow into the left ventricle and mix with the blood that is relatively high in oxygen. Symptoms include a distinct heart murmur, low blood oxygen percent saturation, dyspnea or difficulty in breathing, polycythemia, broadening (clubbing) of the fingers and toes, and in children, difficulty in feeding or failure to grow and develop. It is the most common cause of cyanosis following birth. The term “tetralogy” is derived from the four components of the condition, although only three may be present in an individual patient: pulmonary infundibular stenosis (rigidity of the pulmonary valve), overriding aorta (the aorta is shifted above both ventricles), ventricular septal defect (opening), and right ventricular hypertrophy (enlargement of the right ventricle). Other heart defects may also accompany this condition, which is typically confirmed by echocardiography imaging. Tetralogy of Fallot occurs in approximately 400 out of one million live births. Normal treatment involves extensive surgical repair, including the use of stents to redirect blood flow and replacement of valves and patches to repair the septal defect, but the condition has a relatively high mortality. Survival rates are currently 75 percent during the first year of life; 60 percent by 4 years of age; 30 percent by 10 years; and 5 percent by 40 years. In the case of severe septal defects, including both tetralogy of Fallot and patent foramen ovale, failure of the heart to develop properly can lead to a condition commonly known as a “blue baby.” Regardless of normal skin pigmentation, individuals with this condition have an insufficient supply of oxygenated blood, which leads to cyanosis, a blue or purple coloration of the skin, especially when active. Septal defects are commonly first detected through auscultation, listening to the chest using a stethoscope. In this case, instead of hearing normal heart sounds attributed to the flow of blood and closing of heart valves, unusual heart sounds may be detected. This is often followed by medical imaging to confirm or rule out a diagnosis. In many cases, treatment may not be needed. Some common congenital heart defects are illustrated in Figure 19.10. Figure 19.10 Congenital Heart Defects (a) A patent foramen ovale defect is an abnormal opening in the interatrial septum, or more commonly, a failure of the foramen ovale to close. (b) Coarctation of the aorta is an abnormal narrowing of the aorta. (c) A patent ductus arteriosus is the failure of the ductus arteriosus to close. (d) Tetralogy of Fallot includes an abnormal opening in the interventricular septum. Right Atrium The right atrium serves as the receiving chamber for blood returning to the heart from the systemic circulation. The two major systemic veins, the superior and inferior venae cavae, and the large coronary vein called the coronary sinus that drains the heart myocardium empty into the right atrium. The superior vena cava drains blood from regions superior to the diaphragm: the head, neck, upper limbs, and the thoracic region. It empties into the superior and posterior portions of the right atrium. The inferior vena cava drains blood from areas inferior to the diaphragm: the lower limbs and abdominopelvic region of the body. It, too, empties into the posterior portion of the atria, but inferior to the opening of the superior vena cava. Immediately superior and slightly medial to the opening of the inferior vena cava on the posterior surface of the atrium is the opening of the coronary sinus. This thin-walled vessel drains most of the coronary veins that return systemic blood from the heart. The majority of the internal heart structures discussed in this and subsequent sections are illustrated in Figure 19.9. While the bulk of the internal surface of the right atrium is smooth, the depression of the fossa ovalis is medial, and the anterior surface demonstrates prominent ridges of muscle called the pectinate muscles. The right auricle also has pectinate muscles. The left atrium does not have pectinate muscles except in the auricle. The atria receive venous blood on a nearly continuous basis, preventing venous flow from stopping while the ventricles are contracting. While most ventricular filling occurs while the atria are relaxed, they do demonstrate a contractile phase and actively pump blood into the ventricles just prior to ventricular contraction. The opening between the atrium and ventricle is guarded by the tricuspid valve. Right Ventricle The right ventricle receives blood from the right atrium through the tricuspid valve. Each flap of the valve is attached to strong strands of connective tissue, the chordae tendineae, literally “tendinous cords,” or sometimes more poetically referred to as “heart strings.” There are several chordae tendineae associated with each of the flaps. They are composed of approximately 80 percent collagenous fibers with the remainder consisting of elastic fibers and endothelium. They connect each of the flaps to a papillary muscle that extends from the inferior ventricular surface. There are three papillary muscles in the right ventricle, called the anterior, posterior, and septal muscles, which correspond to the three sections of the valves. When the myocardium of the ventricle contracts, pressure within the ventricular chamber rises. Blood, like any fluid, flows from higher pressure to lower pressure areas, in this case, toward the pulmonary trunk and the atrium. To prevent any potential backflow, the papillary muscles also contract, generating tension on the chordae tendineae. This prevents the flaps of the valves from being forced into the atria and regurgitation of the blood back into the atria during ventricular contraction. Figure 19.11shows papillary muscles and chordae tendineae attached to the tricuspid valve. Figure 19.11 Chordae Tendineae and Papillary Muscles In this frontal section, you can see papillary muscles attached to the tricuspid valve on the right as well as the mitral valve on the left via chordae tendineae. (credit: modification of work by “PV KS”/flickr.com) The walls of the ventricle are lined with trabeculae carneae, ridges of cardiac muscle covered by endocardium. In addition to these muscular ridges, a band of cardiac muscle, also covered by endocardium, known as the moderator band (see Figure 19.9) reinforces the thin walls of the right ventricle and plays a crucial role in cardiac conduction. It arises from the inferior portion of the interventricular septum and crosses the interior space of the right ventricle to connect with the inferior papillary muscle. When the right ventricle contracts, it ejects blood into the pulmonary trunk, which branches into the left and right pulmonary arteries that carry it to each lung. The superior surface of the right ventricle begins to taper as it approaches the pulmonary trunk. At the base of the pulmonary trunk is the pulmonary semilunar valve that prevents backflow from the pulmonary trunk. Left Atrium After exchange of gases in the pulmonary capillaries, blood returns to the left atrium high in oxygen via one of the four pulmonary veins. While the left atrium does not contain pectinate muscles, it does have an auricle that includes these pectinate ridges. Blood flows nearly continuously from the pulmonary veins back into the atrium, which acts as the receiving chamber, and from here through an opening into the left ventricle. Most blood flows passively into the heart while both the atria and ventricles are relaxed, but toward the end of the ventricular relaxation period, the left atrium will contract, pumping blood into the ventricle. This atrial contraction accounts for approximately 20 percent of ventricular filling. The opening between the left atrium and ventricle is guarded by the mitral valve. Left Ventricle Recall that, although both sides of the heart will pump the same amount of blood, the muscular layer is much thicker in the left ventricle compared to the right (see Figure 19.8). Like the right ventricle, the left also has trabeculae carneae, but there is no moderator band. The mitral valve is connected to papillary muscles via chordae tendineae. There are two papillary muscles on the left—the anterior and posterior—as opposed to three on the right. The left ventricle is the major pumping chamber for the systemic circuit; it ejects blood into the aorta through the aortic semilunar valve. Heart Valve Structure and Function A transverse section through the heart slightly above the level of the atrioventricular septum reveals all four heart valves along the same plane (Figure 19.12). The valves ensure unidirectional blood flow through the heart. Between the right atrium and the right ventricle is the right atrioventricular valve, or tricuspid valve. It typically consists of three flaps, or leaflets, made of endocardium reinforced with additional connective tissue. The flaps are connected by chordae tendineae to the papillary muscles, which control the opening and closing of the valves. Figure 19.12 Heart Valves With the atria and major vessels removed, all four valves are clearly visible, although it is difficult to distinguish the three separate cusps of the tricuspid valve. Emerging from the right ventricle at the base of the pulmonary trunk is the pulmonary semilunar valve, or the pulmonary valve; it is also known as the pulmonic valve or the right semilunar valve. The pulmonary valve is comprised of three small flaps of endothelium reinforced with connective tissue. When the ventricle relaxes, the pressure differential causes blood to flow back into the ventricle from the pulmonary trunk. This flow of blood fills the pocket-like flaps of the pulmonary valve, causing the valve to close and producing an audible sound. Unlike the atrioventricular valves, there are no papillary muscles or chordae tendineae associated with the pulmonary valve. Located at the opening between the left atrium and left ventricle is the mitral valve, also called the bicuspid valve or the left atrioventricular valve. Structurally, this valve consists of two cusps, known as the anterior medial cusp and the posterior medial cusp, compared to the three cusps of the tricuspid valve. In a clinical setting, the valve is referred to as the mitral valve, rather than the bicuspid valve. The two cusps of the mitral valve are attached by chordae tendineae to two papillary muscles that project from the wall of the ventricle. At the base of the aorta is the aortic semilunar valve, or the aortic valve, which prevents backflow from the aorta. It normally is composed of three flaps. When the ventricle relaxes and blood attempts to flow back into the ventricle from the aorta, blood will fill the cusps of the valve, causing it to close and producing an audible sound. In Figure 19.13a, the two atrioventricular valves are open and the two semilunar valves are closed. This occurs when both atria and ventricles are relaxed and when the atria contract to pump blood into the ventricles. Figure 19.13b shows a frontal view. Although only the left side of the heart is illustrated, the process is virtually identical on the right. Figure 19.13 Blood Flow from the Left Atrium to the Left Ventricle (a) A transverse section through the heart illustrates the four heart valves. The two atrioventricular valves are open; the two semilunar valves are closed. The atria and vessels have been removed. (b) A frontal section through the heart illustrates blood flow through the mitral valve. When the mitral valve is open, it allows blood to move from the left atrium to the left ventricle. The aortic semilunar valve is closed to prevent backflow of blood from the aorta to the left ventricle. Figure 19.14a shows the atrioventricular valves closed while the two semilunar valves are open. This occurs when the ventricles contract to eject blood into the pulmonary trunk and aorta. Closure of the two atrioventricular valves prevents blood from being forced back into the atria. This stage can be seen from a frontal view in Figure 19.14b. Figure 19.14 Blood Flow from the Left Ventricle into the Great Vessels (a) A transverse section through the heart illustrates the four heart valves during ventricular contraction. The two atrioventricular valves are closed, but the two semilunar valves are open. The atria and vessels have been removed. (b) A frontal view shows the closed mitral (bicuspid) valve that prevents backflow of blood into the left atrium. The aortic semilunar valve is open to allow blood to be ejected into the aorta. When the ventricles begin to contract, pressure within the ventricles rises and blood flows toward the area of lowest pressure, which is initially in the atria. This backflow causes the cusps of the tricuspid and mitral (bicuspid) valves to close. These valves are tied down to the papillary muscles by chordae tendineae. During the relaxation phase of the cardiac cycle, the papillary muscles are also relaxed and the tension on the chordae tendineae is slight (see Figure 19.13b). However, as the myocardium of the ventricle contracts, so do the papillary muscles. This creates tension on the chordae tendineae (see Figure 19.14b), helping to hold the cusps of the atrioventricular valves in place and preventing them from being blown back into the atria. The aortic and pulmonary semilunar valves lack the chordae tendineae and papillary muscles associated with the atrioventricular valves. Instead, they consist of pocket-like folds of endocardium reinforced with additional connective tissue. When the ventricles relax and the change in pressure forces the blood toward the ventricles, the blood presses against these cusps and seals the openings. INTERACTIVE LINK Visit this site to observe an echocardiogram of actual heart valves opening and closing. Although much of the heart has been “removed” from this gif loop so the chordae tendineae are not visible, why is their presence more critical for the atrioventricular valves (tricuspid and mitral) than the semilunar (aortic and pulmonary) valves? DISORDERS OF THE... Heart Valves When heart valves do not function properly, they are often described as incompetent and result in valvular heart disease, which can range from benign to lethal. Some of these conditions are congenital, that is, the individual was born with the defect, whereas others may be attributed to disease processes or trauma. Some malfunctions are treated with medications, others require surgery, and still others may be mild enough that the condition is merely monitored since treatment might trigger more serious consequences. Valvular disorders are often caused by carditis, or inflammation of the heart. One common trigger for this inflammation is rheumatic fever, or scarlet fever, an autoimmune response to the presence of a bacterium, Streptococcus pyogenes, normally a disease of childhood. While any of the heart valves may be involved in valve disorders, mitral regurgitation is the most common, detected in approximately 2 percent of the population, and the pulmonary semilunar valve is the least frequently involved. When a valve malfunctions, the flow of blood to a region will often be disrupted. The resulting inadequate flow of blood to this region will be described in general terms as an insufficiency. The specific type of insufficiency is named for the valve involved: aortic insufficiency, mitral insufficiency, tricuspid insufficiency, or pulmonary insufficiency. If one of the cusps of the valve is forced backward by the force of the blood, the condition is referred to as a prolapsed valve. Prolapse may occur if the chordae tendineae are damaged or broken, causing the closure mechanism to fail. The failure of the valve to close properly disrupts the normal one-way flow of blood and results in regurgitation, when the blood flows backward from its normal path. Using a stethoscope, the disruption to the normal flow of blood produces a heart murmur. Stenosis is a condition in which the heart valves become rigid and may calcify over time. The loss of flexibility of the valve interferes with normal function and may cause the heart to work harder to propel blood through the valve, which eventually weakens the heart. Aortic stenosis affects approximately 2 percent of the population over 65 years of age, and the percentage increases to approximately 4 percent in individuals over 85 years. Occasionally, one or more of the chordae tendineae will tear or the papillary muscle itself may die as a component of a myocardial infarction (heart attack). In this case, the patient’s condition will deteriorate dramatically and rapidly, and immediate surgical intervention may be required. Auscultation, or listening to a patient’s heart sounds, is one of the most useful diagnostic tools, since it is proven, safe, and inexpensive. The term auscultation is derived from the Latin for “to listen,” and the technique has been used for diagnostic purposes as far back as the ancient Egyptians. Valve and septal disorders will trigger abnormal heart sounds. If a valvular disorder is detected or suspected, a test called an echocardiogram, or simply an “echo,” may be ordered. Echocardiograms are sonograms of the heart and can help in the diagnosis of valve disorders as well as a wide variety of heart pathologies. INTERACTIVE LINK Visit this site for a free download, including excellent animations and audio of heart sounds. CAREER CONNECTION Cardiologist Cardiologists are medical doctors that specialize in the diagnosis and treatment of diseases of the heart. After completing 4 years of medical school, cardiologists complete a three-year residency in internal medicine followed by an additional three or more years in cardiology. Following this 10-year period of medical training and clinical experience, they qualify for a rigorous two-day examination administered by the Board of Internal Medicine that tests their academic training and clinical abilities, including diagnostics and treatment. After successful completion of this examination, a physician becomes a board-certified cardiologist. Some board-certified cardiologists may be invited to become a Fellow of the American College of Cardiology (FACC). This professional recognition is awarded to outstanding physicians based upon merit, including outstanding credentials, achievements, and community contributions to cardiovascular medicine. INTERACTIVE LINK Visit this site to learn more about cardiologists. CAREER CONNECTION Cardiovascular Technologist/Technician Cardiovascular technologists/technicians are trained professionals who perform a variety of imaging techniques, such as sonograms or echocardiograms, used by physicians to diagnose and treat diseases of the heart. Nearly all of these positions require an associate degree, and these technicians earn a median salary of $49,410 as of May 2010, according to the U.S. Bureau of Labor Statistics. Growth within the field is fast, projected at 29 percent from 2010 to 2020. There is a considerable overlap and complementary skills between cardiac technicians and vascular technicians, and so the term cardiovascular technician is often used. Special certifications within the field require documenting appropriate experience and completing additional and often expensive certification examinations. These subspecialties include Certified Rhythm Analysis Technician (CRAT), Certified Cardiographic Technician (CCT), Registered Congenital Cardiac Sonographer (RCCS), Registered Cardiac Electrophysiology Specialist (RCES), Registered Cardiovascular Invasive Specialist (RCIS), Registered Cardiac Sonographer (RCS), Registered Vascular Specialist (RVS), and Registered Phlebology Sonographer (RPhS). INTERACTIVE LINK Visit this site for more information on cardiovascular technologists/technicians. Coronary Circulation You will recall that the heart is a remarkable pump composed largely of cardiac muscle cells that are incredibly active throughout life. Like all other cells, a cardiomyocyte requires a reliable supply of oxygen and nutrients, and a way to remove wastes, so it needs a dedicated, complex, and extensive coronary circulation. And because of the critical and nearly ceaseless activity of the heart throughout life, this need for a blood supply is even greater than for a typical cell. However, coronary circulation is not continuous; rather, it cycles, reaching a peak when the heart muscle is relaxed and nearly ceasing while it is contracting. Coronary Arteries Coronary arteries supply blood to the myocardium and other components of the heart. The first portion of the aorta after it arises from the left ventricle gives rise to the coronary arteries. There are three dilations in the wall of the aorta just superior to the aortic semilunar valve. Two of these, the left posterior aortic sinus and anterior aortic sinus, give rise to the left and right coronary arteries, respectively. The third sinus, the right posterior aortic sinus, typically does not give rise to a vessel. Coronary vessel branches that remain on the surface of the artery and follow the sulci are called epicardial coronary arteries. The left coronary artery distributes blood to the left side of the heart, the left atrium and ventricle, and the interventricular septum. The circumflex artery arises from the left coronary artery and follows the coronary sulcus to the left. Eventually, it will fuse with the small branches of the right coronary artery. The larger anterior interventricular artery, also known as the left anterior descending artery (LAD), is the second major branch arising from the left coronary artery. It follows the anterior interventricular sulcus around the pulmonary trunk. Along the way it gives rise to numerous smaller branches that interconnect with the branches of the posterior interventricular artery, forming anastomoses. An anastomosis is an area where vessels unite to form interconnections that normally allow blood to circulate to a region even if there may be partial blockage in another branch. The anastomoses in the heart are very small. Therefore, this ability is somewhat restricted in the heart so a coronary artery blockage often results in death of the cells (myocardial infarction) supplied by the particular vessel. The right coronary artery proceeds along the coronary sulcus and distributes blood to the right atrium, portions of both ventricles, and the heart conduction system. Normally, one or more marginal arteries arise from the right coronary artery inferior to the right atrium. The marginal arteries supply blood to the superficial portions of the right ventricle. On the posterior surface of the heart, the right coronary artery gives rise to the posterior interventricular artery, also known as the posterior descending artery. It runs along the posterior portion of the interventricular sulcus toward the apex of the heart, giving rise to branches that supply the interventricular septum and portions of both ventricles. Figure 19.15 presents views of the coronary circulation from both the anterior and posterior views. Figure 19.15 Coronary Circulation The anterior view of the heart shows the prominent coronary surface vessels. The posterior view of the heart shows the prominent coronary surface vessels. DISEASES OF THE... Heart: Myocardial Infarction Myocardial infarction (MI) is the formal term for what is commonly referred to as a heart attack. It normally results from a lack of blood flow (ischemia) and oxygen (hypoxia) to a region of the heart, resulting in death of the cardiac muscle cells. An MI often occurs when a coronary artery is blocked by the buildup of atherosclerotic plaque consisting of lipids, cholesterol and fatty acids, and white blood cells, primarily macrophages. It can also occur when a portion of an unstable atherosclerotic plaque travels through the coronary arterial system and lodges in one of the smaller vessels. The resulting blockage restricts the flow of blood and oxygen to the myocardium and causes death of the tissue. MIs may be triggered by excessive exercise, in which the partially occluded artery is no longer able to pump sufficient quantities of blood, or severe stress, which may induce spasm of the smooth muscle in the walls of the vessel. In the case of acute MI, there is often sudden pain beneath the sternum (retrosternal pain) called angina pectoris, often radiating down the left arm in males but not in female patients. Until this anomaly between the sexes was discovered, many female patients suffering MIs were misdiagnosed and sent home. In addition, patients typically present with difficulty breathing and shortness of breath (dyspnea), irregular heartbeat (palpations), nausea and vomiting, sweating (diaphoresis), anxiety, and fainting (syncope), although not all of these symptoms may be present. Many of the symptoms are shared with other medical conditions, including anxiety attacks and simple indigestion, so differential diagnosis is critical. It is estimated that between 22 and 64 percent of MIs present without any symptoms. An MI can be confirmed by examining the patient’s ECG, which frequently reveals alterations in the ST and Q components. Some classification schemes of MI are referred to as ST-elevated MI (STEMI) and non-elevated MI (non-STEMI). In addition, echocardiography or cardiac magnetic resonance imaging may be employed. Common blood tests indicating an MI include elevated levels of creatine kinase MB (an enzyme that catalyzes the conversion of creatine to phosphocreatine, consuming ATP) and cardiac troponin (the regulatory protein for muscle contraction), both of which are released by damaged cardiac muscle cells. Immediate treatments for MI are essential and include administering supplemental oxygen, aspirin that helps to break up clots, and nitroglycerine administered sublingually (under the tongue) to facilitate its absorption. Despite its unquestioned success in treatments and use since the 1880s, the mechanism of nitroglycerine is still incompletely understood but is believed to involve the release of nitric oxide, a known vasodilator, and endothelium-derived releasing factor, which also relaxes the smooth muscle in the tunica media of coronary vessels. Longer-term treatments include injections of thrombolytic agents such as streptokinase that dissolve the clot, the anticoagulant heparin, balloon angioplasty and stents to open blocked vessels, and bypass surgery to allow blood to pass around the site of blockage. If the damage is extensive, coronary replacement with a donor heart or coronary assist device, a sophisticated mechanical device that supplements the pumping activity of the heart, may be employed. Despite the attention, development of artificial hearts to augment the severely limited supply of heart donors has proven less than satisfactory but will likely improve in the future. MIs may trigger cardiac arrest, but the two are not synonymous. Important risk factors for MI include cardiovascular disease, age, smoking, high blood levels of the low-density lipoprotein (LDL, often referred to as “bad” cholesterol), low levels of high-density lipoprotein (HDL, or “good” cholesterol), hypertension, diabetes mellitus, obesity, lack of physical exercise, chronic kidney disease, excessive alcohol consumption, and use of illegal drugs. Coronary Veins Coronary veins drain the heart and generally parallel the large surface arteries (see Figure 19.15). The great cardiac vein can be seen initially on the surface of the heart following the interventricular sulcus, but it eventually flows along the coronary sulcus into the coronary sinus on the posterior surface. The great cardiac vein initially parallels the anterior interventricular artery and drains the areas supplied by this vessel. It receives several major branches, including the posterior cardiac vein, the middle cardiac vein, and the small cardiac vein. The posterior cardiac vein parallels and drains the areas supplied by the marginal artery branch of the circumflex artery. The middle cardiac vein parallels and drains the areas supplied by the posterior interventricular artery. The small cardiac vein parallels the right coronary artery and drains the blood from the posterior surfaces of the right atrium and ventricle. The coronary sinus is a large, thin-walled vein on the posterior surface of the heart lying within the atrioventricular sulcus and emptying directly into the right atrium. The anterior cardiac veins parallel the small cardiac arteries and drain the anterior surface of the right ventricle. Unlike these other cardiac veins, it bypasses the coronary sinus and drains directly into the right atrium. DISORDERS OF THE... Heart: Coronary Artery Disease Coronary artery disease is the leading cause of death worldwide. It occurs when the buildup of plaque—a fatty material including cholesterol, connective tissue, white blood cells, and some smooth muscle cells—within the walls of the arteries obstructs the flow of blood and decreases the flexibility or compliance of the vessels. This condition is called atherosclerosis, a hardening of the arteries that involves the accumulation of plaque. As the coronary blood vessels become occluded, the flow of blood to the tissues will be restricted, a condition called ischemia that causes the cells to receive insufficient amounts of oxygen, called hypoxia. Figure 19.16 shows the blockage of coronary arteries highlighted by the injection of dye. Some individuals with coronary artery disease report pain radiating from the chest called angina pectoris, but others remain asymptomatic. If untreated, coronary artery disease can lead to MI or a heart attack. Figure 19.16 Atherosclerotic Coronary Arteries In this coronary angiogram (X-ray), the dye makes visible two occluded coronary arteries. Such blockages can lead to decreased blood flow (ischemia) and insufficient oxygen (hypoxia) delivered to the cardiac tissues. If uncorrected, this can lead to cardiac muscle death (myocardial infarction). The disease progresses slowly and often begins in children and can be seen as fatty “streaks” in the vessels. It then gradually progresses throughout life. Well-documented risk factors include smoking, family history, hypertension, obesity, diabetes, high alcohol consumption, lack of exercise, stress, and hyperlipidemia or high circulating levels of lipids in the blood. Treatments may include medication, changes to diet and exercise, angioplasty with a balloon catheter, insertion of a stent, or coronary bypass procedure. Angioplasty is a procedure in which the occlusion is mechanically widened with a balloon. A specialized catheter with an expandable tip is inserted into a superficial vessel, normally in the leg, and then directed to the site of the occlusion. At this point, the balloon is inflated to compress the plaque material and to open the vessel to increase blood flow. Then, the balloon is deflated and retracted. A stent consisting of a specialized mesh is typically inserted at the site of occlusion to reinforce the weakened and damaged walls. Stent insertions have been routine in cardiology for more than 40 years. Coronary bypass surgery may also be performed. This surgical procedure grafts a replacement vessel obtained from another, less vital portion of the body to bypass the occluded area. This procedure is clearly effective in treating patients experiencing a MI, but overall does not increase longevity. Nor does it seem advisable in patients with stable although diminished cardiac capacity since frequently loss of mental acuity occurs following the procedure. Long-term changes to behavior, emphasizing diet and exercise plus a medicine regime tailored to lower blood pressure, lower cholesterol and lipids, and reduce clotting are equally as effective. Cardiac Muscle and Electrical Activity - Describe the structure of cardiac muscle - Identify and describe the components of the conducting system that distributes electrical impulses through the heart - Compare the effect of ion movement on membrane potential of cardiac conductive and contractile cells - Relate characteristics of an electrocardiogram to events in the cardiac cycle - Identify blocks that can interrupt the cardiac cycle Recall that cardiac muscle shares a few characteristics with both skeletal muscle and smooth muscle, but it has some unique properties of its own. Not the least of these exceptional properties is its ability to initiate an electrical potential at a fixed rate that spreads rapidly from cell to cell to trigger the contractile mechanism. This property is known as autorhythmicity. Neither smooth nor skeletal muscle can do this. Even though cardiac muscle has autorhythmicity, heart rate is modulated by the endocrine and nervous systems. There are two major types of cardiac muscle cells: myocardial contractile cells and myocardial conducting cells. The myocardial contractile cells constitute the bulk (99 percent) of the cells in the atria and ventricles. Contractile cells conduct impulses and are responsible for contractions that pump blood through the body. The myocardial conducting cells (1 percent of the cells) form the conduction system of the heart. Except for Purkinje cells, they are generally much smaller than the contractile cells and have few of the myofibrils or filaments needed for contraction. Their function is similar in many respects to neurons, although they are specialized muscle cells. Myocardial conduction cells initiate and propagate the action potential (the electrical impulse) that travels throughout the heart and triggers the contractions that propel the blood. Structure of Cardiac Muscle Compared to the giant cylinders of skeletal muscle, cardiac muscle cells, or cardiomyocytes, are considerably shorter with much smaller diameters. Cardiac muscle also demonstrates striations, the alternating pattern of dark A bands and light I bands attributed to the precise arrangement of the myofilaments and fibrils that are organized in sarcomeres along the length of the cell (Figure 19.17a). These contractile elements are virtually identical to skeletal muscle. T (transverse) tubules penetrate from the surface plasma membrane, the sarcolemma, to the interior of the cell, allowing the electrical impulse to reach the interior. The T tubules are only found at the Z discs, whereas in skeletal muscle, they are found at the junction of the A and I bands. Therefore, there are one-half as many T tubules in cardiac muscle as in skeletal muscle. In addition, the sarcoplasmic reticulum stores few calcium ions, so most of the calcium ions must come from outside the cells. The result is a slower onset of contraction. Mitochondria are plentiful, providing energy for the contractions of the heart. Typically, cardiomyocytes have a single, central nucleus, but two or more nuclei may be found in some cells. Cardiac muscle cells branch freely. A junction between two adjoining cells is marked by a critical structure called an intercalated disc, which helps support the synchronized contraction of the muscle (Figure 19.17b). The sarcolemmas from adjacent cells bind together at the intercalated discs. They consist of desmosomes, specialized linking proteoglycans, tight junctions, and large numbers of gap junctions that allow the passage of ions between the cells and help to synchronize the contraction (Figure 19.17c). Intercellular connective tissue also helps to bind the cells together. The importance of strongly binding these cells together is necessitated by the forces exerted by contraction. Figure 19.17 Cardiac Muscle (a) Cardiac muscle cells have myofibrils composed of myofilaments arranged in sarcomeres, T tubules to transmit the impulse from the sarcolemma to the interior of the cell, numerous mitochondria for energy, and intercalated discs that are found at the junction of different cardiac muscle cells. (b) A photomicrograph of cardiac muscle cells shows the nuclei and intercalated discs. (c) An intercalated disc connects cardiac muscle cells and consists of desmosomes and gap junctions. LM × 1600. (Micrograph provided by the Regents of the University of Michigan Medical School © 2012) Cardiac muscle undergoes aerobic respiration patterns, primarily metabolizing lipids and carbohydrates. Myoglobin, lipids, and glycogen are all stored within the cytoplasm. Cardiac muscle cells undergo twitch-type contractions with long refractory periods followed by brief relaxation periods. The relaxation is essential so the heart can fill with blood for the next cycle. The refractory period is very long to prevent the possibility of tetany, a condition in which muscle remains involuntarily contracted. In the heart, tetany is not compatible with life, since it would prevent the heart from pumping blood. EVERYDAY CONNECTION Repair and Replacement Damaged cardiac muscle cells have extremely limited abilities to repair themselves or to replace dead cells via mitosis. Recent evidence indicates that at least some stem cells remain within the heart that continue to divide and at least potentially replace these dead cells. However, newly formed or repaired cells are rarely as functional as the original cells, and cardiac function is reduced. In the event of a heart attack or MI, dead cells are often replaced by patches of scar tissue. Autopsies performed on individuals who had successfully received heart transplants show some proliferation of original cells. If researchers can unlock the mechanism that generates new cells and restore full mitotic capabilities to heart muscle, the prognosis for heart attack survivors will be greatly enhanced. To date, myocardial cells produced within the patient (in situ) by cardiac stem cells seem to be nonfunctional, although those grown in Petri dishes (in vitro) do beat. Perhaps soon this mystery will be solved, and new advances in treatment will be commonplace. Conduction System of the Heart If embryonic heart cells are separated into a Petri dish and kept alive, each is capable of generating its own electrical impulse followed by contraction. When two independently beating embryonic cardiac muscle cells are placed together, the cell with the higher inherent rate sets the pace, and the impulse spreads from the faster to the slower cell to trigger a contraction. As more cells are joined together, the fastest cell continues to assume control of the rate. A fully developed adult heart maintains the capability of generating its own electrical impulse, triggered by the fastest cells, as part of the cardiac conduction system. The components of the cardiac conduction system include the sinoatrial node, the atrioventricular node, the atrioventricular bundle, the atrioventricular bundle branches, and the Purkinje cells (Figure 19.18). Figure 19.18 Conduction System of the Heart Specialized conducting components of the heart include the sinoatrial node, the internodal pathways, the atrioventricular node, the atrioventricular bundle, the right and left bundle branches, and the Purkinje fibers. Sinoatrial (SA) Node Normal cardiac rhythm is established by the sinoatrial (SA) node, a specialized clump of myocardial conducting cells located in the superior and posterior walls of the right atrium in close proximity to the orifice of the superior vena cava. The SA node has the highest inherent rate of depolarization and is known as the pacemaker of the heart. It initiates the sinus rhythm, or normal electrical pattern followed by contraction of the heart. This impulse spreads from its initiation in the SA node throughout the atria through specialized internodal pathways, to the atrial myocardial contractile cells and the atrioventricular node. The internodal pathways consist of three bands (anterior, middle, and posterior) that lead directly from the SA node to the next node in the conduction system, the atrioventricular node (see Figure 19.18). The impulse takes approximately 50 ms (milliseconds) to travel between these two nodes. The relative importance of this pathway has been debated since the impulse would reach the atrioventricular node simply following the cell-by-cell pathway through the contractile cells of the myocardium in the atria. In addition, there is a specialized pathway called Bachmann’s bundle or the interatrial band that conducts the impulse directly from the right atrium to the left atrium. Regardless of the pathway, as the impulse reaches the atrioventricular septum, the connective tissue of the cardiac skeleton prevents the impulse from spreading into the myocardial cells in the ventricles except at the atrioventricular node. Figure 19.19illustrates the initiation of the impulse in the SA node that then spreads the impulse throughout the atria to the atrioventricular node. Figure 19.19 Cardiac Conduction (1) The sinoatrial (SA) node and the remainder of the conduction system are at rest. (2) The SA node initiates the action potential, which sweeps across the atria. (3) After reaching the atrioventricular node, there is a delay of approximately 100 ms that allows the atria to complete pumping blood before the impulse is transmitted to the atrioventricular bundle. (4) Following the delay, the impulse travels through the atrioventricular bundle and bundle branches to the Purkinje fibers, and also reaches the right papillary muscle via the moderator band. (5) The impulse spreads to the contractile fibers of the ventricle. (6) Ventricular contraction begins. The electrical event, the wave of depolarization, is the trigger for muscular contraction. The wave of depolarization begins in the right atrium, and the impulse spreads across the superior portions of both atria and then down through the contractile cells. The contractile cells then begin contraction from the superior to the inferior portions of the atria, efficiently pumping blood into the ventricles. Atrioventricular (AV) Node The atrioventricular (AV) node is a second clump of specialized myocardial conductive cells, located in the inferior portion of the right atrium within the atrioventricular septum. The septum prevents the impulse from spreading directly to the ventricles without passing through the AV node. There is a critical pause before the AV node depolarizes and transmits the impulse to the atrioventricular bundle (see Figure 19.19, step 3). This delay in transmission is partially attributable to the small diameter of the cells of the node, which slow the impulse. Also, conduction between nodal cells is less efficient than between conducting cells. These factors mean that it takes the impulse approximately 100 ms to pass through the node. This pause is critical to heart function, as it allows the atrial cardiomyocytes to complete their contraction that pumps blood into the ventricles before the impulse is transmitted to the cells of the ventricle itself. With extreme stimulation by the SA node, the AV node can transmit impulses maximally at 220 per minute. This establishes the typical maximum heart rate in a healthy young individual. Damaged hearts or those stimulated by drugs can contract at higher rates, but at these rates, the heart can no longer effectively pump blood. Atrioventricular Bundle (Bundle of His), Bundle Branches, and Purkinje Fibers Arising from the AV node, the atrioventricular bundle, or bundle of His, proceeds through the interventricular septum before dividing into two atrioventricular bundle branches, commonly called the left and right bundle branches. The left bundle branch has two fascicles. The left bundle branch supplies the left ventricle, and the right bundle branch the right ventricle. Since the left ventricle is much larger than the right, the left bundle branch is also considerably larger than the right. Portions of the right bundle branch are found in the moderator band and supply the right papillary muscles. Because of this connection, each papillary muscle receives the impulse at approximately the same time, so they begin to contract simultaneously just prior to the remainder of the myocardial contractile cells of the ventricles. This is believed to allow tension to develop on the chordae tendineae prior to right ventricular contraction. There is no corresponding moderator band on the left. Both bundle branches descend and reach the apex of the heart where they connect with the Purkinje fibers (see Figure 19.19, step 4). This passage takes approximately 25 ms. The Purkinje fibers are additional myocardial conductive fibers that spread the impulse to the myocardial contractile cells in the ventricles. They extend throughout the myocardium from the apex of the heart toward the atrioventricular septum and the base of the heart. The Purkinje fibers have a fast inherent conduction rate, and the electrical impulse reaches all of the ventricular muscle cells in about 75 ms (see Figure 19.19, step 5). Since the electrical stimulus begins at the apex, the contraction also begins at the apex and travels toward the base of the heart, similar to squeezing a tube of toothpaste from the bottom. This allows the blood to be pumped out of the ventricles and into the aorta and pulmonary trunk. The total time elapsed from the initiation of the impulse in the SA node until depolarization of the ventricles is approximately 225 ms. Membrane Potentials and Ion Movement in Cardiac Conductive Cells Action potentials are considerably different between cardiac conductive cells and cardiac contractive cells. While Na+ and K+play essential roles, Ca2+ is also critical for both types of cells. Unlike skeletal muscles and neurons, cardiac conductive cells do not have a stable resting potential. Conductive cells contain a series of sodium ion channels that allow a normal and slow influx of sodium ions that causes the membrane potential to rise slowly from an initial value of −60 mV up to about –40 mV. The resulting movement of sodium ions creates spontaneous depolarization (or prepotential depolarization). At this point, calcium ion channels open and Ca2+ enters the cell, further depolarizing it at a more rapid rate until it reaches a value of approximately +15 mV. At this point, the calcium ion channels close and K+ channels open, allowing outflux of K+ and resulting in repolarization. When the membrane potential reaches approximately −60 mV, the K+ channels close and Na+ channels open, and the prepotential phase begins again. This phenomenon explains the autorhythmicity properties of cardiac muscle (Figure 19.20). Figure 19.20 Action Potential at the SA Node The prepotential is due to a slow influx of sodium ions until the threshold is reached followed by a rapid depolarization and repolarization. The prepotential accounts for the membrane reaching threshold and initiates the spontaneous depolarization and contraction of the cell. Note the lack of a resting potential. Membrane Potentials and Ion Movement in Cardiac Contractile Cells There is a distinctly different electrical pattern involving the contractile cells. In this case, there is a rapid depolarization, followed by a plateau phase and then repolarization. This phenomenon accounts for the long refractory periods required for the cardiac muscle cells to pump blood effectively before they are capable of firing for a second time. These cardiac myocytes normally do not initiate their own electrical potential but rather wait for an impulse to reach them. Contractile cells demonstrate a much more stable resting phase than conductive cells at approximately −80 mV for cells in the atria and −90 mV for cells in the ventricles. Despite this initial difference, the other components of their action potentials are virtually identical. In both cases, when stimulated by an action potential, voltage-gated channels rapidly open, beginning the positive-feedback mechanism of depolarization. This rapid influx of positively charged ions raises the membrane potential to approximately +30 mV, at which point the sodium channels close. The rapid depolarization period typically lasts 3–5 ms. Depolarization is followed by the plateau phase, in which membrane potential declines relatively slowly. This is due in large part to the opening of the slow Ca2+ channels, allowing Ca2+ to enter the cell while few K+ channels are open, allowing K+ to exit the cell. The relatively long plateau phase lasts approximately 175 ms. Once the membrane potential reaches approximately zero, the Ca2+ channels close and K+ channels open, allowing K+ to exit the cell. The repolarization lasts approximately 75 ms. At this point, membrane potential drops until it reaches resting levels once more and the cycle repeats. The entire event lasts between 250 and 300 ms (Figure 19.21). The absolute refractory period for cardiac contractile muscle lasts approximately 200 ms, and the relative refractory period lasts approximately 50 ms, for a total of 250 ms. This extended period is critical, since the heart muscle must contract to pump blood effectively and the contraction must follow the electrical events. Without extended refractory periods, premature contractions would occur in the heart and would not be compatible with life. Figure 19.21 Action Potential in Cardiac Contractile Cells (a) Note the long plateau phase due to the influx of calcium ions. The extended refractory period allows the cell to fully contract before another electrical event can occur. (b) The action potential for heart muscle is compared to that of skeletal muscle. Calcium Ions Calcium ions play two critical roles in the physiology of cardiac muscle. Their influx through slow calcium channels accounts for the prolonged plateau phase and absolute refractory period that enable cardiac muscle to function properly. Calcium ions also combine with the regulatory protein troponin in the troponin-tropomyosin complex; this complex removes the inhibition that prevents the heads of the myosin molecules from forming cross bridges with the active sites on actin that provide the power stroke of contraction. This mechanism is virtually identical to that of skeletal muscle. Approximately 20 percent of the calcium required for contraction is supplied by the influx of Ca2+ during the plateau phase. The remaining Ca2+ for contraction is released from storage in the sarcoplasmic reticulum. Comparative Rates of Conduction System Firing The pattern of prepotential or spontaneous depolarization, followed by rapid depolarization and repolarization just described, are seen in the SA node and a few other conductive cells in the heart. Since the SA node is the pacemaker, it reaches threshold faster than any other component of the conduction system. It will initiate the impulses spreading to the other conducting cells. The SA node, without nervous or endocrine control, would initiate a heart impulse approximately 80–100 times per minute. Although each component of the conduction system is capable of generating its own impulse, the rate progressively slows as you proceed from the SA node to the Purkinje fibers. Without the SA node, the AV node would generate a heart rate of 40–60 beats per minute. If the AV node were blocked, the atrioventricular bundle would fire at a rate of approximately 30–40 impulses per minute. The bundle branches would have an inherent rate of 20–30 impulses per minute, and the Purkinje fibers would fire at 15–20 impulses per minute. While a few exceptionally trained aerobic athletes demonstrate resting heart rates in the range of 30–40 beats per minute (the lowest recorded figure is 28 beats per minute for Miguel Indurain, a cyclist), for most individuals, rates lower than 50 beats per minute would indicate a condition called bradycardia. Depending upon the specific individual, as rates fall much below this level, the heart would be unable to maintain adequate flow of blood to vital tissues, initially resulting in decreasing loss of function across the systems, unconsciousness, and ultimately death. Electrocardiogram By careful placement of surface electrodes on the body, it is possible to record the complex, compound electrical signal of the heart. This tracing of the electrical signal is the electrocardiogram (ECG), also commonly abbreviated EKG (K coming kardiology, from the German term for cardiology). Careful analysis of the ECG reveals a detailed picture of both normal and abnormal heart function, and is an indispensable clinical diagnostic tool. The standard electrocardiograph (the instrument that generates an ECG) uses 3, 5, or 12 leads. The greater the number of leads an electrocardiograph uses, the more information the ECG provides. The term “lead” may be used to refer to the cable from the electrode to the electrical recorder, but it typically describes the voltage difference between two of the electrodes. The 12-lead electrocardiograph uses 10 electrodes placed in standard locations on the patient’s skin (Figure 19.22). In continuous ambulatory electrocardiographs, the patient wears a small, portable, battery-operated device known as a Holter monitor, or simply a Holter, that continuously monitors heart electrical activity, typically for a period of 24 hours during the patient’s normal routine. Figure 19.22 Standard Placement of ECG Leads In a 12-lead ECG, six electrodes are placed on the chest, and four electrodes are placed on the limbs. A normal ECG tracing is presented in Figure 19.23. Each component, segment, and interval is labeled and corresponds to important electrical events, demonstrating the relationship between these events and contraction in the heart. There are five prominent points on the ECG: the P wave, the QRS complex, and the T wave. The small P wave represents the depolarization of the atria. The atria begin contracting approximately 25 ms after the start of the P wave. The large QRS complex represents the depolarization of the ventricles, which requires a much stronger electrical signal because of the larger size of the ventricular cardiac muscle. The ventricles begin to contract as the QRS reaches the peak of the R wave. Lastly, the T wave represents the repolarization of the ventricles. The repolarization of the atria occurs during the QRS complex, which masks it on an ECG. The major segments and intervals of an ECG tracing are indicated in Figure 19.23. Segments are defined as the regions between two waves. Intervals include one segment plus one or more waves. For example, the PR segment begins at the end of the P wave and ends at the beginning of the QRS complex. The PR interval starts at the beginning of the P wave and ends with the beginning of the QRS complex. The PR interval is more clinically relevant, as it measures the duration from the beginning of atrial depolarization (the P wave) to the initiation of the QRS complex. Since the Q wave may be difficult to view in some tracings, the measurement is often extended to the R that is more easily visible. Should there be a delay in passage of the impulse from the SA node to the AV node, it would be visible in the PR interval. Figure 19.24 correlates events of heart contraction to the corresponding segments and intervals of an ECG. INTERACTIVE LINK Visit this site for a more detailed analysis of ECGs. Figure 19.23 Electrocardiogram A normal tracing shows the P wave, QRS complex, and T wave. Also indicated are the PR, QT, QRS, and ST intervals, plus the P-R and S-T segments. Figure 19.24 ECG Tracing Correlated to the Cardiac Cycle This diagram correlates an ECG tracing with the electrical and mechanical events of a heart contraction. Each segment of an ECG tracing corresponds to one event in the cardiac cycle. EVERYDAY CONNECTION ECG Abnormalities Occassionally, an area of the heart other than the SA node will initiate an impulse that will be followed by a premature contraction. Such an area, which may actually be a component of the conduction system or some other contractile cells, is known as an ectopic focus or ectopic pacemaker. An ectopic focus may be stimulated by localized ischemia; exposure to certain drugs, including caffeine, digitalis, or acetylcholine; elevated stimulation by both sympathetic or parasympathetic divisions of the autonomic nervous system; or a number of disease or pathological conditions. Occasional occurances are generally transitory and nonlife threatening, but if the condition becomes chronic, it may lead to either an arrhythmia, a deviation from the normal pattern of impulse conduction and contraction, or to fibrillation, an uncoordinated beating of the heart. While interpretation of an ECG is possible and extremely valuable after some training, a full understanding of the complexities and intricacies generally requires several years of experience. In general, the size of the electrical variations, the duration of the events, and detailed vector analysis provide the most comprehensive picture of cardiac function. For example, an amplified P wave may indicate enlargement of the atria, an enlarged Q wave may indicate a MI, and an enlarged suppressed or inverted Q wave often indicates enlarged ventricles. T waves often appear flatter when insufficient oxygen is being delivered to the myocardium. An elevation of the ST segment above baseline is often seen in patients with an acute MI, and may appear depressed below the baseline when hypoxia is occurring. As useful as analyzing these electrical recordings may be, there are limitations. For example, not all areas suffering a MI may be obvious on the ECG. Additionally, it will not reveal the effectiveness of the pumping, which requires further testing, such as an ultrasound test called an echocardiogram or nuclear medicine imaging. It is also possible for there to be pulseless electrical activity, which will show up on an ECG tracing, although there is no corresponding pumping action. Common abnormalities that may be detected by the ECGs are shown in Figure 19.25. Figure 19.25 Common ECG Abnormalities (a) In a second-degree or partial block, one-half of the P waves are not followed by the QRS complex and T waves while the other half are. (b) In atrial fibrillation, the electrical pattern is abnormal prior to the QRS complex, and the frequency between the QRS complexes has increased. (c) In ventricular tachycardia, the shape of the QRS complex is abnormal. (d) In ventricular fibrillation, there is no normal electrical activity. (e) In a third-degree block, there is no correlation between atrial activity (the P wave) and ventricular activity (the QRS complex). INTERACTIVE LINK Visit this site for a more complete library of abnormal ECGs. EVERYDAY CONNECTION External Automated Defibrillators In the event that the electrical activity of the heart is severely disrupted, cessation of electrical activity or fibrillation may occur. In fibrillation, the heart beats in a wild, uncontrolled manner, which prevents it from being able to pump effectively. Atrial fibrillation (see Figure 19.25b) is a serious condition, but as long as the ventricles continue to pump blood, the patient’s life may not be in immediate danger. Ventricular fibrillation (see Figure 19.25d) is a medical emergency that requires life support, because the ventricles are not effectively pumping blood. In a hospital setting, it is often described as “code blue.” If untreated for as little as a few minutes, ventricular fibrillation may lead to brain death. The most common treatment is defibrillation, which uses special paddles to apply a charge to the heart from an external electrical source in an attempt to establish a normal sinus rhythm (Figure 19.26). A defibrillator effectively stops the heart so that the SA node can trigger a normal conduction cycle. Because of their effectiveness in reestablishing a normal sinus rhythm, external automated defibrillators (EADs) are being placed in areas frequented by large numbers of people, such as schools, restaurants, and airports. These devices contain simple and direct verbal instructions that can be followed by nonmedical personnel in an attempt to save a life. Figure 19.26 Defibrillators (a) An external automatic defibrillator can be used by nonmedical personnel to reestablish a normal sinus rhythm in a person with fibrillation. (b) Defibrillator paddles are more commonly used in hospital settings. (credit b: “widerider107”/flickr.com) A heart block refers to an interruption in the normal conduction pathway. The nomenclature for these is very straightforward. SA nodal blocks occur within the SA node. AV nodal blocks occur within the AV node. Infra-Hisian blocks involve the bundle of His. Bundle branch blocks occur within either the left or right atrioventricular bundle branches. Hemiblocks are partial and occur within one or more fascicles of the atrioventricular bundle branch. Clinically, the most common types are the AV nodal and infra-Hisian blocks. AV blocks are often described by degrees. A first-degree or partial block indicates a delay in conduction between the SA and AV nodes. This can be recognized on the ECG as an abnormally long PR interval. A second-degree or incomplete block occurs when some impulses from the SA node reach the AV node and continue, while others do not. In this instance, the ECG would reveal some P waves not followed by a QRS complex, while others would appear normal. In the third-degree or complete block, there is no correlation between atrial activity (the P wave) and ventricular activity (the QRS complex). Even in the event of a total SA block, the AV node will assume the role of pacemaker and continue initiating contractions at 40–60 contractions per minute, which is adequate to maintain consciousness. Second- and third-degree blocks are demonstrated on the ECG presented in Figure 19.25. When arrhythmias become a chronic problem, the heart maintains a junctional rhythm, which originates in the AV node. In order to speed up the heart rate and restore full sinus rhythm, a cardiologist can implant an artificial pacemaker, which delivers electrical impulses to the heart muscle to ensure that the heart continues to contract and pump blood effectively. These artificial pacemakers are programmable by the cardiologists and can either provide stimulation temporarily upon demand or on a continuous basis. Some devices also contain built-in defibrillators. Cardiac Muscle Metabolism Normally, cardiac muscle metabolism is entirely aerobic. Oxygen from the lungs is brought to the heart, and every other organ, attached to the hemoglobin molecules within the erythrocytes. Heart cells also store appreciable amounts of oxygen in myoglobin. Normally, these two mechanisms, circulating oxygen and oxygen attached to myoglobin, can supply sufficient oxygen to the heart, even during peak performance. Fatty acids and glucose from the circulation are broken down within the mitochondria to release energy in the form of ATP. Both fatty acid droplets and glycogen are stored within the sarcoplasm and provide additional nutrient supply. (Seek additional content for more detail about metabolism.) Cardiac Cycle - Describe the relationship between blood pressure and blood flow - Summarize the events of the cardiac cycle - Compare atrial and ventricular systole and diastole - Relate heart sounds detected by auscultation to action of heart’s valves The period of time that begins with contraction of the atria and ends with ventricular relaxation is known as the cardiac cycle(Figure 19.27). The period of contraction that the heart undergoes while it pumps blood into circulation is called systole. The period of relaxation that occurs as the chambers fill with blood is called diastole. Both the atria and ventricles undergo systole and diastole, and it is essential that these components be carefully regulated and coordinated to ensure blood is pumped efficiently to the body. Figure 19.27 Overview of the Cardiac Cycle The cardiac cycle begins with atrial systole and progresses to ventricular systole, atrial diastole, and ventricular diastole, when the cycle begins again. Correlations to the ECG are highlighted. Pressures and Flow Fluids, whether gases or liquids, are materials that flow according to pressure gradients—that is, they move from regions that are higher in pressure to regions that are lower in pressure. Accordingly, when the heart chambers are relaxed (diastole), blood will flow into the atria from the veins, which are higher in pressure. As blood flows into the atria, the pressure will rise, so the blood will initially move passively from the atria into the ventricles. When the action potential triggers the muscles in the atria to contract (atrial systole), the pressure within the atria rises further, pumping blood into the ventricles. During ventricular systole, pressure rises in the ventricles, pumping blood into the pulmonary trunk from the right ventricle and into the aorta from the left ventricle. Again, as you consider this flow and relate it to the conduction pathway, the elegance of the system should become apparent. Phases of the Cardiac Cycle At the beginning of the cardiac cycle, both the atria and ventricles are relaxed (diastole). Blood is flowing into the right atrium from the superior and inferior venae cavae and the coronary sinus. Blood flows into the left atrium from the four pulmonary veins. The two atrioventricular valves, the tricuspid and mitral valves, are both open, so blood flows unimpeded from the atria and into the ventricles. Approximately 70–80 percent of ventricular filling occurs by this method. The two semilunar valves, the pulmonary and aortic valves, are closed, preventing backflow of blood into the right and left ventricles from the pulmonary trunk on the right and the aorta on the left. Atrial Systole and Diastole Contraction of the atria follows depolarization, represented by the P wave of the ECG. As the atrial muscles contract from the superior portion of the atria toward the atrioventricular septum, pressure rises within the atria and blood is pumped into the ventricles through the open atrioventricular (tricuspid, and mitral or bicuspid) valves. At the start of atrial systole, the ventricles are normally filled with approximately 70–80 percent of their capacity due to inflow during diastole. Atrial contraction, also referred to as the “atrial kick,” contributes the remaining 20–30 percent of filling (see Figure 19.27). Atrial systole lasts approximately 100 ms and ends prior to ventricular systole, as the atrial muscle returns to diastole. Ventricular Systole Ventricular systole (see Figure 19.27) follows the depolarization of the ventricles and is represented by the QRS complex in the ECG. It may be conveniently divided into two phases, lasting a total of 270 ms. At the end of atrial systole and just prior to atrial contraction, the ventricles contain approximately 130 mL blood in a resting adult in a standing position. This volume is known as the end diastolic volume (EDV) or preload. Initially, as the muscles in the ventricle contract, the pressure of the blood within the chamber rises, but it is not yet high enough to open the semilunar (pulmonary and aortic) valves and be ejected from the heart. However, blood pressure quickly rises above that of the atria that are now relaxed and in diastole. This increase in pressure causes blood to flow back toward the atria, closing the tricuspid and mitral valves. Since blood is not being ejected from the ventricles at this early stage, the volume of blood within the chamber remains constant. Consequently, this initial phase of ventricular systole is known as isovolumic contraction, also called isovolumetric contraction (see Figure 19.27). In the second phase of ventricular systole, the ventricular ejection phase, the contraction of the ventricular muscle has raised the pressure within the ventricle to the point that it is greater than the pressures in the pulmonary trunk and the aorta. Blood is pumped from the heart, pushing open the pulmonary and aortic semilunar valves. Pressure generated by the left ventricle will be appreciably greater than the pressure generated by the right ventricle, since the existing pressure in the aorta will be so much higher. Nevertheless, both ventricles pump the same amount of blood. This quantity is referred to as stroke volume. Stroke volume will normally be in the range of 70–80 mL. Since ventricular systole began with an EDV of approximately 130 mL of blood, this means that there is still 50–60 mL of blood remaining in the ventricle following contraction. This volume of blood is known as the end systolic volume (ESV). Ventricular Diastole Ventricular relaxation, or diastole, follows repolarization of the ventricles and is represented by the T wave of the ECG. It too is divided into two distinct phases and lasts approximately 430 ms. During the early phase of ventricular diastole, as the ventricular muscle relaxes, pressure on the remaining blood within the ventricle begins to fall. When pressure within the ventricles drops below pressure in both the pulmonary trunk and aorta, blood flows back toward the heart, producing the dicrotic notch (small dip) seen in blood pressure tracings. The semilunar valves close to prevent backflow into the heart. Since the atrioventricular valves remain closed at this point, there is no change in the volume of blood in the ventricle, so the early phase of ventricular diastole is called the isovolumic ventricular relaxation phase, also called isovolumetric ventricular relaxation phase (see Figure 19.27). In the second phase of ventricular diastole, called late ventricular diastole, as the ventricular muscle relaxes, pressure on the blood within the ventricles drops even further. Eventually, it drops below the pressure in the atria. When this occurs, blood flows from the atria into the ventricles, pushing open the tricuspid and mitral valves. As pressure drops within the ventricles, blood flows from the major veins into the relaxed atria and from there into the ventricles. Both chambers are in diastole, the atrioventricular valves are open, and the semilunar valves remain closed (see Figure 19.27). The cardiac cycle is complete. Figure 19.28 illustrates the relationship between the cardiac cycle and the ECG. Figure 19.28 Relationship between the Cardiac Cycle and ECG Initially, both the atria and ventricles are relaxed (diastole). The P wave represents depolarization of the atria and is followed by atrial contraction (systole). Atrial systole extends until the QRS complex, at which point, the atria relax. The QRS complex represents depolarization of the ventricles and is followed by ventricular contraction. The T wave represents the repolarization of the ventricles and marks the beginning of ventricular relaxation. Heart Sounds One of the simplest, yet effective, diagnostic techniques applied to assess the state of a patient’s heart is auscultation using a stethoscope. In a normal, healthy heart, there are only two audible heart sounds: S1 and S2. S1 is the sound created by the closing of the atrioventricular valves during ventricular contraction and is normally described as a “lub,” or first heart sound. The second heart sound, S2, is the sound of the closing of the semilunar valves during ventricular diastole and is described as a “dub” (Figure 19.29). In both cases, as the valves close, the openings within the atrioventricular septum guarded by the valves will become reduced, and blood flow through the opening will become more turbulent until the valves are fully closed. There is a third heart sound, S3, but it is rarely heard in healthy individuals. It may be the sound of blood flowing into the atria, or blood sloshing back and forth in the ventricle, or even tensing of the chordae tendineae. S3 may be heard in youth, some athletes, and pregnant women. If the sound is heard later in life, it may indicate congestive heart failure, warranting further tests. Some cardiologists refer to the collective S1, S2, and S3 sounds as the “Kentucky gallop,” because they mimic those produced by a galloping horse. The fourth heart sound, S4, results from the contraction of the atria pushing blood into a stiff or hypertrophic ventricle, indicating failure of the left ventricle. S4 occurs prior to S1 and the collective sounds S4, S1, and S2 are referred to by some cardiologists as the “Tennessee gallop,” because of their similarity to the sound produced by a galloping horse with a different gait. A few individuals may have both S3 and S4, and this combined sound is referred to as S7. Figure 19.29 Heart Sounds and the Cardiac Cycle In this illustration, the x-axis reflects time with a recording of the heart sounds. The y-axis represents pressure. The term murmur is used to describe an unusual sound coming from the heart that is caused by the turbulent flow of blood. Murmurs are graded on a scale of 1 to 6, with 1 being the most common, the most difficult sound to detect, and the least serious. The most severe is a 6. Phonocardiograms or auscultograms can be used to record both normal and abnormal sounds using specialized electronic stethoscopes. During auscultation, it is common practice for the clinician to ask the patient to breathe deeply. This procedure not only allows for listening to airflow, but it may also amplify heart murmurs. Inhalation increases blood flow into the right side of the heart and may increase the amplitude of right-sided heart murmurs. Expiration partially restricts blood flow into the left side of the heart and may amplify left-sided heart murmurs. Figure 19.30 indicates proper placement of the bell of the stethoscope to facilitate auscultation. Figure 19.30 Stethoscope Placement for Auscultation Proper placement of the bell of the stethoscope facilitates auscultation. At each of the four locations on the chest, a different valve can be heard. Cardiac Physiology - Relate heart rate to cardiac output - Describe the effect of exercise on heart rate - Identify cardiovascular centers and cardiac reflexes that regulate heart function - Describe factors affecting heart rate - Distinguish between positive and negative factors that affect heart contractility - Summarize factors affecting stroke volume and cardiac output - Describe the cardiac response to variations in blood flow and pressure The autorhythmicity inherent in cardiac cells keeps the heart beating at a regular pace; however, the heart is regulated by and responds to outside influences as well. Neural and endocrine controls are vital to the regulation of cardiac function. In addition, the heart is sensitive to several environmental factors, including electrolytes. Resting Cardiac Output Cardiac output (CO) is a measurement of the amount of blood pumped by each ventricle in one minute. To calculate this value, multiply stroke volume (SV), the amount of blood pumped by each ventricle, by heart rate (HR), in contractions per minute (or beats per minute, bpm). It can be represented mathematically by the following equation: CO = HR × SV SV is normally measured using an echocardiogram to record EDV and ESV, and calculating the difference: SV = EDV – ESV. SV can also be measured using a specialized catheter, but this is an invasive procedure and far more dangerous to the patient. A mean SV for a resting 70-kg (150-lb) individual would be approximately 70 mL. There are several important variables, including size of the heart, physical and mental condition of the individual, sex, contractility, duration of contraction, preload or EDV, and afterload or resistance. Normal range for SV would be 55–100 mL. An average resting HR would be approximately 75 bpm but could range from 60–100 in some individuals. Using these numbers, the mean CO is 5.25 L/min, with a range of 4.0–8.0 L/min. Remember, however, that these numbers refer to CO from each ventricle separately, not the total for the heart. Factors influencing CO are summarized in Figure 19.31. Figure 19.31 Major Factors Influencing Cardiac Output Cardiac output is influenced by heart rate and stroke volume, both of which are also variable. SVs are also used to calculate ejection fraction, which is the portion of the blood that is pumped or ejected from the heart with each contraction. To calculate ejection fraction, SV is divided by EDV. Despite the name, the ejection fraction is normally expressed as a percentage. Ejection fractions range from approximately 55–70 percent, with a mean of 58 percent. Exercise and Maximum Cardiac Output In healthy young individuals, HR may increase to 150 bpm during exercise. SV can also increase from 70 to approximately 130 mL due to increased strength of contraction. This would increase CO to approximately 19.5 L/min, 4–5 times the resting rate. Top cardiovascular athletes can achieve even higher levels. At their peak performance, they may increase resting CO by 7–8 times. Since the heart is a muscle, exercising it increases its efficiency. The difference between maximum and resting CO is known as the cardiac reserve. It measures the residual capacity of the heart to pump blood. Heart Rates HRs vary considerably, not only with exercise and fitness levels, but also with age. Newborn resting HRs may be 120 bpm. HR gradually decreases until young adulthood and then gradually increases again with age. Maximum HRs are normally in the range of 200–220 bpm, although there are some extreme cases in which they may reach higher levels. As one ages, the ability to generate maximum rates decreases. This may be estimated by taking the maximal value of 220 bpm and subtracting the individual’s age. So a 40-year-old individual would be expected to hit a maximum rate of approximately 180, and a 60-year-old person would achieve a HR of 160. DISORDERS OF THE... Heart: Abnormal Heart Rates For an adult, normal resting HR will be in the range of 60–100 bpm. Bradycardia is the condition in which resting rate drops below 60 bpm, and tachycardia is the condition in which the resting rate is above 100 bpm. Trained athletes typically have very low HRs. If the patient is not exhibiting other symptoms, such as weakness, fatigue, dizziness, fainting, chest discomfort, palpitations, or respiratory distress, bradycardia is not considered clinically significant. However, if any of these symptoms are present, they may indicate that the heart is not providing sufficient oxygenated blood to the tissues. The term relative bradycardia may be used with a patient who has a HR in the normal range but is still suffering from these symptoms. Most patients remain asymptomatic as long as the HR remains above 50 bpm. Bradycardia may be caused by either inherent factors or causes external to the heart. While the condition may be inherited, typically it is acquired in older individuals. Inherent causes include abnormalities in either the SA or AV node. If the condition is serious, a pacemaker may be required. Other causes include ischemia to the heart muscle or diseases of the heart vessels or valves. External causes include metabolic disorders, pathologies of the endocrine system often involving the thyroid, electrolyte imbalances, neurological disorders including inappropriate autonomic responses, autoimmune pathologies, over-prescription of beta blocker drugs that reduce HR, recreational drug use, or even prolonged bed rest. Treatment relies upon establishing the underlying cause of the disorder and may necessitate supplemental oxygen. Tachycardia is not normal in a resting patient but may be detected in pregnant women or individuals experiencing extreme stress. In the latter case, it would likely be triggered by stimulation from the limbic system or disorders of the autonomic nervous system. In some cases, tachycardia may involve only the atria. Some individuals may remain asymptomatic, but when present, symptoms may include dizziness, shortness of breath, lightheadedness, rapid pulse, heart palpations, chest pain, or fainting (syncope). While tachycardia is defined as a HR above 100 bpm, there is considerable variation among people. Further, the normal resting HRs of children are often above 100 bpm, but this is not considered to be tachycardia Many causes of tachycardia may be benign, but the condition may also be correlated with fever, anemia, hypoxia, hyperthyroidism, hypersecretion of catecholamines, some cardiomyopathies, some disorders of the valves, and acute exposure to radiation. Elevated rates in an exercising or resting patient are normal and expected. Resting rate should always be taken after recovery from exercise. Treatment depends upon the underlying cause but may include medications, implantable cardioverter defibrillators, ablation, or surgery. Correlation Between Heart Rates and Cardiac Output Initially, physiological conditions that cause HR to increase also trigger an increase in SV. During exercise, the rate of blood returning to the heart increases. However as the HR rises, there is less time spent in diastole and consequently less time for the ventricles to fill with blood. Even though there is less filling time, SV will initially remain high. However, as HR continues to increase, SV gradually decreases due to decreased filling time. CO will initially stabilize as the increasing HR compensates for the decreasing SV, but at very high rates, CO will eventually decrease as increasing rates are no longer able to compensate for the decreasing SV. Consider this phenomenon in a healthy young individual. Initially, as HR increases from resting to approximately 120 bpm, CO will rise. As HR increases from 120 to 160 bpm, CO remains stable, since the increase in rate is offset by decreasing ventricular filling time and, consequently, SV. As HR continues to rise above 160 bpm, CO actually decreases as SV falls faster than HR increases. So although aerobic exercises are critical to maintain the health of the heart, individuals are cautioned to monitor their HR to ensure they stay within the target heart rate range of between 120 and 160 bpm, so CO is maintained. The target HR is loosely defined as the range in which both the heart and lungs receive the maximum benefit from the aerobic workout and is dependent upon age. Cardiovascular Centers Nervous control over HR is centralized within the two paired cardiovascular centers of the medulla oblongata (Figure 19.32). The cardioaccelerator regions stimulate activity via sympathetic stimulation of the cardioaccelerator nerves, and the cardioinhibitory centers decrease heart activity via parasympathetic stimulation as one component of the vagus nerve, cranial nerve X. During rest, both centers provide slight stimulation to the heart, contributing to autonomic tone. This is a similar concept to tone in skeletal muscles. Normally, vagal stimulation predominates as, left unregulated, the SA node would initiate a sinus rhythm of approximately 100 bpm. Both sympathetic and parasympathetic stimulations flow through a paired complex network of nerve fibers known as the cardiac plexus near the base of the heart. The cardioaccelerator center also sends additional fibers, forming the cardiac nerves via sympathetic ganglia (the cervical ganglia plus superior thoracic ganglia T1–T4) to both the SA and AV nodes, plus additional fibers to the atria and ventricles. The ventricles are more richly innervated by sympathetic fibers than parasympathetic fibers. Sympathetic stimulation causes the release of the neurotransmitter norepinephrine (NE) at the neuromuscular junction of the cardiac nerves. NE shortens the repolarization period, thus speeding the rate of depolarization and contraction, which results in an increase in HR. It opens chemical- or ligand-gated sodium and calcium ion channels, allowing an influx of positively charged ions. NE binds to the beta-1 receptor. Some cardiac medications (for example, beta blockers) work by blocking these receptors, thereby slowing HR and are one possible treatment for hypertension. Overprescription of these drugs may lead to bradycardia and even stoppage of the heart. Figure 19.32 Autonomic Innervation of the Heart Cardioaccelerator and cardioinhibitory areas are components of the paired cardiac centers located in the medulla oblongata of the brain. They innervate the heart via sympathetic cardiac nerves that increase cardiac activity and vagus (parasympathetic) nerves that slow cardiac activity. Parasympathetic stimulation originates from the cardioinhibitory region with impulses traveling via the vagus nerve (cranial nerve X). The vagus nerve sends branches to both the SA and AV nodes, and to portions of both the atria and ventricles. Parasympathetic stimulation releases the neurotransmitter acetylcholine (ACh) at the neuromuscular junction. ACh slows HR by opening chemical- or ligand-gated potassium ion channels to slow the rate of spontaneous depolarization, which extends repolarization and increases the time before the next spontaneous depolarization occurs. Without any nervous stimulation, the SA node would establish a sinus rhythm of approximately 100 bpm. Since resting rates are considerably less than this, it becomes evident that parasympathetic stimulation normally slows HR. This is similar to an individual driving a car with one foot on the brake pedal. To speed up, one need merely remove one’s foot from the break and let the engine increase speed. In the case of the heart, decreasing parasympathetic stimulation decreases the release of ACh, which allows HR to increase up to approximately 100 bpm. Any increases beyond this rate would require sympathetic stimulation. Figure 19.33 illustrates the effects of parasympathetic and sympathetic stimulation on the normal sinus rhythm. Figure 19.33 Effects of Parasympathetic and Sympathetic Stimulation on Normal Sinus Rhythm The wave of depolarization in a normal sinus rhythm shows a stable resting HR. Following parasympathetic stimulation, HR slows. Following sympathetic stimulation, HR increases. Input to the Cardiovascular Center The cardiovascular center receives input from a series of visceral receptors with impulses traveling through visceral sensory fibers within the vagus and sympathetic nerves via the cardiac plexus. Among these receptors are various proprioreceptors, baroreceptors, and chemoreceptors, plus stimuli from the limbic system. Collectively, these inputs normally enable the cardiovascular centers to regulate heart function precisely, a process known as cardiac reflexes. Increased physical activity results in increased rates of firing by various proprioreceptors located in muscles, joint capsules, and tendons. Any such increase in physical activity would logically warrant increased blood flow. The cardiac centers monitor these increased rates of firing, and suppress parasympathetic stimulation and increase sympathetic stimulation as needed in order to increase blood flow. Similarly, baroreceptors are stretch receptors located in the aortic sinus, carotid bodies, the venae cavae, and other locations, including pulmonary vessels and the right side of the heart itself. Rates of firing from the baroreceptors represent blood pressure, level of physical activity, and the relative distribution of blood. The cardiac centers monitor baroreceptor firing to maintain cardiac homeostasis, a mechanism called the baroreceptor reflex. With increased pressure and stretch, the rate of baroreceptor firing increases, and the cardiac centers decrease sympathetic stimulation and increase parasympathetic stimulation. As pressure and stretch decrease, the rate of baroreceptor firing decreases, and the cardiac centers increase sympathetic stimulation and decrease parasympathetic stimulation. There is a similar reflex, called the atrial reflex or Bainbridge reflex, associated with varying rates of blood flow to the atria. Increased venous return stretches the walls of the atria where specialized baroreceptors are located. However, as the atrial baroreceptors increase their rate of firing and as they stretch due to the increased blood pressure, the cardiac center responds by increasing sympathetic stimulation and inhibiting parasympathetic stimulation to increase HR. The opposite is also true. Increased metabolic byproducts associated with increased activity, such as carbon dioxide, hydrogen ions, and lactic acid, plus falling oxygen levels, are detected by a suite of chemoreceptors innervated by the glossopharyngeal and vagus nerves. These chemoreceptors provide feedback to the cardiovascular centers about the need for increased or decreased blood flow, based on the relative levels of these substances. The limbic system can also significantly impact HR related to emotional state. During periods of stress, it is not unusual to identify higher than normal HRs, often accompanied by a surge in the stress hormone cortisol. Individuals experiencing extreme anxiety may manifest panic attacks with symptoms that resemble those of heart attacks. These events are typically transient and treatable. Meditation techniques have been developed to ease anxiety and have been shown to lower HR effectively. Doing simple deep and slow breathing exercises with one’s eyes closed can also significantly reduce this anxiety and HR. DISORDERS OF THE... Heart: Broken Heart Syndrome Extreme stress from such life events as the death of a loved one, an emotional break up, loss of income, or foreclosure of a home may lead to a condition commonly referred to as broken heart syndrome. This condition may also be called Takotsubo cardiomyopathy, transient apical ballooning syndrome, apical ballooning cardiomyopathy, stress-induced cardiomyopathy, Gebrochenes-Herz syndrome, and stress cardiomyopathy. The recognized effects on the heart include congestive heart failure due to a profound weakening of the myocardium not related to lack of oxygen. This may lead to acute heart failure, lethal arrhythmias, or even the rupture of a ventricle. The exact etiology is not known, but several factors have been suggested, including transient vasospasm, dysfunction of the cardiac capillaries, or thickening of the myocardium—particularly in the left ventricle—that may lead to the critical circulation of blood to this region. While many patients survive the initial acute event with treatment to restore normal function, there is a strong correlation with death. Careful statistical analysis by the Cass Business School, a prestigious institution located in London, published in 2008, revealed that within one year of the death of a loved one, women are more than twice as likely to die and males are six times as likely to die as would otherwise be expected. Other Factors Influencing Heart Rate Using a combination of autorhythmicity and innervation, the cardiovascular center is able to provide relatively precise control over HR. However, there are a number of other factors that have an impact on HR as well, including epinephrine, NE, and thyroid hormones; levels of various ions including calcium, potassium, and sodium; body temperature; hypoxia; and pH balance (Table 19.1 and Table 19.2). After reading this section, the importance of maintaining homeostasis should become even more apparent. Major Factors Increasing Heart Rate and Force of Contraction \| Factor \| Effect \| \|---\|---\| \| Cardioaccelerator nerves \| Release of norepinephrine by cardioinhibitory nerves \| \| Proprioreceptors \| Increased firing rates of proprioreceptors (e.g. during exercise) \| \| Chemoreceptors \| Chemoreceptors sensing decreased levels of O2 or increased levels of H+, CO2 and lactic acid \| \| Baroreceptors \| Decreased firing rates of baroreceptors (indicating falling blood volume/pressure) \| \| Limbic system \| Anticipation of physical exercise or strong emotions by the limbic system \| \| Catecholamines \| Increased epinephrine and norepinephrine release by the adrenal glands \| \| Thyroid hormones \| Increased T3 and T4 in the blood (released by thyroid) \| \| Calcium \| Increase in calcium ions in the blood \| \| Potassium \| Decrease in potassium ions in the blood \| \| Sodium \| Decrease in sodium ions in the blood \| \| Body temperature \| Increase in body temperature \| \| Nicotine and caffeine \| Presence of nicotine, caffeine or other stimulants \| Table 19.1 Factors Decreasing Heart Rate and Force of Contraction \| Factor \| Effect \| \|---\|---\| \| Cardioinhibitor nerves (vagus) \| Release of acetylcholine by cardioaccelerator nerves \| \| Proprioreceptors \| Decreased firing rates of proprioreceptors (e.g. during rest) \| \| Chemoreceptors \| Chemoreceptors sensing increased levels of O2 or decreased levels of H+, CO2 and lactic acid \| \| Baroreceptors \| Increased firing rates of baroreceptors (indicating rising blood volume/pressure) \| \| Limbic system \| Anticipation of relaxation by the limbic system \| \| Catecholamines \| Increased epinephrine and norepinephrine release by the adrenal glands \| \| Thyroid hormones \| Decreased T3 and T4 in the blood (released by thyroid) \| \| Calcium \| Increase in calcium ions in the blood \| \| Potassium \| Increase in potassium ions in the blood \| \| Sodium \| Increase in sodium ions in the blood \| \| Body temperature \| Decrease in body temperature \| \| Opiates and tranquilizers \| Presence of opiates (heroin), tranquilizers or other depressants \| Table 19.2 Epinephrine and Norepinephrine The catecholamines, epinephrine and NE, secreted by the adrenal medulla form one component of the extended fight-or-flight mechanism. The other component is sympathetic stimulation. Epinephrine and NE have similar effects: binding to the beta-1 receptors, and opening sodium and calcium ion chemical- or ligand-gated channels. The rate of depolarization is increased by this additional influx of positively charged ions, so the threshold is reached more quickly and the period of repolarization is shortened. However, massive releases of these hormones coupled with sympathetic stimulation may actually lead to arrhythmias. There is no parasympathetic stimulation to the adrenal medulla. Thyroid Hormones In general, increased levels of thyroid hormone, or thyroxin, increase cardiac rate and contractility. The impact of thyroid hormone is typically of a much longer duration than that of the catecholamines. The physiologically active form of thyroid hormone, T3 or triiodothyronine, has been shown to directly enter cardiomyocytes and alter activity at the level of the genome. It also impacts the beta adrenergic response similar to epinephrine and NE described above. Excessive levels of thyroxin may trigger tachycardia. Calcium Calcium ion levels have great impacts upon both HR and contractility; as the levels of calcium ions increase, so do HR and contractility. High levels of calcium ions (hypercalcemia) may be implicated in a short QT interval and a widened T wave in the ECG. The QT interval represents the time from the start of depolarization to repolarization of the ventricles, and includes the period of ventricular systole. Extremely high levels of calcium may induce cardiac arrest. Drugs known as calcium channel blockers slow HR by binding to these channels and blocking or slowing the inward movement of calcium ions. Caffeine and Nicotine Caffeine and nicotine are not found naturally within the body. Both of these nonregulated drugs have an excitatory effect on membranes of neurons in general and have a stimulatory effect on the cardiac centers specifically, causing an increase in HR. Caffeine works by increasing the rates of depolarization at the SA node, whereas nicotine stimulates the activity of the sympathetic neurons that deliver impulses to the heart. Although it is the world’s most widely consumed psychoactive drug, caffeine is legal and not regulated. While precise quantities have not been established, “normal” consumption is not considered harmful to most people, although it may cause disruptions to sleep and acts as a diuretic. Its consumption by pregnant women is cautioned against, although no evidence of negative effects has been confirmed. Tolerance and even physical and mental addiction to the drug result in individuals who routinely consume the substance. Nicotine, too, is a stimulant and produces addiction. While legal and nonregulated, concerns about nicotine’s safety and documented links to respiratory and cardiac disease have resulted in warning labels on cigarette packages. Factors Decreasing Heart Rate HR can be slowed when a person experiences altered sodium and potassium levels, hypoxia, acidosis, alkalosis, and hypothermia (see Table 19.1). The relationship between electrolytes and HR is complex, but maintaining electrolyte balance is critical to the normal wave of depolarization. Of the two ions, potassium has the greater clinical significance. Initially, both hyponatremia (low sodium levels) and hypernatremia (high sodium levels) may lead to tachycardia. Severely high hypernatremia may lead to fibrillation, which may cause CO to cease. Severe hyponatremia leads to both bradycardia and other arrhythmias. Hypokalemia (low potassium levels) also leads to arrhythmias, whereas hyperkalemia (high potassium levels) causes the heart to become weak and flaccid, and ultimately to fail. Acidosis is a condition in which excess hydrogen ions are present, and the patient’s blood expresses a low pH value. Alkalosis is a condition in which there are too few hydrogen ions, and the patient’s blood has an elevated pH. Normal blood pH falls in the range of 7.35–7.45, so a number lower than this range represents acidosis and a higher number represents alkalosis. Recall that enzymes are the regulators or catalysts of virtually all biochemical reactions; they are sensitive to pH and will change shape slightly with values outside their normal range. These variations in pH and accompanying slight physical changes to the active site on the enzyme decrease the rate of formation of the enzyme-substrate complex, subsequently decreasing the rate of many enzymatic reactions, which can have complex effects on HR. Severe changes in pH will lead to denaturation of the enzyme. The last variable is body temperature. Elevated body temperature is called hyperthermia, and suppressed body temperature is called hypothermia. Slight hyperthermia results in increasing HR and strength of contraction. Hypothermia slows the rate and strength of heart contractions. This distinct slowing of the heart is one component of the larger diving reflex that diverts blood to essential organs while submerged. If sufficiently chilled, the heart will stop beating, a technique that may be employed during open heart surgery. In this case, the patient’s blood is normally diverted to an artificial heart-lung machine to maintain the body’s blood supply and gas exchange until the surgery is complete, and sinus rhythm can be restored. Excessive hyperthermia and hypothermia will both result in death, as enzymes drive the body systems to cease normal function, beginning with the central nervous system. Stroke Volume Many of the same factors that regulate HR also impact cardiac function by altering SV. While a number of variables are involved, SV is ultimately dependent upon the difference between EDV and ESV. The three primary factors to consider are preload, or the stretch on the ventricles prior to contraction; the contractility, or the force or strength of the contraction itself; and afterload, the force the ventricles must generate to pump blood against the resistance in the vessels. These factors are summarized in Table 19.1 and Table 19.2. Preload Preload is another way of expressing EDV. Therefore, the greater the EDV is, the greater the preload is. One of the primary factors to consider is filling time, or the duration of ventricular diastole during which filling occurs. The more rapidly the heart contracts, the shorter the filling time becomes, and the lower the EDV and preload are. This effect can be partially overcome by increasing the second variable, contractility, and raising SV, but over time, the heart is unable to compensate for decreased filling time, and preload also decreases. With increasing ventricular filling, both EDV or preload increase, and the cardiac muscle itself is stretched to a greater degree. At rest, there is little stretch of the ventricular muscle, and the sarcomeres remain short. With increased ventricular filling, the ventricular muscle is increasingly stretched and the sarcomere length increases. As the sarcomeres reach their optimal lengths, they will contract more powerfully, because more of the myosin heads can bind to the actin on the thin filaments, forming cross bridges and increasing the strength of contraction and SV. If this process were to continue and the sarcomeres stretched beyond their optimal lengths, the force of contraction would decrease. However, due to the physical constraints of the location of the heart, this excessive stretch is not a concern. The relationship between ventricular stretch and contraction has been stated in the well-known Frank-Starling mechanism or simply Starling’s Law of the Heart. This principle states that, within physiological limits, the force of heart contraction is directly proportional to the initial length of the muscle fiber. This means that the greater the stretch of the ventricular muscle (within limits), the more powerful the contraction is, which in turn increases SV. Therefore, by increasing preload, you increase the second variable, contractility. Otto Frank (1865–1944) was a German physiologist; among his many published works are detailed studies of this important heart relationship. Ernest Starling (1866–1927) was an important English physiologist who also studied the heart. Although they worked largely independently, their combined efforts and similar conclusions have been recognized in the name “Frank-Starling mechanism.” Any sympathetic stimulation to the venous system will increase venous return to the heart, which contributes to ventricular filling, and EDV and preload. While much of the ventricular filling occurs while both atria and ventricles are in diastole, the contraction of the atria, the atrial kick, plays a crucial role by providing the last 20–30 percent of ventricular filling. Contractility It is virtually impossible to consider preload or ESV without including an early mention of the concept of contractility. Indeed, the two parameters are intimately linked. Contractility refers to the force of the contraction of the heart muscle, which controls SV, and is the primary parameter for impacting ESV. The more forceful the contraction is, the greater the SV and smaller the ESV are. Less forceful contractions result in smaller SVs and larger ESVs. Factors that increase contractility are described as positive inotropic factors, and those that decrease contractility are described as negative inotropic factors (ino- = “fiber;” -tropic = “turning toward”). Not surprisingly, sympathetic stimulation is a positive inotrope, whereas parasympathetic stimulation is a negative inotrope. Sympathetic stimulation triggers the release of NE at the neuromuscular junction from the cardiac nerves and also stimulates the adrenal cortex to secrete epinephrine and NE. In addition to their stimulatory effects on HR, they also bind to both alpha and beta receptors on the cardiac muscle cell membrane to increase metabolic rate and the force of contraction. This combination of actions has the net effect of increasing SV and leaving a smaller residual ESV in the ventricles. In comparison, parasympathetic stimulation releases ACh at the neuromuscular junction from the vagus nerve. The membrane hyperpolarizes and inhibits contraction to decrease the strength of contraction and SV, and to raise ESV. Since parasympathetic fibers are more widespread in the atria than in the ventricles, the primary site of action is in the upper chambers. Parasympathetic stimulation in the atria decreases the atrial kick and reduces EDV, which decreases ventricular stretch and preload, thereby further limiting the force of ventricular contraction. Stronger parasympathetic stimulation also directly decreases the force of contraction of the ventricles. Several synthetic drugs, including dopamine and isoproterenol, have been developed that mimic the effects of epinephrine and NE by stimulating the influx of calcium ions from the extracellular fluid. Higher concentrations of intracellular calcium ions increase the strength of contraction. Excess calcium (hypercalcemia) also acts as a positive inotropic agent. The drug digitalis lowers HR and increases the strength of the contraction, acting as a positive inotropic agent by blocking the sequestering of calcium ions into the sarcoplasmic reticulum. This leads to higher intracellular calcium levels and greater strength of contraction. In addition to the catecholamines from the adrenal medulla, other hormones also demonstrate positive inotropic effects. These include thyroid hormones and glucagon from the pancreas. Negative inotropic agents include hypoxia, acidosis, hyperkalemia, and a variety of synthetic drugs. These include numerous beta blockers and calcium channel blockers. Early beta blocker drugs include propranolol and pronethalol, and are credited with revolutionizing treatment of cardiac patients experiencing angina pectoris. There is also a large class of dihydropyridine, phenylalkylamine, and benzothiazepine calcium channel blockers that may be administered decreasing the strength of contraction and SV. Afterload Afterload refers to the tension that the ventricles must develop to pump blood effectively against the resistance in the vascular system. Any condition that increases resistance requires a greater afterload to force open the semilunar valves and pump the blood. Damage to the valves, such as stenosis, which makes them harder to open will also increase afterload. Any decrease in resistance decreases the afterload. Figure 19.34 summarizes the major factors influencing SV, Figure 19.35 summarizes the major factors influencing CO, and Table 19.3 and Table 19.4 summarize cardiac responses to increased and decreased blood flow and pressure in order to restore homeostasis. Figure 19.34 Major Factors Influencing Stroke Volume Multiple factors impact preload, afterload, and contractility, and are the major considerations influencing SV. Figure 19.35 Summary of Major Factors Influencing Cardiac Output The primary factors influencing HR include autonomic innervation plus endocrine control. Not shown are environmental factors, such as electrolytes, metabolic products, and temperature. The primary factors controlling SV include preload, contractility, and afterload. Other factors such as electrolytes may be classified as either positive or negative inotropic agents. Cardiac Response to Decreasing Blood Flow and Pressure Due to Decreasing Cardiac Output \| Baroreceptors (aorta, carotid arteries, venae cavae, and atria) \| Chemoreceptors (both central nervous system and in proximity to baroreceptors) \| \| \|---\|---\|---\| \| Sensitive to \| Decreasing stretch \| Decreasing O2 and increasing CO2, H+, and lactic acid \| \| Target \| Parasympathetic stimulation suppressed \| Sympathetic stimulation increased \| \| Response of heart \| Increasing heart rate and increasing stroke volume \| Increasing heart rate and increasing stroke volume \| \| Overall effect \| Increasing blood flow and pressure due to increasing cardiac output; homeostasis restored \| Increasing blood flow and pressure due to increasing cardiac output; homeostasis restored \| Table 19.3 Cardiac Response to Increasing Blood Flow and Pressure Due to Increasing Cardiac Output \| Baroreceptors (aorta, carotid arteries, venae cavae, and atria) \| Chemoreceptors (both central nervous system and in proximity to baroreceptors) \| \| \|---\|---\|---\| \| Sensitive to \| Increasing stretch \| Increasing O2 and decreasing CO2, H+, and lactic acid \| \| Target \| Parasympathetic stimulation increased \| Sympathetic stimulation suppressed \| \| Response of heart \| Decreasing heart rate and decreasing stroke volume \| Decreasing heart rate and decreasing stroke volume \| \| Overall effect \| Decreasing blood flow and pressure due to decreasing cardiac output; homeostasis restored \| Decreasing blood flow and pressure due to decreasing cardiac output; homeostasis restored \| Table 19.4 Development of the Heart - Describe the embryological development of heart structures - Identify five regions of the fetal heart - Relate fetal heart structures to adult counterparts The human heart is the first functional organ to develop. It begins beating and pumping blood around day 21 or 22, a mere three weeks after fertilization. This emphasizes the critical nature of the heart in distributing blood through the vessels and the vital exchange of nutrients, oxygen, and wastes both to and from the developing baby. The critical early development of the heart is reflected by the prominent heart bulge that appears on the anterior surface of the embryo. The heart forms from an embryonic tissue called mesoderm around 18 to 19 days after fertilization. Mesoderm is one of the three primary germ layers that differentiates early in development that collectively gives rise to all subsequent tissues and organs. The heart begins to develop near the head of the embryo in a region known as the cardiogenic area. Following chemical signals called factors from the underlying endoderm (another of the three primary germ layers), the cardiogenic area begins to form two strands called the cardiogenic cords (Figure 19.36). As the cardiogenic cords develop, a lumen rapidly develops within them. At this point, they are referred to as endocardial tubes. The two tubes migrate together and fuse to form a single primitive heart tube. The primitive heart tube quickly forms five distinct regions. From head to tail, these include the truncus arteriosus, bulbus cordis, primitive ventricle, primitive atrium, and the sinus venosus. Initially, all venous blood flows into the sinus venosus, and contractions propel the blood from tail to head, or from the sinus venosus to the truncus arteriosus. This is a very different pattern from that of an adult. Figure 19.36 Development of the Human Heart This diagram outlines the embryological development of the human heart during the first eight weeks and the subsequent formation of the four heart chambers. The five regions of the primitive heart tube develop into recognizable structures in a fully developed heart. The truncus arteriosus will eventually divide and give rise to the ascending aorta and pulmonary trunk. The bulbus cordis develops into the right ventricle. The primitive ventricle forms the left ventricle. The primitive atrium becomes the anterior portions of both the right and left atria, and the two auricles. The sinus venosus develops into the posterior portion of the right atrium, the SA node, and the coronary sinus. As the primitive heart tube elongates, it begins to fold within the pericardium, eventually forming an S shape, which places the chambers and major vessels into an alignment similar to the adult heart. This process occurs between days 23 and 28. The remainder of the heart development pattern includes development of septa and valves, and remodeling of the actual chambers. Partitioning of the atria and ventricles by the interatrial septum, interventricular septum, and atrioventricular septum is complete by the end of the fifth week, although the fetal blood shunts remain until birth or shortly after. The atrioventricular valves form between weeks five and eight, and the semilunar valves form between weeks five and nine. Key Terms - afterload - force the ventricles must develop to effectively pump blood against the resistance in the vessels - anastomosis - (plural = anastomoses) area where vessels unite to allow blood to circulate even if there may be partial blockage in another branch - anterior cardiac veins - vessels that parallel the small cardiac arteries and drain the anterior surface of the right ventricle; bypass the coronary sinus and drain directly into the right atrium - anterior interventricular artery - (also, left anterior descending artery or LAD) major branch of the left coronary artery that follows the anterior interventricular sulcus - anterior interventricular sulcus - sulcus located between the left and right ventricles on the anterior surface of the heart - aortic valve - (also, aortic semilunar valve) valve located at the base of the aorta - artificial pacemaker - medical device that transmits electrical signals to the heart to ensure that it contracts and pumps blood to the body - atrial reflex - (also, called Bainbridge reflex) autonomic reflex that responds to stretch receptors in the atria that send impulses to the cardioaccelerator area to increase HR when venous flow into the atria increases - atrioventricular (AV) node - clump of myocardial cells located in the inferior portion of the right atrium within the atrioventricular septum; receives the impulse from the SA node, pauses, and then transmits it into specialized conducting cells within the interventricular septum - atrioventricular bundle - (also, bundle of His) group of specialized myocardial conductile cells that transmit the impulse from the AV node through the interventricular septum; form the left and right atrioventricular bundle branches - atrioventricular bundle branches - (also, left or right bundle branches) specialized myocardial conductile cells that arise from the bifurcation of the atrioventricular bundle and pass through the interventricular septum; lead to the Purkinje fibers and also to the right papillary muscle via the moderator band - atrioventricular septum - cardiac septum located between the atria and ventricles; atrioventricular valves are located here - atrioventricular valves - one-way valves located between the atria and ventricles; the valve on the right is called the tricuspid valve, and the one on the left is the mitral or bicuspid valve - atrium - (plural = atria) upper or receiving chamber of the heart that pumps blood into the lower chambers just prior to their contraction; the right atrium receives blood from the systemic circuit that flows into the right ventricle; the left atrium receives blood from the pulmonary circuit that flows into the left ventricle - auricle - extension of an atrium visible on the superior surface of the heart - autonomic tone - contractile state during resting cardiac activity produced by mild sympathetic and parasympathetic stimulation - autorhythmicity - ability of cardiac muscle to initiate its own electrical impulse that triggers the mechanical contraction that pumps blood at a fixed pace without nervous or endocrine control - Bachmann’s bundle - (also, interatrial band) group of specialized conducting cells that transmit the impulse directly from the SA node in the right atrium to the left atrium - Bainbridge reflex - (also, called atrial reflex) autonomic reflex that responds to stretch receptors in the atria that send impulses to the cardioaccelerator area to increase HR when venous flow into the atria increases - baroreceptor reflex - autonomic reflex in which the cardiac centers monitor signals from the baroreceptor stretch receptors and regulate heart function based on blood flow - bicuspid valve - (also, mitral valve or left atrioventricular valve) valve located between the left atrium and ventricle; consists of two flaps of tissue - bulbus cordis - portion of the primitive heart tube that will eventually develop into the right ventricle - bundle of His - (also, atrioventricular bundle) group of specialized myocardial conductile cells that transmit the impulse from the AV node through the interventricular septum; form the left and right atrioventricular bundle branches - cardiac cycle - period of time between the onset of atrial contraction (atrial systole) and ventricular relaxation (ventricular diastole) - cardiac notch - depression in the medial surface of the inferior lobe of the left lung where the apex of the heart is located - cardiac output (CO) - amount of blood pumped by each ventricle during one minute; equals HR multiplied by SV - cardiac plexus - paired complex network of nerve fibers near the base of the heart that receive sympathetic and parasympathetic stimulations to regulate HR - cardiac reflexes - series of autonomic reflexes that enable the cardiovascular centers to regulate heart function based upon sensory information from a variety of visceral sensors - cardiac reserve - difference between maximum and resting CO - cardiac skeleton - (also, skeleton of the heart) reinforced connective tissue located within the atrioventricular septum; includes four rings that surround the openings between the atria and ventricles, and the openings to the pulmonary trunk and aorta; the point of attachment for the heart valves - cardiogenic area - area near the head of the embryo where the heart begins to develop 18–19 days after fertilization - cardiogenic cords - two strands of tissue that form within the cardiogenic area - cardiomyocyte - muscle cell of the heart - chordae tendineae - string-like extensions of tough connective tissue that extend from the flaps of the atrioventricular valves to the papillary muscles - circumflex artery - branch of the left coronary artery that follows coronary sulcus - coronary arteries - branches of the ascending aorta that supply blood to the heart; the left coronary artery feeds the left side of the heart, the left atrium and ventricle, and the interventricular septum; the right coronary artery feeds the right atrium, portions of both ventricles, and the heart conduction system - coronary sinus - large, thin-walled vein on the posterior surface of the heart that lies within the atrioventricular sulcus and drains the heart myocardium directly into the right atrium - coronary sulcus - sulcus that marks the boundary between the atria and ventricles - coronary veins - vessels that drain the heart and generally parallel the large surface arteries - diastole - period of time when the heart muscle is relaxed and the chambers fill with blood - ejection fraction - portion of the blood that is pumped or ejected from the heart with each contraction; mathematically represented by SV divided by EDV - electrocardiogram (ECG) - surface recording of the electrical activity of the heart that can be used for diagnosis of irregular heart function; also abbreviated as EKG - end diastolic volume (EDV) - (also, preload) the amount of blood in the ventricles at the end of atrial systole just prior to ventricular contraction - end systolic volume (ESV) - amount of blood remaining in each ventricle following systole - endocardial tubes - stage in which lumens form within the expanding cardiogenic cords, forming hollow structures - endocardium - innermost layer of the heart lining the heart chambers and heart valves; composed of endothelium reinforced with a thin layer of connective tissue that binds to the myocardium - endothelium - layer of smooth, simple squamous epithelium that lines the endocardium and blood vessels - epicardial coronary arteries - surface arteries of the heart that generally follow the sulci - epicardium - innermost layer of the serous pericardium and the outermost layer of the heart wall - filling time - duration of ventricular diastole during which filling occurs - foramen ovale - opening in the fetal heart that allows blood to flow directly from the right atrium to the left atrium, bypassing the fetal pulmonary circuit - fossa ovalis - oval-shaped depression in the interatrial septum that marks the former location of the foramen ovale - Frank-Starling mechanism - relationship between ventricular stretch and contraction in which the force of heart contraction is directly proportional to the initial length of the muscle fiber - great cardiac vein - vessel that follows the interventricular sulcus on the anterior surface of the heart and flows along the coronary sulcus into the coronary sinus on the posterior surface; parallels the anterior interventricular artery and drains the areas supplied by this vessel - heart block - interruption in the normal conduction pathway - heart bulge - prominent feature on the anterior surface of the heart, reflecting early cardiac development - heart rate (HR) - number of times the heart contracts (beats) per minute - heart sounds - sounds heard via auscultation with a stethoscope of the closing of the atrioventricular valves (“lub”) and semilunar valves (“dub”) - hypertrophic cardiomyopathy - pathological enlargement of the heart, generally for no known reason - inferior vena cava - large systemic vein that returns blood to the heart from the inferior portion of the body - interatrial band - (also, Bachmann’s bundle) group of specialized conducting cells that transmit the impulse directly from the SA node in the right atrium to the left atrium - interatrial septum - cardiac septum located between the two atria; contains the fossa ovalis after birth - intercalated disc - physical junction between adjacent cardiac muscle cells; consisting of desmosomes, specialized linking proteoglycans, and gap junctions that allow passage of ions between the two cells - internodal pathways - specialized conductile cells within the atria that transmit the impulse from the SA node throughout the myocardial cells of the atrium and to the AV node - interventricular septum - cardiac septum located between the two ventricles - isovolumic contraction - (also, isovolumetric contraction) initial phase of ventricular contraction in which tension and pressure in the ventricle increase, but no blood is pumped or ejected from the heart - isovolumic ventricular relaxation phase - initial phase of the ventricular diastole when pressure in the ventricles drops below pressure in the two major arteries, the pulmonary trunk, and the aorta, and blood attempts to flow back into the ventricles, producing the dicrotic notch of the ECG and closing the two semilunar valves - left atrioventricular valve - (also, mitral valve or bicuspid valve) valve located between the left atrium and ventricle; consists of two flaps of tissue - marginal arteries - branches of the right coronary artery that supply blood to the superficial portions of the right ventricle - mesoderm - one of the three primary germ layers that differentiate early in embryonic development - mesothelium - simple squamous epithelial portion of serous membranes, such as the superficial portion of the epicardium (the visceral pericardium) and the deepest portion of the pericardium (the parietal pericardium) - middle cardiac vein - vessel that parallels and drains the areas supplied by the posterior interventricular artery; drains into the great cardiac vein - mitral valve - (also, left atrioventricular valve or bicuspid valve) valve located between the left atrium and ventricle; consists of two flaps of tissue - moderator band - band of myocardium covered by endocardium that arises from the inferior portion of the interventricular septum in the right ventricle and crosses to the anterior papillary muscle; contains conductile fibers that carry electrical signals followed by contraction of the heart - murmur - unusual heart sound detected by auscultation; typically related to septal or valve defects - myocardial conducting cells - specialized cells that transmit electrical impulses throughout the heart and trigger contraction by the myocardial contractile cells - myocardial contractile cells - bulk of the cardiac muscle cells in the atria and ventricles that conduct impulses and contract to propel blood - myocardium - thickest layer of the heart composed of cardiac muscle cells built upon a framework of primarily collagenous fibers and blood vessels that supply it and the nervous fibers that help to regulate it - negative inotropic factors - factors that negatively impact or lower heart contractility - P wave - component of the electrocardiogram that represents the depolarization of the atria - pacemaker - cluster of specialized myocardial cells known as the SA node that initiates the sinus rhythm - papillary muscle - extension of the myocardium in the ventricles to which the chordae tendineae attach - pectinate muscles - muscular ridges seen on the anterior surface of the right atrium - pericardial cavity - cavity surrounding the heart filled with a lubricating serous fluid that reduces friction as the heart contracts - pericardial sac - (also, pericardium) membrane that separates the heart from other mediastinal structures; consists of two distinct, fused sublayers: the fibrous pericardium and the parietal pericardium - pericardium - (also, pericardial sac) membrane that separates the heart from other mediastinal structures; consists of two distinct, fused sublayers: the fibrous pericardium and the parietal pericardium - positive inotropic factors - factors that positively impact or increase heart contractility - posterior cardiac vein - vessel that parallels and drains the areas supplied by the marginal artery branch of the circumflex artery; drains into the great cardiac vein - posterior interventricular artery - (also, posterior descending artery) branch of the right coronary artery that runs along the posterior portion of the interventricular sulcus toward the apex of the heart and gives rise to branches that supply the interventricular septum and portions of both ventricles - posterior interventricular sulcus - sulcus located between the left and right ventricles on the anterior surface of the heart - preload - (also, end diastolic volume) amount of blood in the ventricles at the end of atrial systole just prior to ventricular contraction - prepotential depolarization - (also, spontaneous depolarization) mechanism that accounts for the autorhythmic property of cardiac muscle; the membrane potential increases as sodium ions diffuse through the always-open sodium ion channels and causes the electrical potential to rise - primitive atrium - portion of the primitive heart tube that eventually becomes the anterior portions of both the right and left atria, and the two auricles - primitive heart tube - singular tubular structure that forms from the fusion of the two endocardial tubes - primitive ventricle - portion of the primitive heart tube that eventually forms the left ventricle - pulmonary arteries - left and right branches of the pulmonary trunk that carry deoxygenated blood from the heart to each of the lungs - pulmonary capillaries - capillaries surrounding the alveoli of the lungs where gas exchange occurs: carbon dioxide exits the blood and oxygen enters - pulmonary circuit - blood flow to and from the lungs - pulmonary trunk - large arterial vessel that carries blood ejected from the right ventricle; divides into the left and right pulmonary arteries - pulmonary valve - (also, pulmonary semilunar valve, the pulmonic valve, or the right semilunar valve) valve at the base of the pulmonary trunk that prevents backflow of blood into the right ventricle; consists of three flaps - pulmonary veins - veins that carry highly oxygenated blood into the left atrium, which pumps the blood into the left ventricle, which in turn pumps oxygenated blood into the aorta and to the many branches of the systemic circuit - Purkinje fibers - specialized myocardial conduction fibers that arise from the bundle branches and spread the impulse to the myocardial contraction fibers of the ventricles - QRS complex - component of the electrocardiogram that represents the depolarization of the ventricles and includes, as a component, the repolarization of the atria - right atrioventricular valve - (also, tricuspid valve) valve located between the right atrium and ventricle; consists of three flaps of tissue - semilunar valves - valves located at the base of the pulmonary trunk and at the base of the aorta - septum - (plural = septa) walls or partitions that divide the heart into chambers - septum primum - flap of tissue in the fetus that covers the foramen ovale within a few seconds after birth - sinoatrial (SA) node - known as the pacemaker, a specialized clump of myocardial conducting cells located in the superior portion of the right atrium that has the highest inherent rate of depolarization that then spreads throughout the heart - sinus rhythm - normal contractile pattern of the heart - sinus venosus - develops into the posterior portion of the right atrium, the SA node, and the coronary sinus - small cardiac vein - parallels the right coronary artery and drains blood from the posterior surfaces of the right atrium and ventricle; drains into the great cardiac vein - spontaneous depolarization - (also, prepotential depolarization) the mechanism that accounts for the autorhythmic property of cardiac muscle; the membrane potential increases as sodium ions diffuse through the always-open sodium ion channels and causes the electrical potential to rise - stroke volume (SV) - amount of blood pumped by each ventricle per contraction; also, the difference between EDV and ESV - sulcus - (plural = sulci) fat-filled groove visible on the surface of the heart; coronary vessels are also located in these areas - superior vena cava - large systemic vein that returns blood to the heart from the superior portion of the body - systemic circuit - blood flow to and from virtually all of the tissues of the body - systole - period of time when the heart muscle is contracting - T wave - component of the electrocardiogram that represents the repolarization of the ventricles - target heart rate - range in which both the heart and lungs receive the maximum benefit from an aerobic workout - trabeculae carneae - ridges of muscle covered by endocardium located in the ventricles - tricuspid valve - term used most often in clinical settings for the right atrioventricular valve - truncus arteriosus - portion of the primitive heart that will eventually divide and give rise to the ascending aorta and pulmonary trunk - valve - in the cardiovascular system, a specialized structure located within the heart or vessels that ensures one-way flow of blood - ventricle - one of the primary pumping chambers of the heart located in the lower portion of the heart; the left ventricle is the major pumping chamber on the lower left side of the heart that ejects blood into the systemic circuit via the aorta and receives blood from the left atrium; the right ventricle is the major pumping chamber on the lower right side of the heart that ejects blood into the pulmonary circuit via the pulmonary trunk and receives blood from the right atrium - ventricular ejection phase - second phase of ventricular systole during which blood is pumped from the ventricle Chapter Review 19.1 Heart Anatomy The heart resides within the pericardial sac and is located in the mediastinal space within the thoracic cavity. The pericardial sac consists of two fused layers: an outer fibrous capsule and an inner parietal pericardium lined with a serous membrane. Between the pericardial sac and the heart is the pericardial cavity, which is filled with lubricating serous fluid. The walls of the heart are composed of an outer epicardium, a thick myocardium, and an inner lining layer of endocardium. The human heart consists of a pair of atria, which receive blood and pump it into a pair of ventricles, which pump blood into the vessels. The right atrium receives systemic blood relatively low in oxygen and pumps it into the right ventricle, which pumps it into the pulmonary circuit. Exchange of oxygen and carbon dioxide occurs in the lungs, and blood high in oxygen returns to the left atrium, which pumps blood into the left ventricle, which in turn pumps blood into the aorta and the remainder of the systemic circuit. The septa are the partitions that separate the chambers of the heart. They include the interatrial septum, the interventricular septum, and the atrioventricular septum. Two of these openings are guarded by the atrioventricular valves, the right tricuspid valve and the left mitral valve, which prevent the backflow of blood. Each is attached to chordae tendineae that extend to the papillary muscles, which are extensions of the myocardium, to prevent the valves from being blown back into the atria. The pulmonary valve is located at the base of the pulmonary trunk, and the left semilunar valve is located at the base of the aorta. The right and left coronary arteries are the first to branch off the aorta and arise from two of the three sinuses located near the base of the aorta and are generally located in the sulci. Cardiac veins parallel the small cardiac arteries and generally drain into the coronary sinus. 19.2 Cardiac Muscle and Electrical Activity The heart is regulated by both neural and endocrine control, yet it is capable of initiating its own action potential followed by muscular contraction. The conductive cells within the heart establish the heart rate and transmit it through the myocardium. The contractile cells contract and propel the blood. The normal path of transmission for the conductive cells is the sinoatrial (SA) node, internodal pathways, atrioventricular (AV) node, atrioventricular (AV) bundle of His, bundle branches, and Purkinje fibers. The action potential for the conductive cells consists of a prepotential phase with a slow influx of Na+ followed by a rapid influx of Ca2+ and outflux of K+. Contractile cells have an action potential with an extended plateau phase that results in an extended refractory period to allow complete contraction for the heart to pump blood effectively. Recognizable points on the ECG include the P wave that corresponds to atrial depolarization, the QRS complex that corresponds to ventricular depolarization, and the T wave that corresponds to ventricular repolarization. 19.3 Cardiac Cycle The cardiac cycle comprises a complete relaxation and contraction of both the atria and ventricles, and lasts approximately 0.8 seconds. Beginning with all chambers in diastole, blood flows passively from the veins into the atria and past the atrioventricular valves into the ventricles. The atria begin to contract (atrial systole), following depolarization of the atria, and pump blood into the ventricles. The ventricles begin to contract (ventricular systole), raising pressure within the ventricles. When ventricular pressure rises above the pressure in the atria, blood flows toward the atria, producing the first heart sound, S1 or lub. As pressure in the ventricles rises above two major arteries, blood pushes open the two semilunar valves and moves into the pulmonary trunk and aorta in the ventricular ejection phase. Following ventricular repolarization, the ventricles begin to relax (ventricular diastole), and pressure within the ventricles drops. As ventricular pressure drops, there is a tendency for blood to flow back into the atria from the major arteries, producing the dicrotic notch in the ECG and closing the two semilunar valves. The second heart sound, S2 or dub, occurs when the semilunar valves close. When the pressure falls below that of the atria, blood moves from the atria into the ventricles, opening the atrioventricular valves and marking one complete heart cycle. The valves prevent backflow of blood. Failure of the valves to operate properly produces turbulent blood flow within the heart; the resulting heart murmur can often be heard with a stethoscope. 19.4 Cardiac Physiology Many factors affect HR and SV, and together, they contribute to cardiac function. HR is largely determined and regulated by autonomic stimulation and hormones. There are several feedback loops that contribute to maintaining homeostasis dependent upon activity levels, such as the atrial reflex, which is determined by venous return. SV is regulated by autonomic innervation and hormones, but also by filling time and venous return. Venous return is determined by activity of the skeletal muscles, blood volume, and changes in peripheral circulation. Venous return determines preload and the atrial reflex. Filling time directly related to HR also determines preload. Preload then impacts both EDV and ESV. Autonomic innervation and hormones largely regulate contractility. Contractility impacts EDV as does afterload. CO is the product of HR multiplied by SV. SV is the difference between EDV and ESV. 19.5 Development of the Heart The heart is the first organ to form and become functional, emphasizing the importance of transport of material to and from the developing infant. It originates about day 18 or 19 from the mesoderm and begins beating and pumping blood about day 21 or 22. It forms from the cardiogenic region near the head and is visible as a prominent heart bulge on the surface of the embryo. Originally, it consists of a pair of strands called cardiogenic cords that quickly form a hollow lumen and are referred to as endocardial tubes. These then fuse into a single heart tube and differentiate into the truncus arteriosus, bulbus cordis, primitive ventricle, primitive atrium, and sinus venosus, starting about day 22. The primitive heart begins to form an S shape within the pericardium between days 23 and 28. The internal septa begin to form about day 28, separating the heart into the atria and ventricles, although the foramen ovale persists until shortly after birth. Between weeks five and eight, the atrioventricular valves form. The semilunar valves form between weeks five and nine. Interactive Link Questions 1. Visit this site to observe an echocardiogram of actual heart valves opening and closing. Although much of the heart has been “removed” from this gif loop so the chordae tendineae are not visible, why is their presence more critical for the atrioventricular valves (tricuspid and mitral) than the semilunar (aortic and pulmonary) valves? Review Questions Which of the following is not important in preventing backflow of blood? - chordae tendineae - papillary muscles - AV valves - endocardium Which valve separates the left atrium from the left ventricle? - mitral - tricuspid - pulmonary - aortic Which of the following lists the valves in the order through which the blood flows from the vena cava through the heart? - tricuspid, pulmonary semilunar, bicuspid, aortic semilunar - mitral, pulmonary semilunar, bicuspid, aortic semilunar - aortic semilunar, pulmonary semilunar, tricuspid, bicuspid - bicuspid, aortic semilunar, tricuspid, pulmonary semilunar Which chamber initially receives blood from the systemic circuit? - left atrium - left ventricle - right atrium - right ventricle The ________ layer secretes chemicals that help to regulate ionic environments and strength of contraction and serve as powerful vasoconstrictors. - pericardial sac - endocardium - myocardium - epicardium The myocardium would be the thickest in the ________. - left atrium - left ventricle - right atrium - right ventricle In which septum is it normal to find openings in the adult? - interatrial septum - interventricular septum - atrioventricular septum - all of the above Which of the following is unique to cardiac muscle cells? - Only cardiac muscle contains a sarcoplasmic reticulum. - Only cardiac muscle has gap junctions. - Only cardiac muscle is capable of autorhythmicity - Only cardiac muscle has a high concentration of mitochondria. The influx of which ion accounts for the plateau phase? - sodium - potassium - chloride - calcium Which portion of the ECG corresponds to repolarization of the atria? - P wave - QRS complex - T wave - none of the above: atrial repolarization is masked by ventricular depolarization Which component of the heart conduction system would have the slowest rate of firing? - atrioventricular node - atrioventricular bundle - bundle branches - Purkinje fibers The cardiac cycle consists of a distinct relaxation and contraction phase. Which term is typically used to refer ventricular contraction while no blood is being ejected? - systole - diastole - quiescent - isovolumic contraction Most blood enters the ventricle during ________. - atrial systole - atrial diastole - ventricular systole - isovolumic contraction The first heart sound represents which portion of the cardiac cycle? - atrial systole - ventricular systole - closing of the atrioventricular valves - closing of the semilunar valves Ventricular relaxation immediately follows ________. - atrial depolarization - ventricular repolarization - ventricular depolarization - atrial repolarization The force the heart must overcome to pump blood is known as ________. - preload - afterload - cardiac output - stroke volume The cardiovascular centers are located in which area of the brain? - medulla oblongata - pons - mesencephalon (midbrain) - cerebrum In a healthy young adult, what happens to cardiac output when heart rate increases above 160 bpm? - It increases. - It decreases. - It remains constant. - There is no way to predict. What happens to preload when there is venous constriction in the veins? - It increases. - It decreases. - It remains constant. - There is no way to predict. Which of the following is a positive inotrope? - Na+ - K+ - Ca2+ - both Na+ and K+ The earliest organ to form and begin function within the developing human is the ________. - brain - stomach - lungs - heart Of the three germ layers that give rise to all adult tissues and organs, which gives rise to the heart? - ectoderm - endoderm - mesoderm - placenta The two tubes that eventually fuse to form the heart are referred to as the ________. - primitive heart tubes - endocardial tubes - cardiogenic region - cardiogenic tubes Which primitive area of the heart will give rise to the right ventricle? - bulbus cordis - primitive ventricle - sinus venosus - truncus arteriosus The pulmonary trunk and aorta are derived from which primitive heart structure? - bulbus cordis - primitive ventricle - sinus venosus - truncus arteriosus Critical Thinking Questions Describe how the valves keep the blood moving in one direction. 28.Why is the pressure in the pulmonary circulation lower than in the systemic circulation? 29.Why is the plateau phase so critical to cardiac muscle function? 30.How does the delay of the impulse at the atrioventricular node contribute to cardiac function? 31.How do gap junctions and intercalated disks aid contraction of the heart? 32.Why do the cardiac muscles cells demonstrate autorhythmicity? 33.Describe one cardiac cycle, beginning with both atria and ventricles relaxed. 34.Why does increasing EDV increase contractility? 35.Why is afterload important to cardiac function? 36.Why is it so important for the human heart to develop early and begin functioning within the developing embryo? 37.Describe how the major pumping chambers, the ventricles, form within the developing heart.	oercommons	2025-03-18T00:37:00.905991	null	{ "license": "Creative Commons - Attribution - https://creativecommons.org/licenses/by/4.0/", "url": "https://oercommons.org/courseware/lesson/58765/overview", "title": "Anatomy and Physiology, Fluids and Transport", "author": null }
https://oercommons.org/courseware/lesson/58766/overview	The Cardiovascular System: Blood Vessels and Circulation Introduction Figure 20.1 Blood Vessels While most blood vessels are located deep from the surface and are not visible, the superficial veins of the upper limb provide an indication of the extent, prominence, and importance of these structures to the body. (credit: Colin Davis) CHAPTER OBJECTIVES After studying this chapter, you will be able to: - Compare and contrast the anatomical structure of arteries, arterioles, capillaries, venules, and veins - Accurately describe the forces that account for capillary exchange - List the major factors affecting blood flow, blood pressure, and resistance - Describe how blood flow, blood pressure, and resistance interrelate - Discuss how the neural and endocrine mechanisms maintain homeostasis within the blood vessels - Describe the interaction of the cardiovascular system with other body systems - Label the major blood vessels of the pulmonary and systemic circulations - Identify and describe the hepatic portal system - Describe the development of blood vessels and fetal circulation - Compare fetal circulation to that of an individual after birth In this chapter, you will learn about the vascular part of the cardiovascular system, that is, the vessels that transport blood throughout the body and provide the physical site where gases, nutrients, and other substances are exchanged with body cells. When vessel functioning is reduced, blood-borne substances do not circulate effectively throughout the body. As a result, tissue injury occurs, metabolism is impaired, and the functions of every bodily system are threatened. Structure and Function of Blood Vessels - Compare and contrast the three tunics that make up the walls of most blood vessels Distinguish between elastic arteries, muscular arteries, and arterioles on the basis of structure, location, and function - Describe the basic structure of a capillary bed, from the supplying metarteriole to the venule into which it drains - Explain the structure and function of venous valves in the large veins of the extremities Blood is carried through the body via blood vessels. An artery is a blood vessel that carries blood away from the heart, where it branches into ever-smaller vessels. Eventually, the smallest arteries, vessels called arterioles, further branch into tiny capillaries, where nutrients and wastes are exchanged, and then combine with other vessels that exit capillaries to form venules, small blood vessels that carry blood to a vein, a larger blood vessel that returns blood to the heart. Arteries and veins transport blood in two distinct circuits: the systemic circuit and the pulmonary circuit (Figure 20.2). Systemic arteries provide blood rich in oxygen to the body’s tissues. The blood returned to the heart through systemic veins has less oxygen, since much of the oxygen carried by the arteries has been delivered to the cells. In contrast, in the pulmonary circuit, arteries carry blood low in oxygen exclusively to the lungs for gas exchange. Pulmonary veins then return freshly oxygenated blood from the lungs to the heart to be pumped back out into systemic circulation. Although arteries and veins differ structurally and functionally, they share certain features. Figure 20.2 Cardiovascular Circulation The pulmonary circuit moves blood from the right side of the heart to the lungs and back to the heart. The systemic circuit moves blood from the left side of the heart to the head and body and returns it to the right side of the heart to repeat the cycle. The arrows indicate the direction of blood flow, and the colors show the relative levels of oxygen concentration. Shared Structures Different types of blood vessels vary slightly in their structures, but they share the same general features. Arteries and arterioles have thicker walls than veins and venules because they are closer to the heart and receive blood that is surging at a far greater pressure (Figure 20.3). Each type of vessel has a lumen—a hollow passageway through which blood flows. Arteries have smaller lumens than veins, a characteristic that helps to maintain the pressure of blood moving through the system. Together, their thicker walls and smaller diameters give arterial lumens a more rounded appearance in cross section than the lumens of veins. Figure 20.3 Structure of Blood Vessels (a) Arteries and (b) veins share the same general features, but the walls of arteries are much thicker because of the higher pressure of the blood that flows through them. (c) A micrograph shows the relative differences in thickness. LM × 160. (Micrograph provided by the Regents of the University of Michigan Medical School © 2012) By the time blood has passed through capillaries and entered venules, the pressure initially exerted upon it by heart contractions has diminished. In other words, in comparison to arteries, venules and veins withstand a much lower pressure from the blood that flows through them. Their walls are considerably thinner and their lumens are correspondingly larger in diameter, allowing more blood to flow with less vessel resistance. In addition, many veins of the body, particularly those of the limbs, contain valves that assist the unidirectional flow of blood toward the heart. This is critical because blood flow becomes sluggish in the extremities, as a result of the lower pressure and the effects of gravity. The walls of arteries and veins are largely composed of living cells and their products (including collagenous and elastic fibers); the cells require nourishment and produce waste. Since blood passes through the larger vessels relatively quickly, there is limited opportunity for blood in the lumen of the vessel to provide nourishment to or remove waste from the vessel’s cells. Further, the walls of the larger vessels are too thick for nutrients to diffuse through to all of the cells. Larger arteries and veins contain small blood vessels within their walls known as the vasa vasorum—literally “vessels of the vessel”—to provide them with this critical exchange. Since the pressure within arteries is relatively high, the vasa vasorum must function in the outer layers of the vessel (see Figure 20.3) or the pressure exerted by the blood passing through the vessel would collapse it, preventing any exchange from occurring. The lower pressure within veins allows the vasa vasorum to be located closer to the lumen. The restriction of the vasa vasorum to the outer layers of arteries is thought to be one reason that arterial diseases are more common than venous diseases, since its location makes it more difficult to nourish the cells of the arteries and remove waste products. There are also minute nerves within the walls of both types of vessels that control the contraction and dilation of smooth muscle. These minute nerves are known as the nervi vasorum. Both arteries and veins have the same three distinct tissue layers, called tunics (from the Latin term tunica), for the garments first worn by ancient Romans; the term tunic is also used for some modern garments. From the most interior layer to the outer, these tunics are the tunica intima, the tunica media, and the tunica externa (see Figure 20.3). Table 20.1 compares and contrasts the tunics of the arteries and veins. Comparison of Tunics in Arteries and Veins \| Arteries \| Veins \| \| \|---\|---\|---\| \| General appearance \| Thick walls with small lumens Generally appear rounded \| Thin walls with large lumens Generally appear flattened \| \| Tunica intima \| Endothelium usually appears wavy due to constriction of smooth muscle Internal elastic membrane present in larger vessels \| Endothelium appears smooth Internal elastic membrane absent \| \| Tunica media \| Normally the thickest layer in arteries Smooth muscle cells and elastic fibers predominate (the proportions of these vary with distance from the heart) External elastic membrane present in larger vessels \| Normally thinner than the tunica externa Smooth muscle cells and collagenous fibers predominate Nervi vasorum and vasa vasorum present External elastic membrane absent \| \| Tunica externa \| Normally thinner than the tunica media in all but the largest arteries Collagenous and elastic fibers Nervi vasorum and vasa vasorum present \| Normally the thickest layer in veins Collagenous and smooth fibers predominate Some smooth muscle fibers Nervi vasorum and vasa vasorum present \| Table 20.1 Tunica Intima The tunica intima (also called the tunica interna) is composed of epithelial and connective tissue layers. Lining the tunica intima is the specialized simple squamous epithelium called the endothelium, which is continuous throughout the entire vascular system, including the lining of the chambers of the heart. Damage to this endothelial lining and exposure of blood to the collagenous fibers beneath is one of the primary causes of clot formation. Until recently, the endothelium was viewed simply as the boundary between the blood in the lumen and the walls of the vessels. Recent studies, however, have shown that it is physiologically critical to such activities as helping to regulate capillary exchange and altering blood flow. The endothelium releases local chemicals called endothelins that can constrict the smooth muscle within the walls of the vessel to increase blood pressure. Uncompensated overproduction of endothelins may contribute to hypertension (high blood pressure) and cardiovascular disease. Next to the endothelium is the basement membrane, or basal lamina, that effectively binds the endothelium to the connective tissue. The basement membrane provides strength while maintaining flexibility, and it is permeable, allowing materials to pass through it. The thin outer layer of the tunica intima contains a small amount of areolar connective tissue that consists primarily of elastic fibers to provide the vessel with additional flexibility; it also contains some collagenous fibers to provide additional strength. In larger arteries, there is also a thick, distinct layer of elastic fibers known as the internal elastic membrane (also called the internal elastic lamina) at the boundary with the tunica media. Like the other components of the tunica intima, the internal elastic membrane provides structure while allowing the vessel to stretch. It is permeated with small openings that allow exchange of materials between the tunics. The internal elastic membrane is not apparent in veins. In addition, many veins, particularly in the lower limbs, contain valves formed by sections of thickened endothelium that are reinforced with connective tissue, extending into the lumen. Under the microscope, the lumen and the entire tunica intima of a vein will appear smooth, whereas those of an artery will normally appear wavy because of the partial constriction of the smooth muscle in the tunica media, the next layer of blood vessel walls. Tunica Media The tunica media is the substantial middle layer of the vessel wall (see Figure 20.3). It is generally the thickest layer in arteries, and it is much thicker in arteries than it is in veins. The tunica media consists of layers of smooth muscle supported by connective tissue that is primarily made up of elastic fibers, most of which are arranged in circular sheets. Toward the outer portion of the tunic, there are also layers of longitudinal muscle. Contraction and relaxation of the circular muscles decrease and increase the diameter of the vessel lumen, respectively. Specifically in arteries, vasoconstriction decreases blood flow as the smooth muscle in the walls of the tunica media contracts, making the lumen narrower and increasing blood pressure. Similarly, vasodilation increases blood flow as the smooth muscle relaxes, allowing the lumen to widen and blood pressure to drop. Both vasoconstriction and vasodilation are regulated in part by small vascular nerves, known as nervi vasorum, or “nerves of the vessel,” that run within the walls of blood vessels. These are generally all sympathetic fibers, although some trigger vasodilation and others induce vasoconstriction, depending upon the nature of the neurotransmitter and receptors located on the target cell. Parasympathetic stimulation does trigger vasodilation as well as erection during sexual arousal in the external genitalia of both sexes. Nervous control over vessels tends to be more generalized than the specific targeting of individual blood vessels. Local controls, discussed later, account for this phenomenon. (Seek additional content for more information on these dynamic aspects of the autonomic nervous system.) Hormones and local chemicals also control blood vessels. Together, these neural and chemical mechanisms reduce or increase blood flow in response to changing body conditions, from exercise to hydration. Regulation of both blood flow and blood pressure is discussed in detail later in this chapter. The smooth muscle layers of the tunica media are supported by a framework of collagenous fibers that also binds the tunica media to the inner and outer tunics. Along with the collagenous fibers are large numbers of elastic fibers that appear as wavy lines in prepared slides. Separating the tunica media from the outer tunica externa in larger arteries is the external elastic membrane (also called the external elastic lamina), which also appears wavy in slides. This structure is not usually seen in smaller arteries, nor is it seen in veins. Tunica Externa The outer tunic, the tunica externa (also called the tunica adventitia), is a substantial sheath of connective tissue composed primarily of collagenous fibers. Some bands of elastic fibers are found here as well. The tunica externa in veins also contains groups of smooth muscle fibers. This is normally the thickest tunic in veins and may be thicker than the tunica media in some larger arteries. The outer layers of the tunica externa are not distinct but rather blend with the surrounding connective tissue outside the vessel, helping to hold the vessel in relative position. If you are able to palpate some of the superficial veins on your upper limbs and try to move them, you will find that the tunica externa prevents this. If the tunica externa did not hold the vessel in place, any movement would likely result in disruption of blood flow. Arteries An artery is a blood vessel that conducts blood away from the heart. All arteries have relatively thick walls that can withstand the high pressure of blood ejected from the heart. However, those close to the heart have the thickest walls, containing a high percentage of elastic fibers in all three of their tunics. This type of artery is known as an elastic artery (Figure 20.4). Vessels larger than 10 mm in diameter are typically elastic. Their abundant elastic fibers allow them to expand, as blood pumped from the ventricles passes through them, and then to recoil after the surge has passed. If artery walls were rigid and unable to expand and recoil, their resistance to blood flow would greatly increase and blood pressure would rise to even higher levels, which would in turn require the heart to pump harder to increase the volume of blood expelled by each pump (the stroke volume) and maintain adequate pressure and flow. Artery walls would have to become even thicker in response to this increased pressure. The elastic recoil of the vascular wall helps to maintain the pressure gradient that drives the blood through the arterial system. An elastic artery is also known as a conducting artery, because the large diameter of the lumen enables it to accept a large volume of blood from the heart and conduct it to smaller branches. Figure 20.4 Types of Arteries and Arterioles Comparison of the walls of an elastic artery, a muscular artery, and an arteriole is shown. In terms of scale, the diameter of an arteriole is measured in micrometers compared to millimeters for elastic and muscular arteries. Farther from the heart, where the surge of blood has dampened, the percentage of elastic fibers in an artery’s tunica intima decreases and the amount of smooth muscle in its tunica media increases. The artery at this point is described as a muscular artery. The diameter of muscular arteries typically ranges from 0.1 mm to 10 mm. Their thick tunica media allows muscular arteries to play a leading role in vasoconstriction. In contrast, their decreased quantity of elastic fibers limits their ability to expand. Fortunately, because the blood pressure has eased by the time it reaches these more distant vessels, elasticity has become less important. Notice that although the distinctions between elastic and muscular arteries are important, there is no “line of demarcation” where an elastic artery suddenly becomes muscular. Rather, there is a gradual transition as the vascular tree repeatedly branches. In turn, muscular arteries branch to distribute blood to the vast network of arterioles. For this reason, a muscular artery is also known as a distributing artery. Arterioles An arteriole is a very small artery that leads to a capillary. Arterioles have the same three tunics as the larger vessels, but the thickness of each is greatly diminished. The critical endothelial lining of the tunica intima is intact. The tunica media is restricted to one or two smooth muscle cell layers in thickness. The tunica externa remains but is very thin (see Figure 20.4). With a lumen averaging 30 micrometers or less in diameter, arterioles are critical in slowing down—or resisting—blood flow and, thus, causing a substantial drop in blood pressure. Because of this, you may see them referred to as resistance vessels. The muscle fibers in arterioles are normally slightly contracted, causing arterioles to maintain a consistent muscle tone—in this case referred to as vascular tone—in a similar manner to the muscular tone of skeletal muscle. In reality, all blood vessels exhibit vascular tone due to the partial contraction of smooth muscle. The importance of the arterioles is that they will be the primary site of both resistance and regulation of blood pressure. The precise diameter of the lumen of an arteriole at any given moment is determined by neural and chemical controls, and vasoconstriction and vasodilation in the arterioles are the primary mechanisms for distribution of blood flow. Capillaries A capillary is a microscopic channel that supplies blood to the tissues themselves, a process called perfusion. Exchange of gases and other substances occurs in the capillaries between the blood and the surrounding cells and their tissue fluid (interstitial fluid). The diameter of a capillary lumen ranges from 5–10 micrometers; the smallest are just barely wide enough for an erythrocyte to squeeze through. Flow through capillaries is often described as microcirculation. The wall of a capillary consists of the endothelial layer surrounded by a basement membrane with occasional smooth muscle fibers. There is some variation in wall structure: In a large capillary, several endothelial cells bordering each other may line the lumen; in a small capillary, there may be only a single cell layer that wraps around to contact itself. For capillaries to function, their walls must be leaky, allowing substances to pass through. There are three major types of capillaries, which differ according to their degree of “leakiness:” continuous, fenestrated, and sinusoid capillaries (Figure 20.5). Continuous Capillaries The most common type of capillary, the continuous capillary, is found in almost all vascularized tissues. Continuous capillaries are characterized by a complete endothelial lining with tight junctions between endothelial cells. Although a tight junction is usually impermeable and only allows for the passage of water and ions, they are often incomplete in capillaries, leaving intercellular clefts that allow for exchange of water and other very small molecules between the blood plasma and the interstitial fluid. Substances that can pass between cells include metabolic products, such as glucose, water, and small hydrophobic molecules like gases and hormones, as well as various leukocytes. Continuous capillaries not associated with the brain are rich in transport vesicles, contributing to either endocytosis or exocytosis. Those in the brain are part of the blood-brain barrier. Here, there are tight junctions and no intercellular clefts, plus a thick basement membrane and astrocyte extensions called end feet; these structures combine to prevent the movement of nearly all substances. Figure 20.5 Types of Capillaries The three major types of capillaries: continuous, fenestrated, and sinusoid. Fenestrated Capillaries A fenestrated capillary is one that has pores (or fenestrations) in addition to tight junctions in the endothelial lining. These make the capillary permeable to larger molecules. The number of fenestrations and their degree of permeability vary, however, according to their location. Fenestrated capillaries are common in the small intestine, which is the primary site of nutrient absorption, as well as in the kidneys, which filter the blood. They are also found in the choroid plexus of the brain and many endocrine structures, including the hypothalamus, pituitary, pineal, and thyroid glands. Sinusoid Capillaries A sinusoid capillary (or sinusoid) is the least common type of capillary. Sinusoid capillaries are flattened, and they have extensive intercellular gaps and incomplete basement membranes, in addition to intercellular clefts and fenestrations. This gives them an appearance not unlike Swiss cheese. These very large openings allow for the passage of the largest molecules, including plasma proteins and even cells. Blood flow through sinusoids is very slow, allowing more time for exchange of gases, nutrients, and wastes. Sinusoids are found in the liver and spleen, bone marrow, lymph nodes (where they carry lymph, not blood), and many endocrine glands including the pituitary and adrenal glands. Without these specialized capillaries, these organs would not be able to provide their myriad of functions. For example, when bone marrow forms new blood cells, the cells must enter the blood supply and can only do so through the large openings of a sinusoid capillary; they cannot pass through the small openings of continuous or fenestrated capillaries. The liver also requires extensive specialized sinusoid capillaries in order to process the materials brought to it by the hepatic portal vein from both the digestive tract and spleen, and to release plasma proteins into circulation. Metarterioles and Capillary Beds A metarteriole is a type of vessel that has structural characteristics of both an arteriole and a capillary. Slightly larger than the typical capillary, the smooth muscle of the tunica media of the metarteriole is not continuous but forms rings of smooth muscle (sphincters) prior to the entrance to the capillaries. Each metarteriole arises from a terminal arteriole and branches to supply blood to a capillary bed that may consist of 10–100 capillaries. The precapillary sphincters, circular smooth muscle cells that surround the capillary at its origin with the metarteriole, tightly regulate the flow of blood from a metarteriole to the capillaries it supplies. Their function is critical: If all of the capillary beds in the body were to open simultaneously, they would collectively hold every drop of blood in the body and there would be none in the arteries, arterioles, venules, veins, or the heart itself. Normally, the precapillary sphincters are closed. When the surrounding tissues need oxygen and have excess waste products, the precapillary sphincters open, allowing blood to flow through and exchange to occur before closing once more (Figure 20.6). If all of the precapillary sphincters in a capillary bed are closed, blood will flow from the metarteriole directly into a thoroughfare channel and then into the venous circulation, bypassing the capillary bed entirely. This creates what is known as a vascular shunt. In addition, an arteriovenous anastomosis may bypass the capillary bed and lead directly to the venous system. Although you might expect blood flow through a capillary bed to be smooth, in reality, it moves with an irregular, pulsating flow. This pattern is called vasomotion and is regulated by chemical signals that are triggered in response to changes in internal conditions, such as oxygen, carbon dioxide, hydrogen ion, and lactic acid levels. For example, during strenuous exercise when oxygen levels decrease and carbon dioxide, hydrogen ion, and lactic acid levels all increase, the capillary beds in skeletal muscle are open, as they would be in the digestive system when nutrients are present in the digestive tract. During sleep or rest periods, vessels in both areas are largely closed; they open only occasionally to allow oxygen and nutrient supplies to travel to the tissues to maintain basic life processes. Figure 20.6 Capillary Bed In a capillary bed, arterioles give rise to metarterioles. Precapillary sphincters located at the junction of a metarteriole with a capillary regulate blood flow. A thoroughfare channel connects the metarteriole to a venule. An arteriovenous anastomosis, which directly connects the arteriole with the venule, is shown at the bottom. Venules A venule is an extremely small vein, generally 8–100 micrometers in diameter. Postcapillary venules join multiple capillaries exiting from a capillary bed. Multiple venules join to form veins. The walls of venules consist of endothelium, a thin middle layer with a few muscle cells and elastic fibers, plus an outer layer of connective tissue fibers that constitute a very thin tunica externa (Figure 20.7). Venules as well as capillaries are the primary sites of emigration or diapedesis, in which the white blood cells adhere to the endothelial lining of the vessels and then squeeze through adjacent cells to enter the tissue fluid. Veins A vein is a blood vessel that conducts blood toward the heart. Compared to arteries, veins are thin-walled vessels with large and irregular lumens (see Figure 20.7). Because they are low-pressure vessels, larger veins are commonly equipped with valves that promote the unidirectional flow of blood toward the heart and prevent backflow toward the capillaries caused by the inherent low blood pressure in veins as well as the pull of gravity. Table 20.2 compares the features of arteries and veins. Figure 20.7 Comparison of Veins and Venules Many veins have valves to prevent back flow of blood, whereas venules do not. In terms of scale, the diameter of a venule is measured in micrometers compared to millimeters for veins. Comparison of Arteries and Veins \| Arteries \| Veins \| \| \|---\|---\|---\| \| Direction of blood flow \| Conducts blood away from the heart \| Conducts blood toward the heart \| \| General appearance \| Rounded \| Irregular, often collapsed \| \| Pressure \| High \| Low \| \| Wall thickness \| Thick \| Thin \| \| Relative oxygen concentration \| Higher in systemic arteries Lower in pulmonary arteries \| Lower in systemic veins Higher in pulmonary veins \| \| Valves \| Not present \| Present most commonly in limbs and in veins inferior to the heart \| Table 20.2 DISORDERS OF THE... Cardiovascular System: Edema and Varicose Veins Despite the presence of valves and the contributions of other anatomical and physiological adaptations we will cover shortly, over the course of a day, some blood will inevitably pool, especially in the lower limbs, due to the pull of gravity. Any blood that accumulates in a vein will increase the pressure within it, which can then be reflected back into the smaller veins, venules, and eventually even the capillaries. Increased pressure will promote the flow of fluids out of the capillaries and into the interstitial fluid. The presence of excess tissue fluid around the cells leads to a condition called edema. Most people experience a daily accumulation of tissue fluid, especially if they spend much of their work life on their feet (like most health professionals). However, clinical edema goes beyond normal swelling and requires medical treatment. Edema has many potential causes, including hypertension and heart failure, severe protein deficiency, renal failure, and many others. In order to treat edema, which is a sign rather than a discrete disorder, the underlying cause must be diagnosed and alleviated. Figure 20.8 Varicose Veins Varicose veins are commonly found in the lower limbs. (credit: Thomas Kriese) Edema may be accompanied by varicose veins, especially in the superficial veins of the legs (Figure 20.8). This disorder arises when defective valves allow blood to accumulate within the veins, causing them to distend, twist, and become visible on the surface of the integument. Varicose veins may occur in both sexes, but are more common in women and are often related to pregnancy. More than simple cosmetic blemishes, varicose veins are often painful and sometimes itchy or throbbing. Without treatment, they tend to grow worse over time. The use of support hose, as well as elevating the feet and legs whenever possible, may be helpful in alleviating this condition. Laser surgery and interventional radiologic procedures can reduce the size and severity of varicose veins. Severe cases may require conventional surgery to remove the damaged vessels. As there are typically redundant circulation patterns, that is, anastomoses, for the smaller and more superficial veins, removal does not typically impair the circulation. There is evidence that patients with varicose veins suffer a greater risk of developing a thrombus or clot. Veins as Blood Reservoirs In addition to their primary function of returning blood to the heart, veins may be considered blood reservoirs, since systemic veins contain approximately 64 percent of the blood volume at any given time (Figure 20.9). Their ability to hold this much blood is due to their high capacitance, that is, their capacity to distend (expand) readily to store a high volume of blood, even at a low pressure. The large lumens and relatively thin walls of veins make them far more distensible than arteries; thus, they are said to be capacitance vessels. Figure 20.9 Distribution of Blood Flow When blood flow needs to be redistributed to other portions of the body, the vasomotor center located in the medulla oblongata sends sympathetic stimulation to the smooth muscles in the walls of the veins, causing constriction—or in this case, venoconstriction. Less dramatic than the vasoconstriction seen in smaller arteries and arterioles, venoconstriction may be likened to a “stiffening” of the vessel wall. This increases pressure on the blood within the veins, speeding its return to the heart. As you will note in Figure 20.9, approximately 21 percent of the venous blood is located in venous networks within the liver, bone marrow, and integument. This volume of blood is referred to as venous reserve. Through venoconstriction, this “reserve” volume of blood can get back to the heart more quickly for redistribution to other parts of the circulation. CAREER CONNECTION Vascular Surgeons and Technicians Vascular surgery is a specialty in which the physician deals primarily with diseases of the vascular portion of the cardiovascular system. This includes repair and replacement of diseased or damaged vessels, removal of plaque from vessels, minimally invasive procedures including the insertion of venous catheters, and traditional surgery. Following completion of medical school, the physician generally completes a 5-year surgical residency followed by an additional 1 to 2 years of vascular specialty training. In the United States, most vascular surgeons are members of the Society of Vascular Surgery. Vascular technicians are specialists in imaging technologies that provide information on the health of the vascular system. They may also assist physicians in treating disorders involving the arteries and veins. This profession often overlaps with cardiovascular technology, which would also include treatments involving the heart. Although recognized by the American Medical Association, there are currently no licensing requirements for vascular technicians, and licensing is voluntary. Vascular technicians typically have an Associate’s degree or certificate, involving 18 months to 2 years of training. The United States Bureau of Labor projects this profession to grow by 29 percent from 2010 to 2020. INTERACTIVE LINK Visit this site to learn more about vascular surgery. INTERACTIVE LINK Visit this site to learn more about vascular technicians. Blood Flow, Blood Pressure, and Resistance - Distinguish between systolic pressure, diastolic pressure, pulse pressure, and mean arterial pressure - Describe the clinical measurement of pulse and blood pressure - Identify and discuss five variables affecting arterial blood flow and blood pressure - Discuss several factors affecting blood flow in the venous system Blood flow refers to the movement of blood through a vessel, tissue, or organ, and is usually expressed in terms of volume of blood per unit of time. It is initiated by the contraction of the ventricles of the heart. Ventricular contraction ejects blood into the major arteries, resulting in flow from regions of higher pressure to regions of lower pressure, as blood encounters smaller arteries and arterioles, then capillaries, then the venules and veins of the venous system. This section discusses a number of critical variables that contribute to blood flow throughout the body. It also discusses the factors that impede or slow blood flow, a phenomenon known as resistance. As noted earlier, hydrostatic pressure is the force exerted by a fluid due to gravitational pull, usually against the wall of the container in which it is located. One form of hydrostatic pressure is blood pressure, the force exerted by blood upon the walls of the blood vessels or the chambers of the heart. Blood pressure may be measured in capillaries and veins, as well as the vessels of the pulmonary circulation; however, the term blood pressure without any specific descriptors typically refers to systemic arterial blood pressure—that is, the pressure of blood flowing in the arteries of the systemic circulation. In clinical practice, this pressure is measured in mm Hg and is usually obtained using the brachial artery of the arm. Components of Arterial Blood Pressure Arterial blood pressure in the larger vessels consists of several distinct components (Figure 20.10): systolic and diastolic pressures, pulse pressure, and mean arterial pressure. Systolic and Diastolic Pressures When systemic arterial blood pressure is measured, it is recorded as a ratio of two numbers (e.g., 120/80 is a normal adult blood pressure), expressed as systolic pressure over diastolic pressure. The systolic pressure is the higher value (typically around 120 mm Hg) and reflects the arterial pressure resulting from the ejection of blood during ventricular contraction, or systole. The diastolic pressure is the lower value (usually about 80 mm Hg) and represents the arterial pressure of blood during ventricular relaxation, or diastole. Figure 20.10 Systemic Blood Pressure The graph shows the components of blood pressure throughout the blood vessels, including systolic, diastolic, mean arterial, and pulse pressures. Pulse Pressure As shown in Figure 20.10, the difference between the systolic pressure and the diastolic pressure is the pulse pressure. For example, an individual with a systolic pressure of 120 mm Hg and a diastolic pressure of 80 mm Hg would have a pulse pressure of 40 mmHg. Generally, a pulse pressure should be at least 25 percent of the systolic pressure. A pulse pressure below this level is described as low or narrow. This may occur, for example, in patients with a low stroke volume, which may be seen in congestive heart failure, stenosis of the aortic valve, or significant blood loss following trauma. In contrast, a high or wide pulse pressure is common in healthy people following strenuous exercise, when their resting pulse pressure of 30–40 mm Hg may increase temporarily to 100 mm Hg as stroke volume increases. A persistently high pulse pressure at or above 100 mm Hg may indicate excessive resistance in the arteries and can be caused by a variety of disorders. Chronic high resting pulse pressures can degrade the heart, brain, and kidneys, and warrant medical treatment. Mean Arterial Pressure Mean arterial pressure (MAP) represents the “average” pressure of blood in the arteries, that is, the average force driving blood into vessels that serve the tissues. Mean is a statistical concept and is calculated by taking the sum of the values divided by the number of values. Although complicated to measure directly and complicated to calculate, MAP can be approximated by adding the diastolic pressure to one-third of the pulse pressure or systolic pressure minus the diastolic pressure: MAP = diastolic BP + (systolic-diastolic BP)3MAP = diastolic BP + (systolic-diastolic BP)3 In Figure 20.10, this value is approximately 80 + (120 − 80) / 3, or 93.33. Normally, the MAP falls within the range of 70–110 mm Hg. If the value falls below 60 mm Hg for an extended time, blood pressure will not be high enough to ensure circulation to and through the tissues, which results in ischemia, or insufficient blood flow. A condition called hypoxia, inadequate oxygenation of tissues, commonly accompanies ischemia. The term hypoxemia refers to low levels of oxygen in systemic arterial blood. Neurons are especially sensitive to hypoxia and may die or be damaged if blood flow and oxygen supplies are not quickly restored. Pulse After blood is ejected from the heart, elastic fibers in the arteries help maintain a high-pressure gradient as they expand to accommodate the blood, then recoil. This expansion and recoiling effect, known as the pulse, can be palpated manually or measured electronically. Although the effect diminishes over distance from the heart, elements of the systolic and diastolic components of the pulse are still evident down to the level of the arterioles. Because pulse indicates heart rate, it is measured clinically to provide clues to a patient’s state of health. It is recorded as beats per minute. Both the rate and the strength of the pulse are important clinically. A high or irregular pulse rate can be caused by physical activity or other temporary factors, but it may also indicate a heart condition. The pulse strength indicates the strength of ventricular contraction and cardiac output. If the pulse is strong, then systolic pressure is high. If it is weak, systolic pressure has fallen, and medical intervention may be warranted. Pulse can be palpated manually by placing the tips of the fingers across an artery that runs close to the body surface and pressing lightly. While this procedure is normally performed using the radial artery in the wrist or the common carotid artery in the neck, any superficial artery that can be palpated may be used (Figure 20.11). Common sites to find a pulse include temporal and facial arteries in the head, brachial arteries in the upper arm, femoral arteries in the thigh, popliteal arteries behind the knees, posterior tibial arteries near the medial tarsal regions, and dorsalis pedis arteries in the feet. A variety of commercial electronic devices are also available to measure pulse. Figure 20.11 Pulse Sites The pulse is most readily measured at the radial artery, but can be measured at any of the pulse points shown. Measurement of Blood Pressure Blood pressure is one of the critical parameters measured on virtually every patient in every healthcare setting. The technique used today was developed more than 100 years ago by a pioneering Russian physician, Dr. Nikolai Korotkoff. Turbulent blood flow through the vessels can be heard as a soft ticking while measuring blood pressure; these sounds are known as Korotkoff sounds. The technique of measuring blood pressure requires the use of a sphygmomanometer (a blood pressure cuff attached to a measuring device) and a stethoscope. The technique is as follows: - The clinician wraps an inflatable cuff tightly around the patient’s arm at about the level of the heart. - The clinician squeezes a rubber pump to inject air into the cuff, raising pressure around the artery and temporarily cutting off blood flow into the patient’s arm. - The clinician places the stethoscope on the patient’s antecubital region and, while gradually allowing air within the cuff to escape, listens for the Korotkoff sounds. Although there are five recognized Korotkoff sounds, only two are normally recorded. Initially, no sounds are heard since there is no blood flow through the vessels, but as air pressure drops, the cuff relaxes, and blood flow returns to the arm. As shown in Figure 20.12, the first sound heard through the stethoscope—the first Korotkoff sound—indicates systolic pressure. As more air is released from the cuff, blood is able to flow freely through the brachial artery and all sounds disappear. The point at which the last sound is heard is recorded as the patient’s diastolic pressure. Figure 20.12 Blood Pressure Measurement When pressure in a sphygmomanometer cuff is released, a clinician can hear the Korotkoff sounds. In this graph, a blood pressure tracing is aligned to a measurement of systolic and diastolic pressures. The majority of hospitals and clinics have automated equipment for measuring blood pressure that work on the same principles. An even more recent innovation is a small instrument that wraps around a patient’s wrist. The patient then holds the wrist over the heart while the device measures blood flow and records pressure. Variables Affecting Blood Flow and Blood Pressure Five variables influence blood flow and blood pressure: - Cardiac output - Compliance - Volume of the blood - Viscosity of the blood - Blood vessel length and diameter Recall that blood moves from higher pressure to lower pressure. It is pumped from the heart into the arteries at high pressure. If you increase pressure in the arteries (afterload), and cardiac function does not compensate, blood flow will actually decrease. In the venous system, the opposite relationship is true. Increased pressure in the veins does not decrease flow as it does in arteries, but actually increases flow. Since pressure in the veins is normally relatively low, for blood to flow back into the heart, the pressure in the atria during atrial diastole must be even lower. It normally approaches zero, except when the atria contract (see Figure 20.10). Cardiac Output Cardiac output is the measurement of blood flow from the heart through the ventricles, and is usually measured in liters per minute. Any factor that causes cardiac output to increase, by elevating heart rate or stroke volume or both, will elevate blood pressure and promote blood flow. These factors include sympathetic stimulation, the catecholamines epinephrine and norepinephrine, thyroid hormones, and increased calcium ion levels. Conversely, any factor that decreases cardiac output, by decreasing heart rate or stroke volume or both, will decrease arterial pressure and blood flow. These factors include parasympathetic stimulation, elevated or decreased potassium ion levels, decreased calcium levels, anoxia, and acidosis. Compliance Compliance is the ability of any compartment to expand to accommodate increased content. A metal pipe, for example, is not compliant, whereas a balloon is. The greater the compliance of an artery, the more effectively it is able to expand to accommodate surges in blood flow without increased resistance or blood pressure. Veins are more compliant than arteries and can expand to hold more blood. When vascular disease causes stiffening of arteries, compliance is reduced and resistance to blood flow is increased. The result is more turbulence, higher pressure within the vessel, and reduced blood flow. This increases the work of the heart. A Mathematical Approach to Factors Affecting Blood Flow Jean Louis Marie Poiseuille was a French physician and physiologist who devised a mathematical equation describing blood flow and its relationship to known parameters. The same equation also applies to engineering studies of the flow of fluids. Although understanding the math behind the relationships among the factors affecting blood flow is not necessary to understand blood flow, it can help solidify an understanding of their relationships. Please note that even if the equation looks intimidating, breaking it down into its components and following the relationships will make these relationships clearer, even if you are weak in math. Focus on the three critical variables: radius (r), vessel length (λ), and viscosity (η). Poiseuille’s equation: Blood flow = π ΔP r48ηλBlood flow = π ΔP r48ηλ- π is the Greek letter pi, used to represent the mathematical constant that is the ratio of a circle’s circumference to its diameter. It may commonly be represented as 3.14, although the actual number extends to infinity. - ΔP represents the difference in pressure. - r4 is the radius (one-half of the diameter) of the vessel to the fourth power. - η is the Greek letter eta and represents the viscosity of the blood. - λ is the Greek letter lambda and represents the length of a blood vessel. One of several things this equation allows us to do is calculate the resistance in the vascular system. Normally this value is extremely difficult to measure, but it can be calculated from this known relationship: Blood flow = ΔPResistanceBlood flow = ΔPResistanceIf we rearrange this slightly, Resistance = ΔPBlood flowResistance = ΔPBlood flowThen by substituting Pouseille’s equation for blood flow: Resistance =8ηλπr4Resistance =8ηλπr4By examining this equation, you can see that there are only three variables: viscosity, vessel length, and radius, since 8 and π are both constants. The important thing to remember is this: Two of these variables, viscosity and vessel length, will change slowly in the body. Only one of these factors, the radius, can be changed rapidly by vasoconstriction and vasodilation, thus dramatically impacting resistance and flow. Further, small changes in the radius will greatly affect flow, since it is raised to the fourth power in the equation. We have briefly considered how cardiac output and blood volume impact blood flow and pressure; the next step is to see how the other variables (contraction, vessel length, and viscosity) articulate with Pouseille’s equation and what they can teach us about the impact on blood flow. Blood Volume The relationship between blood volume, blood pressure, and blood flow is intuitively obvious. Water may merely trickle along a creek bed in a dry season, but rush quickly and under great pressure after a heavy rain. Similarly, as blood volume decreases, pressure and flow decrease. As blood volume increases, pressure and flow increase. Under normal circumstances, blood volume varies little. Low blood volume, called hypovolemia, may be caused by bleeding, dehydration, vomiting, severe burns, or some medications used to treat hypertension. It is important to recognize that other regulatory mechanisms in the body are so effective at maintaining blood pressure that an individual may be asymptomatic until 10–20 percent of the blood volume has been lost. Treatment typically includes intravenous fluid replacement. Hypervolemia, excessive fluid volume, may be caused by retention of water and sodium, as seen in patients with heart failure, liver cirrhosis, some forms of kidney disease, hyperaldosteronism, and some glucocorticoid steroid treatments. Restoring homeostasis in these patients depends upon reversing the condition that triggered the hypervolemia. Blood Viscosity Viscosity is the thickness of fluids that affects their ability to flow. Clean water, for example, is less viscous than mud. The viscosity of blood is directly proportional to resistance and inversely proportional to flow; therefore, any condition that causes viscosity to increase will also increase resistance and decrease flow. For example, imagine sipping milk, then a milkshake, through the same size straw. You experience more resistance and therefore less flow from the milkshake. Conversely, any condition that causes viscosity to decrease (such as when the milkshake melts) will decrease resistance and increase flow. Normally the viscosity of blood does not change over short periods of time. The two primary determinants of blood viscosity are the formed elements and plasma proteins. Since the vast majority of formed elements are erythrocytes, any condition affecting erythropoiesis, such as polycythemia or anemia, can alter viscosity. Since most plasma proteins are produced by the liver, any condition affecting liver function can also change the viscosity slightly and therefore alter blood flow. Liver abnormalities such as hepatitis, cirrhosis, alcohol damage, and drug toxicities result in decreased levels of plasma proteins, which decrease blood viscosity. While leukocytes and platelets are normally a small component of the formed elements, there are some rare conditions in which severe overproduction can impact viscosity as well. Vessel Length and Diameter The length of a vessel is directly proportional to its resistance: the longer the vessel, the greater the resistance and the lower the flow. As with blood volume, this makes intuitive sense, since the increased surface area of the vessel will impede the flow of blood. Likewise, if the vessel is shortened, the resistance will decrease and flow will increase. The length of our blood vessels increases throughout childhood as we grow, of course, but is unchanging in adults under normal physiological circumstances. Further, the distribution of vessels is not the same in all tissues. Adipose tissue does not have an extensive vascular supply. One pound of adipose tissue contains approximately 200 miles of vessels, whereas skeletal muscle contains more than twice that. Overall, vessels decrease in length only during loss of mass or amputation. An individual weighing 150 pounds has approximately 60,000 miles of vessels in the body. Gaining about 10 pounds adds from 2000 to 4000 miles of vessels, depending upon the nature of the gained tissue. One of the great benefits of weight reduction is the reduced stress to the heart, which does not have to overcome the resistance of as many miles of vessels. In contrast to length, the diameter of blood vessels changes throughout the body, according to the type of vessel, as we discussed earlier. The diameter of any given vessel may also change frequently throughout the day in response to neural and chemical signals that trigger vasodilation and vasoconstriction. The vascular tone of the vessel is the contractile state of the smooth muscle and the primary determinant of diameter, and thus of resistance and flow. The effect of vessel diameter on resistance is inverse: Given the same volume of blood, an increased diameter means there is less blood contacting the vessel wall, thus lower friction and lower resistance, subsequently increasing flow. A decreased diameter means more of the blood contacts the vessel wall, and resistance increases, subsequently decreasing flow. The influence of lumen diameter on resistance is dramatic: A slight increase or decrease in diameter causes a huge decrease or increase in resistance. This is because resistance is inversely proportional to the radius of the blood vessel (one-half of the vessel’s diameter) raised to the fourth power (R = 1/r4). This means, for example, that if an artery or arteriole constricts to one-half of its original radius, the resistance to flow will increase 16 times. And if an artery or arteriole dilates to twice its initial radius, then resistance in the vessel will decrease to 1/16 of its original value and flow will increase 16 times. The Roles of Vessel Diameter and Total Area in Blood Flow and Blood Pressure Recall that we classified arterioles as resistance vessels, because given their small lumen, they dramatically slow the flow of blood from arteries. In fact, arterioles are the site of greatest resistance in the entire vascular network. This may seem surprising, given that capillaries have a smaller size. How can this phenomenon be explained? Figure 20.13 compares vessel diameter, total cross-sectional area, average blood pressure, and blood velocity through the systemic vessels. Notice in parts (a) and (b) that the total cross-sectional area of the body’s capillary beds is far greater than any other type of vessel. Although the diameter of an individual capillary is significantly smaller than the diameter of an arteriole, there are vastly more capillaries in the body than there are other types of blood vessels. Part (c) shows that blood pressure drops unevenly as blood travels from arteries to arterioles, capillaries, venules, and veins, and encounters greater resistance. However, the site of the most precipitous drop, and the site of greatest resistance, is the arterioles. This explains why vasodilation and vasoconstriction of arterioles play more significant roles in regulating blood pressure than do the vasodilation and vasoconstriction of other vessels. Part (d) shows that the velocity (speed) of blood flow decreases dramatically as the blood moves from arteries to arterioles to capillaries. This slow flow rate allows more time for exchange processes to occur. As blood flows through the veins, the rate of velocity increases, as blood is returned to the heart. Figure 20.13 Relationships among Vessels in the Systemic Circuit The relationships among blood vessels that can be compared include (a) vessel diameter, (b) total cross-sectional area, (c) average blood pressure, and (d) velocity of blood flow. DISORDERS OF THE... Cardiovascular System: Arteriosclerosis Compliance allows an artery to expand when blood is pumped through it from the heart, and then to recoil after the surge has passed. This helps promote blood flow. In arteriosclerosis, compliance is reduced, and pressure and resistance within the vessel increase. This is a leading cause of hypertension and coronary heart disease, as it causes the heart to work harder to generate a pressure great enough to overcome the resistance. Arteriosclerosis begins with injury to the endothelium of an artery, which may be caused by irritation from high blood glucose, infection, tobacco use, excessive blood lipids, and other factors. Artery walls that are constantly stressed by blood flowing at high pressure are also more likely to be injured—which means that hypertension can promote arteriosclerosis, as well as result from it. Recall that tissue injury causes inflammation. As inflammation spreads into the artery wall, it weakens and scars it, leaving it stiff (sclerotic). As a result, compliance is reduced. Moreover, circulating triglycerides and cholesterol can seep between the damaged lining cells and become trapped within the artery wall, where they are frequently joined by leukocytes, calcium, and cellular debris. Eventually, this buildup, called plaque, can narrow arteries enough to impair blood flow. The term for this condition, atherosclerosis (athero- = “porridge”) describes the mealy deposits (Figure 20.14). Figure 20.14 Atherosclerosis (a) Atherosclerosis can result from plaques formed by the buildup of fatty, calcified deposits in an artery. (b) Plaques can also take other forms, as shown in this micrograph of a coronary artery that has a buildup of connective tissue within the artery wall. LM × 40. (Micrograph provided by the Regents of University of Michigan Medical School © 2012) Sometimes a plaque can rupture, causing microscopic tears in the artery wall that allow blood to leak into the tissue on the other side. When this happens, platelets rush to the site to clot the blood. This clot can further obstruct the artery and—if it occurs in a coronary or cerebral artery—cause a sudden heart attack or stroke. Alternatively, plaque can break off and travel through the bloodstream as an embolus until it blocks a more distant, smaller artery. Even without total blockage, vessel narrowing leads to ischemia—reduced blood flow—to the tissue region “downstream” of the narrowed vessel. Ischemia in turn leads to hypoxia—decreased supply of oxygen to the tissues. Hypoxia involving cardiac muscle or brain tissue can lead to cell death and severe impairment of brain or heart function. A major risk factor for both arteriosclerosis and atherosclerosis is advanced age, as the conditions tend to progress over time. Arteriosclerosis is normally defined as the more generalized loss of compliance, “hardening of the arteries,” whereas atherosclerosis is a more specific term for the build-up of plaque in the walls of the vessel and is a specific type of arteriosclerosis. There is also a distinct genetic component, and pre-existing hypertension and/or diabetes also greatly increase the risk. However, obesity, poor nutrition, lack of physical activity, and tobacco use all are major risk factors. Treatment includes lifestyle changes, such as weight loss, smoking cessation, regular exercise, and adoption of a diet low in sodium and saturated fats. Medications to reduce cholesterol and blood pressure may be prescribed. For blocked coronary arteries, surgery is warranted. In angioplasty, a catheter is inserted into the vessel at the point of narrowing, and a second catheter with a balloon-like tip is inflated to widen the opening. To prevent subsequent collapse of the vessel, a small mesh tube called a stent is often inserted. In an endarterectomy, plaque is surgically removed from the walls of a vessel. This operation is typically performed on the carotid arteries of the neck, which are a prime source of oxygenated blood for the brain. In a coronary bypass procedure, a non-vital superficial vessel from another part of the body (often the great saphenous vein) or a synthetic vessel is inserted to create a path around the blocked area of a coronary artery. Venous System The pumping action of the heart propels the blood into the arteries, from an area of higher pressure toward an area of lower pressure. If blood is to flow from the veins back into the heart, the pressure in the veins must be greater than the pressure in the atria of the heart. Two factors help maintain this pressure gradient between the veins and the heart. First, the pressure in the atria during diastole is very low, often approaching zero when the atria are relaxed (atrial diastole). Second, two physiologic “pumps” increase pressure in the venous system. The use of the term “pump” implies a physical device that speeds flow. These physiological pumps are less obvious. Skeletal Muscle Pump In many body regions, the pressure within the veins can be increased by the contraction of the surrounding skeletal muscle. This mechanism, known as the skeletal muscle pump (Figure 20.15), helps the lower-pressure veins counteract the force of gravity, increasing pressure to move blood back to the heart. As leg muscles contract, for example during walking or running, they exert pressure on nearby veins with their numerous one-way valves. This increased pressure causes blood to flow upward, opening valves superior to the contracting muscles so blood flows through. Simultaneously, valves inferior to the contracting muscles close; thus, blood should not seep back downward toward the feet. Military recruits are trained to flex their legs slightly while standing at attention for prolonged periods. Failure to do so may allow blood to pool in the lower limbs rather than returning to the heart. Consequently, the brain will not receive enough oxygenated blood, and the individual may lose consciousness. Figure 20.15 Skeletal Muscle Pump The contraction of skeletal muscles surrounding a vein compresses the blood and increases the pressure in that area. This action forces blood closer to the heart where venous pressure is lower. Note the importance of the one-way valves to assure that blood flows only in the proper direction. Respiratory Pump The respiratory pump aids blood flow through the veins of the thorax and abdomen. During inhalation, the volume of the thorax increases, largely through the contraction of the diaphragm, which moves downward and compresses the abdominal cavity. The elevation of the chest caused by the contraction of the external intercostal muscles also contributes to the increased volume of the thorax. The volume increase causes air pressure within the thorax to decrease, allowing us to inhale. Additionally, as air pressure within the thorax drops, blood pressure in the thoracic veins also decreases, falling below the pressure in the abdominal veins. This causes blood to flow along its pressure gradient from veins outside the thorax, where pressure is higher, into the thoracic region, where pressure is now lower. This in turn promotes the return of blood from the thoracic veins to the atria. During exhalation, when air pressure increases within the thoracic cavity, pressure in the thoracic veins increases, speeding blood flow into the heart while valves in the veins prevent blood from flowing backward from the thoracic and abdominal veins. Pressure Relationships in the Venous System Although vessel diameter increases from the smaller venules to the larger veins and eventually to the venae cavae (singular = vena cava), the total cross-sectional area actually decreases (see Figure 20.15a and b). The individual veins are larger in diameter than the venules, but their total number is much lower, so their total cross-sectional area is also lower. Also notice that, as blood moves from venules to veins, the average blood pressure drops (see Figure 20.15c), but the blood velocity actually increases (see Figure 20.15). This pressure gradient drives blood back toward the heart. Again, the presence of one-way valves and the skeletal muscle and respiratory pumps contribute to this increased flow. Since approximately 64 percent of the total blood volume resides in systemic veins, any action that increases the flow of blood through the veins will increase venous return to the heart. Maintaining vascular tone within the veins prevents the veins from merely distending, dampening the flow of blood, and as you will see, vasoconstriction actually enhances the flow. The Role of Venoconstriction in Resistance, Blood Pressure, and Flow As previously discussed, vasoconstriction of an artery or arteriole decreases the radius, increasing resistance and pressure, but decreasing flow. Venoconstriction, on the other hand, has a very different outcome. The walls of veins are thin but irregular; thus, when the smooth muscle in those walls constricts, the lumen becomes more rounded. The more rounded the lumen, the less surface area the blood encounters, and the less resistance the vessel offers. Vasoconstriction increases pressure within a vein as it does in an artery, but in veins, the increased pressure increases flow. Recall that the pressure in the atria, into which the venous blood will flow, is very low, approaching zero for at least part of the relaxation phase of the cardiac cycle. Thus, venoconstriction increases the return of blood to the heart. Another way of stating this is that venoconstriction increases the preload or stretch of the cardiac muscle and increases contraction. Capillary Exchange - Identify the primary mechanisms of capillary exchange - Distinguish between capillary hydrostatic pressure and blood colloid osmotic pressure, explaining the contribution of each to net filtration pressure - Compare filtration and reabsorption - Explain the fate of fluid that is not reabsorbed from the tissues into the vascular capillaries The primary purpose of the cardiovascular system is to circulate gases, nutrients, wastes, and other substances to and from the cells of the body. Small molecules, such as gases, lipids, and lipid-soluble molecules, can diffuse directly through the membranes of the endothelial cells of the capillary wall. Glucose, amino acids, and ions—including sodium, potassium, calcium, and chloride—use transporters to move through specific channels in the membrane by facilitated diffusion. Glucose, ions, and larger molecules may also leave the blood through intercellular clefts. Larger molecules can pass through the pores of fenestrated capillaries, and even large plasma proteins can pass through the great gaps in the sinusoids. Some large proteins in blood plasma can move into and out of the endothelial cells packaged within vesicles by endocytosis and exocytosis. Water moves by osmosis. Bulk Flow The mass movement of fluids into and out of capillary beds requires a transport mechanism far more efficient than mere diffusion. This movement, often referred to as bulk flow, involves two pressure-driven mechanisms: Volumes of fluid move from an area of higher pressure in a capillary bed to an area of lower pressure in the tissues via filtration. In contrast, the movement of fluid from an area of higher pressure in the tissues into an area of lower pressure in the capillaries is reabsorption. Two types of pressure interact to drive each of these movements: hydrostatic pressure and osmotic pressure. Hydrostatic Pressure The primary force driving fluid transport between the capillaries and tissues is hydrostatic pressure, which can be defined as the pressure of any fluid enclosed in a space. Blood hydrostatic pressure is the force exerted by the blood confined within blood vessels or heart chambers. Even more specifically, the pressure exerted by blood against the wall of a capillary is called capillary hydrostatic pressure (CHP), and is the same as capillary blood pressure. CHP is the force that drives fluid out of capillaries and into the tissues. As fluid exits a capillary and moves into tissues, the hydrostatic pressure in the interstitial fluid correspondingly rises. This opposing hydrostatic pressure is called the interstitial fluid hydrostatic pressure (IFHP). Generally, the CHP originating from the arterial pathways is considerably higher than the IFHP, because lymphatic vessels are continually absorbing excess fluid from the tissues. Thus, fluid generally moves out of the capillary and into the interstitial fluid. This process is called filtration. Osmotic Pressure The net pressure that drives reabsorption—the movement of fluid from the interstitial fluid back into the capillaries—is called osmotic pressure (sometimes referred to as oncotic pressure). Whereas hydrostatic pressure forces fluid out of the capillary, osmotic pressure draws fluid back in. Osmotic pressure is determined by osmotic concentration gradients, that is, the difference in the solute-to-water concentrations in the blood and tissue fluid. A region higher in solute concentration (and lower in water concentration) draws water across a semipermeable membrane from a region higher in water concentration (and lower in solute concentration). As we discuss osmotic pressure in blood and tissue fluid, it is important to recognize that the formed elements of blood do not contribute to osmotic concentration gradients. Rather, it is the plasma proteins that play the key role. Solutes also move across the capillary wall according to their concentration gradient, but overall, the concentrations should be similar and not have a significant impact on osmosis. Because of their large size and chemical structure, plasma proteins are not truly solutes, that is, they do not dissolve but are dispersed or suspended in their fluid medium, forming a colloid rather than a solution. The pressure created by the concentration of colloidal proteins in the blood is called the blood colloidal osmotic pressure (BCOP). Its effect on capillary exchange accounts for the reabsorption of water. The plasma proteins suspended in blood cannot move across the semipermeable capillary cell membrane, and so they remain in the plasma. As a result, blood has a higher colloidal concentration and lower water concentration than tissue fluid. It therefore attracts water. We can also say that the BCOP is higher than the interstitial fluid colloidal osmotic pressure (IFCOP), which is always very low because interstitial fluid contains few proteins. Thus, water is drawn from the tissue fluid back into the capillary, carrying dissolved molecules with it. This difference in colloidal osmotic pressure accounts for reabsorption. Interaction of Hydrostatic and Osmotic Pressures The normal unit used to express pressures within the cardiovascular system is millimeters of mercury (mm Hg). When blood leaving an arteriole first enters a capillary bed, the CHP is quite high—about 35 mm Hg. Gradually, this initial CHP declines as the blood moves through the capillary so that by the time the blood has reached the venous end, the CHP has dropped to approximately 18 mm Hg. In comparison, the plasma proteins remain suspended in the blood, so the BCOP remains fairly constant at about 25 mm Hg throughout the length of the capillary and considerably below the osmotic pressure in the interstitial fluid. The net filtration pressure (NFP) represents the interaction of the hydrostatic and osmotic pressures, driving fluid out of the capillary. It is equal to the difference between the CHP and the BCOP. Since filtration is, by definition, the movement of fluid out of the capillary, when reabsorption is occurring, the NFP is a negative number. NFP changes at different points in a capillary bed (Figure 20.16). Close to the arterial end of the capillary, it is approximately 10 mm Hg, because the CHP of 35 mm Hg minus the BCOP of 25 mm Hg equals 10 mm Hg. Recall that the hydrostatic and osmotic pressures of the interstitial fluid are essentially negligible. Thus, the NFP of 10 mm Hg drives a net movement of fluid out of the capillary at the arterial end. At approximately the middle of the capillary, the CHP is about the same as the BCOP of 25 mm Hg, so the NFP drops to zero. At this point, there is no net change of volume: Fluid moves out of the capillary at the same rate as it moves into the capillary. Near the venous end of the capillary, the CHP has dwindled to about 18 mm Hg due to loss of fluid. Because the BCOP remains steady at 25 mm Hg, water is drawn into the capillary, that is, reabsorption occurs. Another way of expressing this is to say that at the venous end of the capillary, there is an NFP of −7 mm Hg. Figure 20.16 Capillary Exchange Net filtration occurs near the arterial end of the capillary since capillary hydrostatic pressure (CHP) is greater than blood colloidal osmotic pressure (BCOP). There is no net movement of fluid near the midpoint since CHP = BCOP. Net reabsorption occurs near the venous end since BCOP is greater than CHP. The Role of Lymphatic Capillaries Since overall CHP is higher than BCOP, it is inevitable that more net fluid will exit the capillary through filtration at the arterial end than enters through reabsorption at the venous end. Considering all capillaries over the course of a day, this can be quite a substantial amount of fluid: Approximately 24 liters per day are filtered, whereas 20.4 liters are reabsorbed. This excess fluid is picked up by capillaries of the lymphatic system. These extremely thin-walled vessels have copious numbers of valves that ensure unidirectional flow through ever-larger lymphatic vessels that eventually drain into the subclavian veins in the neck. An important function of the lymphatic system is to return the fluid (lymph) to the blood. Lymph may be thought of as recycled blood plasma. (Seek additional content for more detail on the lymphatic system.) INTERACTIVE LINK Watch this video to explore capillaries and how they function in the body. Capillaries are never more than 100 micrometers away. What is the main component of interstitial fluid? Homeostatic Regulation of the Vascular System - Discuss the mechanisms involved in the neural regulation of vascular homeostasis - Describe the contribution of a variety of hormones to the renal regulation of blood pressure - Identify the effects of exercise on vascular homeostasis - Discuss how hypertension, hemorrhage, and circulatory shock affect vascular health In order to maintain homeostasis in the cardiovascular system and provide adequate blood to the tissues, blood flow must be redirected continually to the tissues as they become more active. In a very real sense, the cardiovascular system engages in resource allocation, because there is not enough blood flow to distribute blood equally to all tissues simultaneously. For example, when an individual is exercising, more blood will be directed to skeletal muscles, the heart, and the lungs. Following a meal, more blood is directed to the digestive system. Only the brain receives a more or less constant supply of blood whether you are active, resting, thinking, or engaged in any other activity. Table 20.3 provides the distribution of systemic blood at rest and during exercise. Although most of the data appears logical, the values for the distribution of blood to the integument may seem surprising. During exercise, the body distributes more blood to the body surface where it can dissipate the excess heat generated by increased activity into the environment. Systemic Blood Flow During Rest, Mild Exercise, and Maximal Exercise in a Healthy Young Individual \| Organ \| Resting (mL/min) \| Mild exercise (mL/min) \| Maximal exercise (mL/min) \| \|---\|---\|---\|---\| \| Skeletal muscle \| 1200 \| 4500 \| 12,500 \| \| Heart \| 250 \| 350 \| 750 \| \| Brain \| 750 \| 750 \| 750 \| \| Integument \| 500 \| 1500 \| 1900 \| \| Kidney \| 1100 \| 900 \| 600 \| \| Gastrointestinal \| 1400 \| 1100 \| 600 \| \| Others (i.e., liver, spleen) \| 600 \| 400 \| 400 \| \| Total \| 5800 \| 9500 \| 17,500 \| Table 20.3 Three homeostatic mechanisms ensure adequate blood flow, blood pressure, distribution, and ultimately perfusion: neural, endocrine, and autoregulatory mechanisms. They are summarized in Figure 20.17. Figure 20.17 Summary of Factors Maintaining Vascular Homeostasis Adequate blood flow, blood pressure, distribution, and perfusion involve autoregulatory, neural, and endocrine mechanisms. Neural Regulation The nervous system plays a critical role in the regulation of vascular homeostasis. The primary regulatory sites include the cardiovascular centers in the brain that control both cardiac and vascular functions. In addition, more generalized neural responses from the limbic system and the autonomic nervous system are factors. The Cardiovascular Centers in the Brain Neurological regulation of blood pressure and flow depends on the cardiovascular centers located in the medulla oblongata. This cluster of neurons responds to changes in blood pressure as well as blood concentrations of oxygen, carbon dioxide, and hydrogen ions. The cardiovascular center contains three distinct paired components: - The cardioaccelerator centers stimulate cardiac function by regulating heart rate and stroke volume via sympathetic stimulation from the cardiac accelerator nerve. - The cardioinhibitor centers slow cardiac function by decreasing heart rate and stroke volume via parasympathetic stimulation from the vagus nerve. - The vasomotor centers control vessel tone or contraction of the smooth muscle in the tunica media. Changes in diameter affect peripheral resistance, pressure, and flow, which affect cardiac output. The majority of these neurons act via the release of the neurotransmitter norepinephrine from sympathetic neurons. Although each center functions independently, they are not anatomically distinct. There is also a small population of neurons that control vasodilation in the vessels of the brain and skeletal muscles by relaxing the smooth muscle fibers in the vessel tunics. Many of these are cholinergic neurons, that is, they release acetylcholine, which in turn stimulates the vessels’ endothelial cells to release nitric oxide (NO), which causes vasodilation. Others release norepinephrine that binds to β2 receptors. A few neurons release NO directly as a neurotransmitter. Recall that mild stimulation of the skeletal muscles maintains muscle tone. A similar phenomenon occurs with vascular tone in vessels. As noted earlier, arterioles are normally partially constricted: With maximal stimulation, their radius may be reduced to one-half of the resting state. Full dilation of most arterioles requires that this sympathetic stimulation be suppressed. When it is, an arteriole can expand by as much as 150 percent. Such a significant increase can dramatically affect resistance, pressure, and flow. Baroreceptor Reflexes Baroreceptors are specialized stretch receptors located within thin areas of blood vessels and heart chambers that respond to the degree of stretch caused by the presence of blood. They send impulses to the cardiovascular center to regulate blood pressure. Vascular baroreceptors are found primarily in sinuses (small cavities) within the aorta and carotid arteries: The aortic sinuses are found in the walls of the ascending aorta just superior to the aortic valve, whereas the carotid sinuses are in the base of the internal carotid arteries. There are also low-pressure baroreceptors located in the walls of the venae cavae and right atrium. When blood pressure increases, the baroreceptors are stretched more tightly and initiate action potentials at a higher rate. At lower blood pressures, the degree of stretch is lower and the rate of firing is slower. When the cardiovascular center in the medulla oblongata receives this input, it triggers a reflex that maintains homeostasis (Figure 20.18): - When blood pressure rises too high, the baroreceptors fire at a higher rate and trigger parasympathetic stimulation of the heart. As a result, cardiac output falls. Sympathetic stimulation of the peripheral arterioles will also decrease, resulting in vasodilation. Combined, these activities cause blood pressure to fall. - When blood pressure drops too low, the rate of baroreceptor firing decreases. This will trigger an increase in sympathetic stimulation of the heart, causing cardiac output to increase. It will also trigger sympathetic stimulation of the peripheral vessels, resulting in vasoconstriction. Combined, these activities cause blood pressure to rise. Figure 20.18 Baroreceptor Reflexes for Maintaining Vascular Homeostasis Increased blood pressure results in increased rates of baroreceptor firing, whereas decreased blood pressure results in slower rates of fire, both initiating the homeostatic mechanism to restore blood pressure. The baroreceptors in the venae cavae and right atrium monitor blood pressure as the blood returns to the heart from the systemic circulation. Normally, blood flow into the aorta is the same as blood flow back into the right atrium. If blood is returning to the right atrium more rapidly than it is being ejected from the left ventricle, the atrial receptors will stimulate the cardiovascular centers to increase sympathetic firing and increase cardiac output until homeostasis is achieved. The opposite is also true. This mechanism is referred to as the atrial reflex. Chemoreceptor Reflexes In addition to the baroreceptors are chemoreceptors that monitor levels of oxygen, carbon dioxide, and hydrogen ions (pH), and thereby contribute to vascular homeostasis. Chemoreceptors monitoring the blood are located in close proximity to the baroreceptors in the aortic and carotid sinuses. They signal the cardiovascular center as well as the respiratory centers in the medulla oblongata. Since tissues consume oxygen and produce carbon dioxide and acids as waste products, when the body is more active, oxygen levels fall and carbon dioxide levels rise as cells undergo cellular respiration to meet the energy needs of activities. This causes more hydrogen ions to be produced, causing the blood pH to drop. When the body is resting, oxygen levels are higher, carbon dioxide levels are lower, more hydrogen is bound, and pH rises. (Seek additional content for more detail about pH.) The chemoreceptors respond to increasing carbon dioxide and hydrogen ion levels (falling pH) by stimulating the cardioaccelerator and vasomotor centers, increasing cardiac output and constricting peripheral vessels. The cardioinhibitor centers are suppressed. With falling carbon dioxide and hydrogen ion levels (increasing pH), the cardioinhibitor centers are stimulated, and the cardioaccelerator and vasomotor centers are suppressed, decreasing cardiac output and causing peripheral vasodilation. In order to maintain adequate supplies of oxygen to the cells and remove waste products such as carbon dioxide, it is essential that the respiratory system respond to changing metabolic demands. In turn, the cardiovascular system will transport these gases to the lungs for exchange, again in accordance with metabolic demands. This interrelationship of cardiovascular and respiratory control cannot be overemphasized. Other neural mechanisms can also have a significant impact on cardiovascular function. These include the limbic system that links physiological responses to psychological stimuli, as well as generalized sympathetic and parasympathetic stimulation. Endocrine Regulation Endocrine control over the cardiovascular system involves the catecholamines, epinephrine and norepinephrine, as well as several hormones that interact with the kidneys in the regulation of blood volume. Epinephrine and Norepinephrine The catecholamines epinephrine and norepinephrine are released by the adrenal medulla, and enhance and extend the body’s sympathetic or “fight-or-flight” response (see Figure 20.17). They increase heart rate and force of contraction, while temporarily constricting blood vessels to organs not essential for flight-or-fight responses and redirecting blood flow to the liver, muscles, and heart. Antidiuretic Hormone Antidiuretic hormone (ADH), also known as vasopressin, is secreted by the cells in the hypothalamus and transported via the hypothalamic-hypophyseal tracts to the posterior pituitary where it is stored until released upon nervous stimulation. The primary trigger prompting the hypothalamus to release ADH is increasing osmolarity of tissue fluid, usually in response to significant loss of blood volume. ADH signals its target cells in the kidneys to reabsorb more water, thus preventing the loss of additional fluid in the urine. This will increase overall fluid levels and help restore blood volume and pressure. In addition, ADH constricts peripheral vessels. Renin-Angiotensin-Aldosterone Mechanism The renin-angiotensin-aldosterone mechanism has a major effect upon the cardiovascular system (Figure 20.19). Renin is an enzyme, although because of its importance in the renin-angiotensin-aldosterone pathway, some sources identify it as a hormone. Specialized cells in the kidneys found in the juxtaglomerular apparatus respond to decreased blood flow by secreting renin into the blood. Renin converts the plasma protein angiotensinogen, which is produced by the liver, into its active form—angiotensin I. Angiotensin I circulates in the blood and is then converted into angiotensin II in the lungs. This reaction is catalyzed by the enzyme angiotensin-converting enzyme (ACE). Angiotensin II is a powerful vasoconstrictor, greatly increasing blood pressure. It also stimulates the release of ADH and aldosterone, a hormone produced by the adrenal cortex. Aldosterone increases the reabsorption of sodium into the blood by the kidneys. Since water follows sodium, this increases the reabsorption of water. This in turn increases blood volume, raising blood pressure. Angiotensin II also stimulates the thirst center in the hypothalamus, so an individual will likely consume more fluids, again increasing blood volume and pressure. Figure 20.19 Hormones Involved in Renal Control of Blood Pressure In the renin-angiotensin-aldosterone mechanism, increasing angiotensin II will stimulate the production of antidiuretic hormone and aldosterone. In addition to renin, the kidneys produce erythropoietin, which stimulates the production of red blood cells, further increasing blood volume. Erythropoietin Erythropoietin (EPO) is released by the kidneys when blood flow and/or oxygen levels decrease. EPO stimulates the production of erythrocytes within the bone marrow. Erythrocytes are the major formed element of the blood and may contribute 40 percent or more to blood volume, a significant factor of viscosity, resistance, pressure, and flow. In addition, EPO is a vasoconstrictor. Overproduction of EPO or excessive intake of synthetic EPO, often to enhance athletic performance, will increase viscosity, resistance, and pressure, and decrease flow in addition to its contribution as a vasoconstrictor. Atrial Natriuretic Hormone Secreted by cells in the atria of the heart, atrial natriuretic hormone (ANH) (also known as atrial natriuretic peptide) is secreted when blood volume is high enough to cause extreme stretching of the cardiac cells. Cells in the ventricle produce a hormone with similar effects, called B-type natriuretic hormone. Natriuretic hormones are antagonists to angiotensin II. They promote loss of sodium and water from the kidneys, and suppress renin, aldosterone, and ADH production and release. All of these actions promote loss of fluid from the body, so blood volume and blood pressure drop. Autoregulation of Perfusion As the name would suggest, autoregulation mechanisms require neither specialized nervous stimulation nor endocrine control. Rather, these are local, self-regulatory mechanisms that allow each region of tissue to adjust its blood flow—and thus its perfusion. These local mechanisms include chemical signals and myogenic controls. Chemical Signals Involved in Autoregulation Chemical signals work at the level of the precapillary sphincters to trigger either constriction or relaxation. As you know, opening a precapillary sphincter allows blood to flow into that particular capillary, whereas constricting a precapillary sphincter temporarily shuts off blood flow to that region. The factors involved in regulating the precapillary sphincters include the following: - Opening of the sphincter is triggered in response to decreased oxygen concentrations; increased carbon dioxide concentrations; increasing levels of lactic acid or other byproducts of cellular metabolism; increasing concentrations of potassium ions or hydrogen ions (falling pH); inflammatory chemicals such as histamines; and increased body temperature. These conditions in turn stimulate the release of NO, a powerful vasodilator, from endothelial cells (see Figure 20.17). - Contraction of the precapillary sphincter is triggered by the opposite levels of the regulators, which prompt the release of endothelins, powerful vasoconstricting peptides secreted by endothelial cells. Platelet secretions and certain prostaglandins may also trigger constriction. Again, these factors alter tissue perfusion via their effects on the precapillary sphincter mechanism, which regulates blood flow to capillaries. Since the amount of blood is limited, not all capillaries can fill at once, so blood flow is allocated based upon the needs and metabolic state of the tissues as reflected in these parameters. Bear in mind, however, that dilation and constriction of the arterioles feeding the capillary beds is the primary control mechanism. The Myogenic Response The myogenic response is a reaction to the stretching of the smooth muscle in the walls of arterioles as changes in blood flow occur through the vessel. This may be viewed as a largely protective function against dramatic fluctuations in blood pressure and blood flow to maintain homeostasis. If perfusion of an organ is too low (ischemia), the tissue will experience low levels of oxygen (hypoxia). In contrast, excessive perfusion could damage the organ’s smaller and more fragile vessels. The myogenic response is a localized process that serves to stabilize blood flow in the capillary network that follows that arteriole. When blood flow is low, the vessel’s smooth muscle will be only minimally stretched. In response, it relaxes, allowing the vessel to dilate and thereby increase the movement of blood into the tissue. When blood flow is too high, the smooth muscle will contract in response to the increased stretch, prompting vasoconstriction that reduces blood flow. Figure 20.20 summarizes the effects of nervous, endocrine, and local controls on arterioles. Figure 20.20 Summary of Mechanisms Regulating Arteriole Smooth Muscle and Veins Effect of Exercise on Vascular Homeostasis The heart is a muscle and, like any muscle, it responds dramatically to exercise. For a healthy young adult, cardiac output (heart rate × stroke volume) increases in the nonathlete from approximately 5.0 liters (5.25 quarts) per minute to a maximum of about 20 liters (21 quarts) per minute. Accompanying this will be an increase in blood pressure from about 120/80 to 185/75. However, well-trained aerobic athletes can increase these values substantially. For these individuals, cardiac output soars from approximately 5.3 liters (5.57 quarts) per minute resting to more than 30 liters (31.5 quarts) per minute during maximal exercise. Along with this increase in cardiac output, blood pressure increases from 120/80 at rest to 200/90 at maximum values. In addition to improved cardiac function, exercise increases the size and mass of the heart. The average weight of the heart for the nonathlete is about 300 g, whereas in an athlete it will increase to 500 g. This increase in size generally makes the heart stronger and more efficient at pumping blood, increasing both stroke volume and cardiac output. Tissue perfusion also increases as the body transitions from a resting state to light exercise and eventually to heavy exercise (see Figure 20.20). These changes result in selective vasodilation in the skeletal muscles, heart, lungs, liver, and integument. Simultaneously, vasoconstriction occurs in the vessels leading to the kidneys and most of the digestive and reproductive organs. The flow of blood to the brain remains largely unchanged whether at rest or exercising, since the vessels in the brain largely do not respond to regulatory stimuli, in most cases, because they lack the appropriate receptors. As vasodilation occurs in selected vessels, resistance drops and more blood rushes into the organs they supply. This blood eventually returns to the venous system. Venous return is further enhanced by both the skeletal muscle and respiratory pumps. As blood returns to the heart more quickly, preload rises and the Frank-Starling principle tells us that contraction of the cardiac muscle in the atria and ventricles will be more forceful. Eventually, even the best-trained athletes will fatigue and must undergo a period of rest following exercise. Cardiac output and distribution of blood then return to normal. Regular exercise promotes cardiovascular health in a variety of ways. Because an athlete’s heart is larger than a nonathlete’s, stroke volume increases, so the athletic heart can deliver the same amount of blood as the nonathletic heart but with a lower heart rate. This increased efficiency allows the athlete to exercise for longer periods of time before muscles fatigue and places less stress on the heart. Exercise also lowers overall cholesterol levels by removing from the circulation a complex form of cholesterol, triglycerides, and proteins known as low-density lipoproteins (LDLs), which are widely associated with increased risk of cardiovascular disease. Although there is no way to remove deposits of plaque from the walls of arteries other than specialized surgery, exercise does promote the health of vessels by decreasing the rate of plaque formation and reducing blood pressure, so the heart does not have to generate as much force to overcome resistance. Generally as little as 30 minutes of noncontinuous exercise over the course of each day has beneficial effects and has been shown to lower the rate of heart attack by nearly 50 percent. While it is always advisable to follow a healthy diet, stop smoking, and lose weight, studies have clearly shown that fit, overweight people may actually be healthier overall than sedentary slender people. Thus, the benefits of moderate exercise are undeniable. Clinical Considerations in Vascular Homeostasis Any disorder that affects blood volume, vascular tone, or any other aspect of vascular functioning is likely to affect vascular homeostasis as well. That includes hypertension, hemorrhage, and shock. Hypertension and Hypotension Chronically elevated blood pressure is known clinically as hypertension. It is defined as chronic and persistent blood pressure measurements of 140/90 mm Hg or above. Pressures between 120/80 and 140/90 mm Hg are defined as prehypertension. About 68 million Americans currently suffer from hypertension. Unfortunately, hypertension is typically a silent disorder; therefore, hypertensive patients may fail to recognize the seriousness of their condition and fail to follow their treatment plan. The result is often a heart attack or stroke. Hypertension may also lead to an aneurism (ballooning of a blood vessel caused by a weakening of the wall), peripheral arterial disease (obstruction of vessels in peripheral regions of the body), chronic kidney disease, or heart failure. INTERACTIVE LINK Listen to this CDC podcast to learn about hypertension, often described as a “silent killer.” What steps can you take to reduce your risk of a heart attack or stroke? Hemorrhage Minor blood loss is managed by hemostasis and repair. Hemorrhage is a loss of blood that cannot be controlled by hemostatic mechanisms. Initially, the body responds to hemorrhage by initiating mechanisms aimed at increasing blood pressure and maintaining blood flow. Ultimately, however, blood volume will need to be restored, either through physiological processes or through medical intervention. In response to blood loss, stimuli from the baroreceptors trigger the cardiovascular centers to stimulate sympathetic responses to increase cardiac output and vasoconstriction. This typically prompts the heart rate to increase to about 180–200 contractions per minute, restoring cardiac output to normal levels. Vasoconstriction of the arterioles increases vascular resistance, whereas constriction of the veins increases venous return to the heart. Both of these steps will help increase blood pressure. Sympathetic stimulation also triggers the release of epinephrine and norepinephrine, which enhance both cardiac output and vasoconstriction. If blood loss were less than 20 percent of total blood volume, these responses together would usually return blood pressure to normal and redirect the remaining blood to the tissues. Additional endocrine involvement is necessary, however, to restore the lost blood volume. The angiotensin-renin-aldosterone mechanism stimulates the thirst center in the hypothalamus, which increases fluid consumption to help restore the lost blood. More importantly, it increases renal reabsorption of sodium and water, reducing water loss in urine output. The kidneys also increase the production of EPO, stimulating the formation of erythrocytes that not only deliver oxygen to the tissues but also increase overall blood volume. Figure 20.21 summarizes the responses to loss of blood volume. Figure 20.21 Homeostatic Responses to Loss of Blood Volume Circulatory Shock The loss of too much blood may lead to circulatory shock, a life-threatening condition in which the circulatory system is unable to maintain blood flow to adequately supply sufficient oxygen and other nutrients to the tissues to maintain cellular metabolism. It should not be confused with emotional or psychological shock. Typically, the patient in circulatory shock will demonstrate an increased heart rate but decreased blood pressure, but there are cases in which blood pressure will remain normal. Urine output will fall dramatically, and the patient may appear confused or lose consciousness. Urine output less than 1 mL/kg body weight/hour is cause for concern. Unfortunately, shock is an example of a positive-feedback loop that, if uncorrected, may lead to the death of the patient. There are several recognized forms of shock: - Hypovolemic shock in adults is typically caused by hemorrhage, although in children it may be caused by fluid losses related to severe vomiting or diarrhea. Other causes for hypovolemic shock include extensive burns, exposure to some toxins, and excessive urine loss related to diabetes insipidus or ketoacidosis. Typically, patients present with a rapid, almost tachycardic heart rate; a weak pulse often described as “thread;” cool, clammy skin, particularly in the extremities, due to restricted peripheral blood flow; rapid, shallow breathing; hypothermia; thirst; and dry mouth. Treatments generally involve providing intravenous fluids to restore the patient to normal function and various drugs such as dopamine, epinephrine, and norepinephrine to raise blood pressure. - Cardiogenic shock results from the inability of the heart to maintain cardiac output. Most often, it results from a myocardial infarction (heart attack), but it may also be caused by arrhythmias, valve disorders, cardiomyopathies, cardiac failure, or simply insufficient flow of blood through the cardiac vessels. Treatment involves repairing the damage to the heart or its vessels to resolve the underlying cause, rather than treating cardiogenic shock directly. - Vascular shock occurs when arterioles lose their normal muscular tone and dilate dramatically. It may arise from a variety of causes, and treatments almost always involve fluid replacement and medications, called inotropic or pressor agents, which restore tone to the muscles of the vessels. In addition, eliminating or at least alleviating the underlying cause of the condition is required. This might include antibiotics and antihistamines, or select steroids, which may aid in the repair of nerve damage. A common cause is sepsis (or septicemia), also called “blood poisoning,” which is a widespread bacterial infection that results in an organismal-level inflammatory response known as septic shock. Neurogenic shock is a form of vascular shock that occurs with cranial or spinal injuries that damage the cardiovascular centers in the medulla oblongata or the nervous fibers originating from this region. Anaphylactic shock is a severe allergic response that causes the widespread release of histamines, triggering vasodilation throughout the body. - Obstructive shock, as the name would suggest, occurs when a significant portion of the vascular system is blocked. It is not always recognized as a distinct condition and may be grouped with cardiogenic shock, including pulmonary embolism and cardiac tamponade. Treatments depend upon the underlying cause and, in addition to administering fluids intravenously, often include the administration of anticoagulants, removal of fluid from the pericardial cavity, or air from the thoracic cavity, and surgery as required. The most common cause is a pulmonary embolism, a clot that lodges in the pulmonary vessels and interrupts blood flow. Other causes include stenosis of the aortic valve; cardiac tamponade, in which excess fluid in the pericardial cavity interferes with the ability of the heart to fully relax and fill with blood (resulting in decreased preload); and a pneumothorax, in which an excessive amount of air is present in the thoracic cavity, outside of the lungs, which interferes with venous return, pulmonary function, and delivery of oxygen to the tissues. Circulatory Pathways - Identify the vessels through which blood travels within the pulmonary circuit, beginning from the right ventricle of the heart and ending at the left atrium - Create a flow chart showing the major systemic arteries through which blood travels from the aorta and its major branches, to the most significant arteries feeding into the right and left upper and lower limbs - Create a flow chart showing the major systemic veins through which blood travels from the feet to the right atrium of the heart Virtually every cell, tissue, organ, and system in the body is impacted by the circulatory system. This includes the generalized and more specialized functions of transport of materials, capillary exchange, maintaining health by transporting white blood cells and various immunoglobulins (antibodies), hemostasis, regulation of body temperature, and helping to maintain acid-base balance. In addition to these shared functions, many systems enjoy a unique relationship with the circulatory system. Figure 20.22 summarizes these relationships. Figure 20.22 Interaction of the Circulatory System with Other Body Systems As you learn about the vessels of the systemic and pulmonary circuits, notice that many arteries and veins share the same names, parallel one another throughout the body, and are very similar on the right and left sides of the body. These pairs of vessels will be traced through only one side of the body. Where differences occur in branching patterns or when vessels are singular, this will be indicated. For example, you will find a pair of femoral arteries and a pair of femoral veins, with one vessel on each side of the body. In contrast, some vessels closer to the midline of the body, such as the aorta, are unique. Moreover, some superficial veins, such as the great saphenous vein in the femoral region, have no arterial counterpart. Another phenomenon that can make the study of vessels challenging is that names of vessels can change with location. Like a street that changes name as it passes through an intersection, an artery or vein can change names as it passes an anatomical landmark. For example, the left subclavian artery becomes the axillary artery as it passes through the body wall and into the axillary region, and then becomes the brachial artery as it flows from the axillary region into the upper arm (or brachium). You will also find examples of anastomoses where two blood vessels that previously branched reconnect. Anastomoses are especially common in veins, where they help maintain blood flow even when one vessel is blocked or narrowed, although there are some important ones in the arteries supplying the brain. As you read about circular pathways, notice that there is an occasional, very large artery referred to as a trunk, a term indicating that the vessel gives rise to several smaller arteries. For example, the celiac trunk gives rise to the left gastric, common hepatic, and splenic arteries. As you study this section, imagine you are on a “Voyage of Discovery” similar to Lewis and Clark’s expedition in 1804–1806, which followed rivers and streams through unfamiliar territory, seeking a water route from the Atlantic to the Pacific Ocean. You might envision being inside a miniature boat, exploring the various branches of the circulatory system. This simple approach has proven effective for many students in mastering these major circulatory patterns. Another approach that works well for many students is to create simple line drawings similar to the ones provided, labeling each of the major vessels. It is beyond the scope of this text to name every vessel in the body. However, we will attempt to discuss the major pathways for blood and acquaint you with the major named arteries and veins in the body. Also, please keep in mind that individual variations in circulation patterns are not uncommon. INTERACTIVE LINK Visit this site for a brief summary of the arteries. Pulmonary Circulation Recall that blood returning from the systemic circuit enters the right atrium (Figure 20.23) via the superior and inferior venae cavae and the coronary sinus, which drains the blood supply of the heart muscle. These vessels will be described more fully later in this section. This blood is relatively low in oxygen and relatively high in carbon dioxide, since much of the oxygen has been extracted for use by the tissues and the waste gas carbon dioxide was picked up to be transported to the lungs for elimination. From the right atrium, blood moves into the right ventricle, which pumps it to the lungs for gas exchange. This system of vessels is referred to as the pulmonary circuit. The single vessel exiting the right ventricle is the pulmonary trunk. At the base of the pulmonary trunk is the pulmonary semilunar valve, which prevents backflow of blood into the right ventricle during ventricular diastole. As the pulmonary trunk reaches the superior surface of the heart, it curves posteriorly and rapidly bifurcates (divides) into two branches, a left and a right pulmonary artery. To prevent confusion between these vessels, it is important to refer to the vessel exiting the heart as the pulmonary trunk, rather than also calling it a pulmonary artery. The pulmonary arteries in turn branch many times within the lung, forming a series of smaller arteries and arterioles that eventually lead to the pulmonary capillaries. The pulmonary capillaries surround lung structures known as alveoli that are the sites of oxygen and carbon dioxide exchange. Once gas exchange is completed, oxygenated blood flows from the pulmonary capillaries into a series of pulmonary venules that eventually lead to a series of larger pulmonary veins. Four pulmonary veins, two on the left and two on the right, return blood to the left atrium. At this point, the pulmonary circuit is complete. Table 20.4 defines the major arteries and veins of the pulmonary circuit discussed in the text. Figure 20.23 Pulmonary Circuit Blood exiting from the right ventricle flows into the pulmonary trunk, which bifurcates into the two pulmonary arteries. These vessels branch to supply blood to the pulmonary capillaries, where gas exchange occurs within the lung alveoli. Blood returns via the pulmonary veins to the left atrium. Pulmonary Arteries and Veins \| Vessel \| Description \| \|---\|---\| \| Pulmonary trunk \| Single large vessel exiting the right ventricle that divides to form the right and left pulmonary arteries \| \| Pulmonary arteries \| Left and right vessels that form from the pulmonary trunk and lead to smaller arterioles and eventually to the pulmonary capillaries \| \| Pulmonary veins \| Two sets of paired vessels—one pair on each side—that are formed from the small venules, leading away from the pulmonary capillaries to flow into the left atrium \| Table 20.4 Overview of Systemic Arteries Blood relatively high in oxygen concentration is returned from the pulmonary circuit to the left atrium via the four pulmonary veins. From the left atrium, blood moves into the left ventricle, which pumps blood into the aorta. The aorta and its branches—the systemic arteries—send blood to virtually every organ of the body (Figure 20.24). Figure 20.24 Systemic Arteries The major systemic arteries shown here deliver oxygenated blood throughout the body. The Aorta The aorta is the largest artery in the body (Figure 20.25). It arises from the left ventricle and eventually descends to the abdominal region, where it bifurcates at the level of the fourth lumbar vertebra into the two common iliac arteries. The aorta consists of the ascending aorta, the aortic arch, and the descending aorta, which passes through the diaphragm and a landmark that divides into the superior thoracic and inferior abdominal components. Arteries originating from the aorta ultimately distribute blood to virtually all tissues of the body. At the base of the aorta is the aortic semilunar valve that prevents backflow of blood into the left ventricle while the heart is relaxing. After exiting the heart, the ascending aorta moves in a superior direction for approximately 5 cm and ends at the sternal angle. Following this ascent, it reverses direction, forming a graceful arc to the left, called the aortic arch. The aortic arch descends toward the inferior portions of the body and ends at the level of the intervertebral disk between the fourth and fifth thoracic vertebrae. Beyond this point, the descending aorta continues close to the bodies of the vertebrae and passes through an opening in the diaphragm known as the aortic hiatus. Superior to the diaphragm, the aorta is called the thoracic aorta, and inferior to the diaphragm, it is called the abdominal aorta. The abdominal aorta terminates when it bifurcates into the two common iliac arteries at the level of the fourth lumbar vertebra. See Figure 20.25 for an illustration of the ascending aorta, the aortic arch, and the initial segment of the descending aorta plus major branches; Table 20.5 summarizes the structures of the aorta. Figure 20.25 Aorta The aorta has distinct regions, including the ascending aorta, aortic arch, and the descending aorta, which includes the thoracic and abdominal regions. Components of the Aorta \| Vessel \| Description \| \|---\|---\| \| Aorta \| Largest artery in the body, originating from the left ventricle and descending to the abdominal region, where it bifurcates into the common iliac arteries at the level of the fourth lumbar vertebra; arteries originating from the aorta distribute blood to virtually all tissues of the body \| \| Ascending aorta \| Initial portion of the aorta, rising superiorly from the left ventricle for a distance of approximately 5 cm \| \| Aortic arch \| Graceful arc to the left that connects the ascending aorta to the descending aorta; ends at the intervertebral disk between the fourth and fifth thoracic vertebrae \| \| Descending aorta \| Portion of the aorta that continues inferiorly past the end of the aortic arch; subdivided into the thoracic aorta and the abdominal aorta \| \| Thoracic aorta \| Portion of the descending aorta superior to the aortic hiatus \| \| Abdominal aorta \| Portion of the aorta inferior to the aortic hiatus and superior to the common iliac arteries \| Table 20.5 Coronary Circulation The first vessels that branch from the ascending aorta are the paired coronary arteries (see Figure 20.25), which arise from two of the three sinuses in the ascending aorta just superior to the aortic semilunar valve. These sinuses contain the aortic baroreceptors and chemoreceptors critical to maintain cardiac function. The left coronary artery arises from the left posterior aortic sinus. The right coronary artery arises from the anterior aortic sinus. Normally, the right posterior aortic sinus does not give rise to a vessel. The coronary arteries encircle the heart, forming a ring-like structure that divides into the next level of branches that supplies blood to the heart tissues. (Seek additional content for more detail on cardiac circulation.) Aortic Arch Branches There are three major branches of the aortic arch: the brachiocephalic artery, the left common carotid artery, and the left subclavian (literally “under the clavicle”) artery. As you would expect based upon proximity to the heart, each of these vessels is classified as an elastic artery. The brachiocephalic artery is located only on the right side of the body; there is no corresponding artery on the left. The brachiocephalic artery branches into the right subclavian artery and the right common carotid artery. The left subclavian and left common carotid arteries arise independently from the aortic arch but otherwise follow a similar pattern and distribution to the corresponding arteries on the right side (see Figure 20.23). Each subclavian artery supplies blood to the arms, chest, shoulders, back, and central nervous system. It then gives rise to three major branches: the internal thoracic artery, the vertebral artery, and the thyrocervical artery. The internal thoracic artery, or mammary artery, supplies blood to the thymus, the pericardium of the heart, and the anterior chest wall. The vertebral arterypasses through the vertebral foramen in the cervical vertebrae and then through the foramen magnum into the cranial cavity to supply blood to the brain and spinal cord. The paired vertebral arteries join together to form the large basilar artery at the base of the medulla oblongata. This is an example of an anastomosis. The subclavian artery also gives rise to the thyrocervical artery that provides blood to the thyroid, the cervical region of the neck, and the upper back and shoulder. The common carotid artery divides into internal and external carotid arteries. The right common carotid artery arises from the brachiocephalic artery and the left common carotid artery arises directly from the aortic arch. The external carotid artery supplies blood to numerous structures within the face, lower jaw, neck, esophagus, and larynx. These branches include the lingual, facial, occipital, maxillary, and superficial temporal arteries. The internal carotid artery initially forms an expansion known as the carotid sinus, containing the carotid baroreceptors and chemoreceptors. Like their counterparts in the aortic sinuses, the information provided by these receptors is critical to maintaining cardiovascular homeostasis (see Figure 20.23). The internal carotid arteries along with the vertebral arteries are the two primary suppliers of blood to the human brain. Given the central role and vital importance of the brain to life, it is critical that blood supply to this organ remains uninterrupted. Recall that blood flow to the brain is remarkably constant, with approximately 20 percent of blood flow directed to this organ at any given time. When blood flow is interrupted, even for just a few seconds, a transient ischemic attack (TIA), or mini-stroke, may occur, resulting in loss of consciousness or temporary loss of neurological function. In some cases, the damage may be permanent. Loss of blood flow for longer periods, typically between 3 and 4 minutes, will likely produce irreversible brain damage or a stroke, also called a cerebrovascular accident (CVA). The locations of the arteries in the brain not only provide blood flow to the brain tissue but also prevent interruption in the flow of blood. Both the carotid and vertebral arteries branch once they enter the cranial cavity, and some of these branches form a structure known as the arterial circle (or circle of Willis), an anastomosis that is remarkably like a traffic circle that sends off branches (in this case, arterial branches to the brain). As a rule, branches to the anterior portion of the cerebrum are normally fed by the internal carotid arteries; the remainder of the brain receives blood flow from branches associated with the vertebral arteries. The internal carotid artery continues through the carotid canal of the temporal bone and enters the base of the brain through the carotid foramen where it gives rise to several branches (Figure 20.26 and Figure 20.27). One of these branches is the anterior cerebral artery that supplies blood to the frontal lobe of the cerebrum. Another branch, the middle cerebral artery, supplies blood to the temporal and parietal lobes, which are the most common sites of CVAs. The ophthalmic artery, the third major branch, provides blood to the eyes. The right and left anterior cerebral arteries join together to form an anastomosis called the anterior communicating artery. The initial segments of the anterior cerebral arteries and the anterior communicating artery form the anterior portion of the arterial circle. The posterior portion of the arterial circle is formed by a left and a right posterior communicating artery that branches from the posterior cerebral artery, which arises from the basilar artery. It provides blood to the posterior portion of the cerebrum and brain stem. The basilar artery is an anastomosis that begins at the junction of the two vertebral arteries and sends branches to the cerebellum and brain stem. It flows into the posterior cerebral arteries. Table 20.6 summarizes the aortic arch branches, including the major branches supplying the brain. Figure 20.26 Arteries Supplying the Head and Neck The common carotid artery gives rise to the external and internal carotid arteries. The external carotid artery remains superficial and gives rise to many arteries of the head. The internal carotid artery first forms the carotid sinus and then reaches the brain via the carotid canal and carotid foramen, emerging into the cranium via the foramen lacerum. The vertebral artery branches from the subclavian artery and passes through the transverse foramen in the cervical vertebrae, entering the base of the skull at the vertebral foramen. The subclavian artery continues toward the arm as the axillary artery. Figure 20.27 Arteries Serving the Brain This inferior view shows the network of arteries serving the brain. The structure is referred to as the arterial circle or circle of Willis. Aortic Arch Branches and Brain Circulation \| Vessel \| Description \| \|---\|---\| \| Brachiocephalic artery \| Single vessel located on the right side of the body; the first vessel branching from the aortic arch; gives rise to the right subclavian artery and the right common carotid artery; supplies blood to the head, neck, upper limb, and wall of the thoracic region \| \| Subclavian artery \| The right subclavian artery arises from the brachiocephalic artery while the left subclavian artery arises from the aortic arch; gives rise to the internal thoracic, vertebral, and thyrocervical arteries; supplies blood to the arms, chest, shoulders, back, and central nervous system \| \| Internal thoracic artery \| Also called the mammary artery; arises from the subclavian artery; supplies blood to the thymus, pericardium of the heart, and anterior chest wall \| \| Vertebral artery \| Arises from the subclavian artery and passes through the vertebral foramen through the foramen magnum to the brain; joins with the internal carotid artery to form the arterial circle; supplies blood to the brain and spinal cord \| \| Thyrocervical artery \| Arises from the subclavian artery; supplies blood to the thyroid, the cervical region, the upper back, and shoulder \| \| Common carotid artery \| The right common carotid artery arises from the brachiocephalic artery and the left common carotid artery arises from the aortic arch; each gives rise to the external and internal carotid arteries; supplies the respective sides of the head and neck \| \| External carotid artery \| Arises from the common carotid artery; supplies blood to numerous structures within the face, lower jaw, neck, esophagus, and larynx \| \| Internal carotid artery \| Arises from the common carotid artery and begins with the carotid sinus; goes through the carotid canal of the temporal bone to the base of the brain; combines with the branches of the vertebral artery, forming the arterial circle; supplies blood to the brain \| \| Arterial circle or circle of Willis \| An anastomosis located at the base of the brain that ensures continual blood supply; formed from the branches of the internal carotid and vertebral arteries; supplies blood to the brain \| \| Anterior cerebral artery \| Arises from the internal carotid artery; supplies blood to the frontal lobe of the cerebrum \| \| Middle cerebral artery \| Another branch of the internal carotid artery; supplies blood to the temporal and parietal lobes of the cerebrum \| \| Ophthalmic artery \| Branch of the internal carotid artery; supplies blood to the eyes \| \| Anterior communicating artery \| An anastomosis of the right and left internal carotid arteries; supplies blood to the brain \| \| Posterior communicating artery \| Branches of the posterior cerebral artery that form part of the posterior portion of the arterial circle; supplies blood to the brain \| \| Posterior cerebral artery \| Branch of the basilar artery that forms a portion of the posterior segment of the arterial circle of Willis; supplies blood to the posterior portion of the cerebrum and brain stem \| \| Basilar artery \| Formed from the fusion of the two vertebral arteries; sends branches to the cerebellum, brain stem, and the posterior cerebral arteries; the main blood supply to the brain stem \| Table 20.6 Thoracic Aorta and Major Branches The thoracic aorta begins at the level of vertebra T5 and continues through to the diaphragm at the level of T12, initially traveling within the mediastinum to the left of the vertebral column. As it passes through the thoracic region, the thoracic aorta gives rise to several branches, which are collectively referred to as visceral branches and parietal branches (Figure 20.28). Those branches that supply blood primarily to visceral organs are known as the visceral branches and include the bronchial arteries, pericardial arteries, esophageal arteries, and the mediastinal arteries, each named after the tissues it supplies. Each bronchial artery (typically two on the left and one on the right) supplies systemic blood to the lungs and visceral pleura, in addition to the blood pumped to the lungs for oxygenation via the pulmonary circuit. The bronchial arteries follow the same path as the respiratory branches, beginning with the bronchi and ending with the bronchioles. There is considerable, but not total, intermingling of the systemic and pulmonary blood at anastomoses in the smaller branches of the lungs. This may sound incongruous—that is, the mixing of systemic arterial blood high in oxygen with the pulmonary arterial blood lower in oxygen—but the systemic vessels also deliver nutrients to the lung tissue just as they do elsewhere in the body. The mixed blood drains into typical pulmonary veins, whereas the bronchial artery branches remain separate and drain into bronchial veins described later. Each pericardial artery supplies blood to the pericardium, the esophageal artery provides blood to the esophagus, and the mediastinal artery provides blood to the mediastinum. The remaining thoracic aorta branches are collectively referred to as parietal branches or somatic branches, and include the intercostal and superior phrenic arteries. Each intercostal artery provides blood to the muscles of the thoracic cavity and vertebral column. The superior phrenic artery provides blood to the superior surface of the diaphragm. Table 20.7 lists the arteries of the thoracic region. Figure 20.28 Arteries of the Thoracic and Abdominal Regions The thoracic aorta gives rise to the arteries of the visceral and parietal branches. Arteries of the Thoracic Region \| Vessel \| Description \| \|---\|---\| \| Visceral branches \| A group of arterial branches of the thoracic aorta; supplies blood to the viscera (i.e., organs) of the thorax \| \| Bronchial artery \| Systemic branch from the aorta that provides oxygenated blood to the lungs; this blood supply is in addition to the pulmonary circuit that brings blood for oxygenation \| \| Pericardial artery \| Branch of the thoracic aorta; supplies blood to the pericardium \| \| Esophageal artery \| Branch of the thoracic aorta; supplies blood to the esophagus \| \| Mediastinal artery \| Branch of the thoracic aorta; supplies blood to the mediastinum \| \| Parietal branches \| Also called somatic branches, a group of arterial branches of the thoracic aorta; include those that supply blood to the thoracic wall, vertebral column, and the superior surface of the diaphragm \| \| Intercostal artery \| Branch of the thoracic aorta; supplies blood to the muscles of the thoracic cavity and vertebral column \| \| Superior phrenic artery \| Branch of the thoracic aorta; supplies blood to the superior surface of the diaphragm \| Table 20.7 Abdominal Aorta and Major Branches After crossing through the diaphragm at the aortic hiatus, the thoracic aorta is called the abdominal aorta (see Figure 20.28). This vessel remains to the left of the vertebral column and is embedded in adipose tissue behind the peritoneal cavity. It formally ends at approximately the level of vertebra L4, where it bifurcates to form the common iliac arteries. Before this division, the abdominal aorta gives rise to several important branches. A single celiac trunk (artery) emerges and divides into the left gastric artery to supply blood to the stomach and esophagus, the splenic artery to supply blood to the spleen, and the common hepatic artery, which in turn gives rise to the hepatic artery proper to supply blood to the liver, the right gastric artery to supply blood to the stomach, the cystic artery to supply blood to the gall bladder, and several branches, one to supply blood to the duodenum and another to supply blood to the pancreas. Two additional single vessels arise from the abdominal aorta. These are the superior and inferior mesenteric arteries. The superior mesenteric artery arises approximately 2.5 cm after the celiac trunk and branches into several major vessels that supply blood to the small intestine (duodenum, jejunum, and ileum), the pancreas, and a majority of the large intestine. The inferior mesenteric artery supplies blood to the distal segment of the large intestine, including the rectum. It arises approximately 5 cm superior to the common iliac arteries. In addition to these single branches, the abdominal aorta gives rise to several significant paired arteries along the way. These include the inferior phrenic arteries, the adrenal arteries, the renal arteries, the gonadal arteries, and the lumbar arteries. Each inferior phrenic artery is a counterpart of a superior phrenic artery and supplies blood to the inferior surface of the diaphragm. The adrenal artery supplies blood to the adrenal (suprarenal) glands and arises near the superior mesenteric artery. Each renal arterybranches approximately 2.5 cm inferior to the superior mesenteric arteries and supplies a kidney. The right renal artery is longer than the left since the aorta lies to the left of the vertebral column and the vessel must travel a greater distance to reach its target. Renal arteries branch repeatedly to supply blood to the kidneys. Each gonadal artery supplies blood to the gonads, or reproductive organs, and is also described as either an ovarian artery or a testicular artery (internal spermatic), depending upon the sex of the individual. An ovarian artery supplies blood to an ovary, uterine (Fallopian) tube, and the uterus, and is located within the suspensory ligament of the uterus. It is considerably shorter than a testicular artery, which ultimately travels outside the body cavity to the testes, forming one component of the spermatic cord. The gonadal arteries arise inferior to the renal arteries and are generally retroperitoneal. The ovarian artery continues to the uterus where it forms an anastomosis with the uterine artery that supplies blood to the uterus. Both the uterine arteries and vaginal arteries, which distribute blood to the vagina, are branches of the internal iliac artery. The four paired lumbar arteries are the counterparts of the intercostal arteries and supply blood to the lumbar region, the abdominal wall, and the spinal cord. In some instances, a fifth pair of lumbar arteries emerges from the median sacral artery. The aorta divides at approximately the level of vertebra L4 into a left and a right common iliac artery but continues as a small vessel, the median sacral artery, into the sacrum. The common iliac arteries provide blood to the pelvic region and ultimately to the lower limbs. They split into external and internal iliac arteries approximately at the level of the lumbar-sacral articulation. Each internal iliac artery sends branches to the urinary bladder, the walls of the pelvis, the external genitalia, and the medial portion of the femoral region. In females, they also provide blood to the uterus and vagina. The much larger external iliac artery supplies blood to each of the lower limbs. Figure 20.29 shows the distribution of the major branches of the aorta into the thoracic and abdominal regions. Figure 20.30 shows the distribution of the major branches of the common iliac arteries. Table 20.8 summarizes the major branches of the abdominal aorta. Figure 20.29 Major Branches of the Aorta The flow chart summarizes the distribution of the major branches of the aorta into the thoracic and abdominal regions. Figure 20.30 Major Branches of the Iliac Arteries The flow chart summarizes the distribution of the major branches of the common iliac arteries into the pelvis and lower limbs. The left side follows a similar pattern to the right. Vessels of the Abdominal Aorta \| Vessel \| Description \| \|---\|---\| \| Celiac trunk \| Also called the celiac artery; a major branch of the abdominal aorta; gives rise to the left gastric artery, the splenic artery, and the common hepatic artery that forms the hepatic artery to the liver, the right gastric artery to the stomach, and the cystic artery to the gall bladder \| \| Left gastric artery \| Branch of the celiac trunk; supplies blood to the stomach \| \| Splenic artery \| Branch of the celiac trunk; supplies blood to the spleen \| \| Common hepatic artery \| Branch of the celiac trunk that forms the hepatic artery, the right gastric artery, and the cystic artery \| \| Hepatic artery proper \| Branch of the common hepatic artery; supplies systemic blood to the liver \| \| Right gastric artery \| Branch of the common hepatic artery; supplies blood to the stomach \| \| Cystic artery \| Branch of the common hepatic artery; supplies blood to the gall bladder \| \| Superior mesenteric artery \| Branch of the abdominal aorta; supplies blood to the small intestine (duodenum, jejunum, and ileum), the pancreas, and a majority of the large intestine \| \| Inferior mesenteric artery \| Branch of the abdominal aorta; supplies blood to the distal segment of the large intestine and rectum \| \| Inferior phrenic arteries \| Branches of the abdominal aorta; supply blood to the inferior surface of the diaphragm \| \| Adrenal artery \| Branch of the abdominal aorta; supplies blood to the adrenal (suprarenal) glands \| \| Renal artery \| Branch of the abdominal aorta; supplies each kidney \| \| Gonadal artery \| Branch of the abdominal aorta; supplies blood to the gonads or reproductive organs; also described as ovarian arteries or testicular arteries, depending upon the sex of the individual \| \| Ovarian artery \| Branch of the abdominal aorta; supplies blood to ovary, uterine (Fallopian) tube, and uterus \| \| Testicular artery \| Branch of the abdominal aorta; ultimately travels outside the body cavity to the testes and forms one component of the spermatic cord \| \| Lumbar arteries \| Branches of the abdominal aorta; supply blood to the lumbar region, the abdominal wall, and spinal cord \| \| Common iliac artery \| Branch of the aorta that leads to the internal and external iliac arteries \| \| Median sacral artery \| Continuation of the aorta into the sacrum \| \| Internal iliac artery \| Branch from the common iliac arteries; supplies blood to the urinary bladder, walls of the pelvis, external genitalia, and the medial portion of the femoral region; in females, also provides blood to the uterus and vagina \| \| External iliac artery \| Branch of the common iliac artery that leaves the body cavity and becomes a femoral artery; supplies blood to the lower limbs \| Table 20.8 Arteries Serving the Upper Limbs As the subclavian artery exits the thorax into the axillary region, it is renamed the axillary artery. Although it does branch and supply blood to the region near the head of the humerus (via the humeral circumflex arteries), the majority of the vessel continues into the upper arm, or brachium, and becomes the brachial artery (Figure 20.31). The brachial artery supplies blood to much of the brachial region and divides at the elbow into several smaller branches, including the deep brachial arteries, which provide blood to the posterior surface of the arm, and the ulnar collateral arteries, which supply blood to the region of the elbow. As the brachial artery approaches the coronoid fossa, it bifurcates into the radial and ulnar arteries, which continue into the forearm, or antebrachium. The radial artery and ulnar artery parallel their namesake bones, giving off smaller branches until they reach the wrist, or carpal region. At this level, they fuse to form the superficial and deep palmar arches that supply blood to the hand, as well as the digital arteries that supply blood to the digits. Figure 20.32 shows the distribution of systemic arteries from the heart into the upper limb. Table 20.9 summarizes the arteries serving the upper limbs. Figure 20.31 Major Arteries Serving the Thorax and Upper Limb The arteries that supply blood to the arms and hands are extensions of the subclavian arteries. Figure 20.32 Major Arteries of the Upper Limb The flow chart summarizes the distribution of the major arteries from the heart into the upper limb. Arteries Serving the Upper Limbs \| Vessel \| Description \| \|---\|---\| \| Axillary artery \| Continuation of the subclavian artery as it penetrates the body wall and enters the axillary region; supplies blood to the region near the head of the humerus (humeral circumflex arteries); the majority of the vessel continues into the brachium and becomes the brachial artery \| \| Brachial artery \| Continuation of the axillary artery in the brachium; supplies blood to much of the brachial region; gives off several smaller branches that provide blood to the posterior surface of the arm in the region of the elbow; bifurcates into the radial and ulnar arteries at the coronoid fossa \| \| Radial artery \| Formed at the bifurcation of the brachial artery; parallels the radius; gives off smaller branches until it reaches the carpal region where it fuses with the ulnar artery to form the superficial and deep palmar arches; supplies blood to the lower arm and carpal region \| \| Ulnar artery \| Formed at the bifurcation of the brachial artery; parallels the ulna; gives off smaller branches until it reaches the carpal region where it fuses with the radial artery to form the superficial and deep palmar arches; supplies blood to the lower arm and carpal region \| \| Palmar arches (superficial and deep) \| Formed from anastomosis of the radial and ulnar arteries; supply blood to the hand and digital arteries \| \| Digital arteries \| Formed from the superficial and deep palmar arches; supply blood to the digits \| Table 20.9 Arteries Serving the Lower Limbs The external iliac artery exits the body cavity and enters the femoral region of the lower leg (Figure 20.33). As it passes through the body wall, it is renamed the femoral artery. It gives off several smaller branches as well as the lateral deep femoral artery that in turn gives rise to a lateral circumflex artery. These arteries supply blood to the deep muscles of the thigh as well as ventral and lateral regions of the integument. The femoral artery also gives rise to the genicular artery, which provides blood to the region of the knee. As the femoral artery passes posterior to the knee near the popliteal fossa, it is called the popliteal artery. The popliteal artery branches into the anterior and posterior tibial arteries. The anterior tibial artery is located between the tibia and fibula, and supplies blood to the muscles and integument of the anterior tibial region. Upon reaching the tarsal region, it becomes the dorsalis pedis artery, which branches repeatedly and provides blood to the tarsal and dorsal regions of the foot. The posterior tibial artery provides blood to the muscles and integument on the posterior surface of the tibial region. The fibular or peroneal artery branches from the posterior tibial artery. It bifurcates and becomes the medial plantar artery and lateral plantar artery, providing blood to the plantar surfaces. There is an anastomosis with the dorsalis pedis artery, and the medial and lateral plantar arteries form two arches called the dorsal arch (also called the arcuate arch) and the plantar arch, which provide blood to the remainder of the foot and toes. Figure 20.34 shows the distribution of the major systemic arteries in the lower limb. Table 20.10 summarizes the major systemic arteries discussed in the text. Figure 20.33 Major Arteries Serving the Lower Limb Major arteries serving the lower limb are shown in anterior and posterior views. Figure 20.34 Systemic Arteries of the Lower Limb The flow chart summarizes the distribution of the systemic arteries from the external iliac artery into the lower limb. Arteries Serving the Lower Limbs \| Vessel \| Description \| \|---\|---\| \| Femoral artery \| Continuation of the external iliac artery after it passes through the body cavity; divides into several smaller branches, the lateral deep femoral artery, and the genicular artery; becomes the popliteal artery as it passes posterior to the knee \| \| Deep femoral artery \| Branch of the femoral artery; gives rise to the lateral circumflex arteries \| \| Lateral circumflex artery \| Branch of the deep femoral artery; supplies blood to the deep muscles of the thigh and the ventral and lateral regions of the integument \| \| Genicular artery \| Branch of the femoral artery; supplies blood to the region of the knee \| \| Popliteal artery \| Continuation of the femoral artery posterior to the knee; branches into the anterior and posterior tibial arteries \| \| Anterior tibial artery \| Branches from the popliteal artery; supplies blood to the anterior tibial region; becomes the dorsalis pedis artery \| \| Dorsalis pedis artery \| Forms from the anterior tibial artery; branches repeatedly to supply blood to the tarsal and dorsal regions of the foot \| \| Posterior tibial artery \| Branches from the popliteal artery and gives rise to the fibular or peroneal artery; supplies blood to the posterior tibial region \| \| Medial plantar artery \| Arises from the bifurcation of the posterior tibial arteries; supplies blood to the medial plantar surfaces of the foot \| \| Lateral plantar artery \| Arises from the bifurcation of the posterior tibial arteries; supplies blood to the lateral plantar surfaces of the foot \| \| Dorsal or arcuate arch \| Formed from the anastomosis of the dorsalis pedis artery and the medial and plantar arteries; branches supply the distal portions of the foot and digits \| \| Plantar arch \| Formed from the anastomosis of the dorsalis pedis artery and the medial and plantar arteries; branches supply the distal portions of the foot and digits \| Table 20.10 Overview of Systemic Veins Systemic veins return blood to the right atrium. Since the blood has already passed through the systemic capillaries, it will be relatively low in oxygen concentration. In many cases, there will be veins draining organs and regions of the body with the same name as the arteries that supplied these regions and the two often parallel one another. This is often described as a “complementary” pattern. However, there is a great deal more variability in the venous circulation than normally occurs in the arteries. For the sake of brevity and clarity, this text will discuss only the most commonly encountered patterns. However, keep this variation in mind when you move from the classroom to clinical practice. In both the neck and limb regions, there are often both superficial and deeper levels of veins. The deeper veins generally correspond to the complementary arteries. The superficial veins do not normally have direct arterial counterparts, but in addition to returning blood, they also make contributions to the maintenance of body temperature. When the ambient temperature is warm, more blood is diverted to the superficial veins where heat can be more easily dissipated to the environment. In colder weather, there is more constriction of the superficial veins and blood is diverted deeper where the body can retain more of the heat. The “Voyage of Discovery” analogy and stick drawings mentioned earlier remain valid techniques for the study of systemic veins, but veins present a more difficult challenge because there are numerous anastomoses and multiple branches. It is like following a river with many tributaries and channels, several of which interconnect. Tracing blood flow through arteries follows the current in the direction of blood flow, so that we move from the heart through the large arteries and into the smaller arteries to the capillaries. From the capillaries, we move into the smallest veins and follow the direction of blood flow into larger veins and back to the heart. Figure 20.35 outlines the path of the major systemic veins. INTERACTIVE LINK Visit this site for a brief online summary of the veins. Figure 20.35 Major Systemic Veins of the Body The major systemic veins of the body are shown here in an anterior view. The right atrium receives all of the systemic venous return. Most of the blood flows into either the superior vena cava or inferior vena cava. If you draw an imaginary line at the level of the diaphragm, systemic venous circulation from above that line will generally flow into the superior vena cava; this includes blood from the head, neck, chest, shoulders, and upper limbs. The exception to this is that most venous blood flow from the coronary veins flows directly into the coronary sinus and from there directly into the right atrium. Beneath the diaphragm, systemic venous flow enters the inferior vena cava, that is, blood from the abdominal and pelvic regions and the lower limbs. The Superior Vena Cava The superior vena cava drains most of the body superior to the diaphragm (Figure 20.36). On both the left and right sides, the subclavian vein forms when the axillary vein passes through the body wall from the axillary region. It fuses with the external and internal jugular veins from the head and neck to form the brachiocephalic vein. Each vertebral vein also flows into the brachiocephalic vein close to this fusion. These veins arise from the base of the brain and the cervical region of the spinal cord, and flow largely through the intervertebral foramina in the cervical vertebrae. They are the counterparts of the vertebral arteries. Each internal thoracic vein, also known as an internal mammary vein, drains the anterior surface of the chest wall and flows into the brachiocephalic vein. The remainder of the blood supply from the thorax drains into the azygos vein. Each intercostal vein drains muscles of the thoracic wall, each esophageal vein delivers blood from the inferior portions of the esophagus, each bronchial vein drains the systemic circulation from the lungs, and several smaller veins drain the mediastinal region. Bronchial veins carry approximately 13 percent of the blood that flows into the bronchial arteries; the remainder intermingles with the pulmonary circulation and returns to the heart via the pulmonary veins. These veins flow into the azygos vein, and with the smaller hemiazygos vein (hemi- = “half”) on the left of the vertebral column, drain blood from the thoracic region. The hemiazygos vein does not drain directly into the superior vena cava but enters the brachiocephalic vein via the superior intercostal vein. The azygos vein passes through the diaphragm from the thoracic cavity on the right side of the vertebral column and begins in the lumbar region of the thoracic cavity. It flows into the superior vena cava at approximately the level of T2, making a significant contribution to the flow of blood. It combines with the two large left and right brachiocephalic veins to form the superior vena cava. Table 20.11 summarizes the veins of the thoracic region that flow into the superior vena cava. Figure 20.36 Veins of the Thoracic and Abdominal Regions Veins of the thoracic and abdominal regions drain blood from the area above the diaphragm, returning it to the right atrium via the superior vena cava. Veins of the Thoracic Region \| Vessel \| Description \| \|---\|---\| \| Superior vena cava \| Large systemic vein; drains blood from most areas superior to the diaphragm; empties into the right atrium \| \| Subclavian vein \| Located deep in the thoracic cavity; formed by the axillary vein as it enters the thoracic cavity from the axillary region; drains the axillary and smaller local veins near the scapular region and leads to the brachiocephalic vein \| \| Brachiocephalic veins \| Pair of veins that form from a fusion of the external and internal jugular veins and the subclavian vein; subclavian, external and internal jugulars, vertebral, and internal thoracic veins flow into it; drain the upper thoracic region and lead to the superior vena cava \| \| Vertebral vein \| Arises from the base of the brain and the cervical region of the spinal cord; passes through the intervertebral foramina in the cervical vertebrae; drains smaller veins from the cranium, spinal cord, and vertebrae, and leads to the brachiocephalic vein; counterpart of the vertebral artery \| \| Internal thoracic veins \| Also called internal mammary veins; drain the anterior surface of the chest wall and lead to the brachiocephalic vein \| \| Intercostal vein \| Drains the muscles of the thoracic wall and leads to the azygos vein \| \| Esophageal vein \| Drains the inferior portions of the esophagus and leads to the azygos vein \| \| Bronchial vein \| Drains the systemic circulation from the lungs and leads to the azygos vein \| \| Azygos vein \| Originates in the lumbar region and passes through the diaphragm into the thoracic cavity on the right side of the vertebral column; drains blood from the intercostal veins, esophageal veins, bronchial veins, and other veins draining the mediastinal region, and leads to the superior vena cava \| \| Hemiazygos vein \| Smaller vein complementary to the azygos vein; drains the esophageal veins from the esophagus and the left intercostal veins, and leads to the brachiocephalic vein via the superior intercostal vein \| Table 20.11 Veins of the Head and Neck Blood from the brain and the superficial facial vein flow into each internal jugular vein (Figure 20.37). Blood from the more superficial portions of the head, scalp, and cranial regions, including the temporal vein and maxillary vein, flow into each external jugular vein. Although the external and internal jugular veins are separate vessels, there are anastomoses between them close to the thoracic region. Blood from the external jugular vein empties into the subclavian vein. Table 20.12 summarizes the major veins of the head and neck. Major Veins of the Head and Neck \| Vessel \| Description \| \|---\|---\| \| Internal jugular vein \| Parallel to the common carotid artery, which is more or less its counterpart, and passes through the jugular foramen and canal; primarily drains blood from the brain, receives the superficial facial vein, and empties into the subclavian vein \| \| Temporal vein \| Drains blood from the temporal region and flows into the external jugular vein \| \| Maxillary vein \| Drains blood from the maxillary region and flows into the external jugular vein \| \| External jugular vein \| Drains blood from the more superficial portions of the head, scalp, and cranial regions, and leads to the subclavian vein \| Table 20.12 Venous Drainage of the Brain Circulation to the brain is both critical and complex (see Figure 20.37). Many smaller veins of the brain stem and the superficial veins of the cerebrum lead to larger vessels referred to as intracranial sinuses. These include the superior and inferior sagittal sinuses, straight sinus, cavernous sinuses, left and right sinuses, the petrosal sinuses, and the occipital sinuses. Ultimately, sinuses will lead back to either the inferior jugular vein or vertebral vein. Most of the veins on the superior surface of the cerebrum flow into the largest of the sinuses, the superior sagittal sinus. It is located midsagittally between the meningeal and periosteal layers of the dura mater within the falx cerebri and, at first glance in images or models, can be mistaken for the subarachnoid space. Most reabsorption of cerebrospinal fluid occurs via the chorionic villi (arachnoid granulations) into the superior sagittal sinus. Blood from most of the smaller vessels originating from the inferior cerebral veins flows into the great cerebral vein and into the straight sinus. Other cerebral veins and those from the eye socket flow into the cavernous sinus, which flows into the petrosal sinus and then into the internal jugular vein. The occipital sinus, sagittal sinus, and straight sinuses all flow into the left and right transverse sinuses near the lambdoid suture. The transverse sinuses in turn flow into the sigmoid sinuses that pass through the jugular foramen and into the internal jugular vein. The internal jugular vein flows parallel to the common carotid artery and is more or less its counterpart. It empties into the brachiocephalic vein. The veins draining the cervical vertebrae and the posterior surface of the skull, including some blood from the occipital sinus, flow into the vertebral veins. These parallel the vertebral arteries and travel through the transverse foramina of the cervical vertebrae. The vertebral veins also flow into the brachiocephalic veins. Table 20.13 summarizes the major veins of the brain. Figure 20.37 Veins of the Head and Neck This left lateral view shows the veins of the head and neck, including the intercranial sinuses. Major Veins of the Brain \| Vessel \| Description \| \|---\|---\| \| Superior sagittal sinus \| Enlarged vein located midsagittally between the meningeal and periosteal layers of the dura mater within the falx cerebri; receives most of the blood drained from the superior surface of the cerebrum and leads to the inferior jugular vein and the vertebral vein \| \| Great cerebral vein \| Receives most of the smaller vessels from the inferior cerebral veins and leads to the straight sinus \| \| Straight sinus \| Enlarged vein that drains blood from the brain; receives most of the blood from the great cerebral vein and leads to the left or right transverse sinus \| \| Cavernous sinus \| Enlarged vein that receives blood from most of the other cerebral veins and the eye socket, and leads to the petrosal sinus \| \| Petrosal sinus \| Enlarged vein that receives blood from the cavernous sinus and leads into the internal jugular veins \| \| Occipital sinus \| Enlarged vein that drains the occipital region near the falx cerebelli and leads to the left and right transverse sinuses, and also the vertebral veins \| \| Transverse sinuses \| Pair of enlarged veins near the lambdoid suture that drains the occipital, sagittal, and straight sinuses, and leads to the sigmoid sinuses \| \| Sigmoid sinuses \| Enlarged vein that receives blood from the transverse sinuses and leads through the jugular foramen to the internal jugular vein \| Table 20.13 Veins Draining the Upper Limbs The digital veins in the fingers come together in the hand to form the palmar venous arches (Figure 20.38). From here, the veins come together to form the radial vein, the ulnar vein, and the median antebrachial vein. The radial vein and the ulnar vein parallel the bones of the forearm and join together at the antebrachium to form the brachial vein, a deep vein that flows into the axillary vein in the brachium. The median antebrachial vein parallels the ulnar vein, is more medial in location, and joins the basilic vein in the forearm. As the basilic vein reaches the antecubital region, it gives off a branch called the median cubital vein that crosses at an angle to join the cephalic vein. The median cubital vein is the most common site for drawing venous blood in humans. The basilic vein continues through the arm medially and superficially to the axillary vein. The cephalic vein begins in the antebrachium and drains blood from the superficial surface of the arm into the axillary vein. It is extremely superficial and easily seen along the surface of the biceps brachii muscle in individuals with good muscle tone and in those without excessive subcutaneous adipose tissue in the arms. The subscapular vein drains blood from the subscapular region and joins the cephalic vein to form the axillary vein. As it passes through the body wall and enters the thorax, the axillary vein becomes the subclavian vein. Many of the larger veins of the thoracic and abdominal region and upper limb are further represented in the flow chart in Figure 20.39. Table 20.14 summarizes the veins of the upper limbs. Figure 20.38 Veins of the Upper Limb This anterior view shows the veins that drain the upper limb. Figure 20.39 Veins Flowing into the Superior Vena Cava The flow chart summarizes the distribution of the veins flowing into the superior vena cava. Veins of the Upper Limbs \| Vessel \| Description \| \|---\|---\| \| Digital veins \| Drain the digits and lead to the palmar arches of the hand and dorsal venous arch of the foot \| \| Palmar venous arches \| Drain the hand and digits, and lead to the radial vein, ulnar veins, and the median antebrachial vein \| \| Radial vein \| Vein that parallels the radius and radial artery; arises from the palmar venous arches and leads to the brachial vein \| \| Ulnar vein \| Vein that parallels the ulna and ulnar artery; arises from the palmar venous arches and leads to the brachial vein \| \| Brachial vein \| Deeper vein of the arm that forms from the radial and ulnar veins in the lower arm; leads to the axillary vein \| \| Median antebrachial vein \| Vein that parallels the ulnar vein but is more medial in location; intertwines with the palmar venous arches; leads to the basilic vein \| \| Basilic vein \| Superficial vein of the arm that arises from the median antebrachial vein, intersects with the median cubital vein, parallels the ulnar vein, and continues into the upper arm; along with the brachial vein, it leads to the axillary vein \| \| Median cubital vein \| Superficial vessel located in the antecubital region that links the cephalic vein to the basilic vein in the form of a v; a frequent site from which to draw blood \| \| Cephalic vein \| Superficial vessel in the upper arm; leads to the axillary vein \| \| Subscapular vein \| Drains blood from the subscapular region and leads to the axillary vein \| \| Axillary vein \| The major vein in the axillary region; drains the upper limb and becomes the subclavian vein \| Table 20.14 The Inferior Vena Cava Other than the small amount of blood drained by the azygos and hemiazygos veins, most of the blood inferior to the diaphragm drains into the inferior vena cava before it is returned to the heart (see Figure 20.36). Lying just beneath the parietal peritoneum in the abdominal cavity, the inferior vena cava parallels the abdominal aorta, where it can receive blood from abdominal veins. The lumbar portions of the abdominal wall and spinal cord are drained by a series of lumbar veins, usually four on each side. The ascending lumbar veins drain into either the azygos vein on the right or the hemiazygos vein on the left, and return to the superior vena cava. The remaining lumbar veins drain directly into the inferior vena cava. Blood supply from the kidneys flows into each renal vein, normally the largest veins entering the inferior vena cava. A number of other, smaller veins empty into the left renal vein. Each adrenal vein drains the adrenal or suprarenal glands located immediately superior to the kidneys. The right adrenal vein enters the inferior vena cava directly, whereas the left adrenal vein enters the left renal vein. From the male reproductive organs, each testicular vein flows from the scrotum, forming a portion of the spermatic cord. Each ovarian vein drains an ovary in females. Each of these veins is generically called a gonadal vein. The right gonadal vein empties directly into the inferior vena cava, and the left gonadal vein empties into the left renal vein. Each side of the diaphragm drains into a phrenic vein; the right phrenic vein empties directly into the inferior vena cava, whereas the left phrenic vein empties into the left renal vein. Blood supply from the liver drains into each hepatic vein and directly into the inferior vena cava. Since the inferior vena cava lies primarily to the right of the vertebral column and aorta, the left renal vein is longer, as are the left phrenic, adrenal, and gonadal veins. The longer length of the left renal vein makes the left kidney the primary target of surgeons removing this organ for donation. Figure 20.40 provides a flow chart of the veins flowing into the inferior vena cava. Table 20.15 summarizes the major veins of the abdominal region. Figure 20.40 Venous Flow into Inferior Vena Cava The flow chart summarizes veins that deliver blood to the inferior vena cava. Major Veins of the Abdominal Region \| Vessel \| Description \| \|---\|---\| \| Inferior vena cava \| Large systemic vein that drains blood from areas largely inferior to the diaphragm; empties into the right atrium \| \| Lumbar veins \| Series of veins that drain the lumbar portion of the abdominal wall and spinal cord; the ascending lumbar veins drain into the azygos vein on the right or the hemiazygos vein on the left; the remaining lumbar veins drain directly into the inferior vena cava \| \| Renal vein \| Largest vein entering the inferior vena cava; drains the kidneys and flows into the inferior vena cava \| \| Adrenal vein \| Drains the adrenal or suprarenal; the right adrenal vein enters the inferior vena cava directly and the left adrenal vein enters the left renal vein \| \| Testicular vein \| Drains the testes and forms part of the spermatic cord; the right testicular vein empties directly into the inferior vena cava and the left testicular vein empties into the left renal vein \| \| Ovarian vein \| Drains the ovary; the right ovarian vein empties directly into the inferior vena cava and the left ovarian vein empties into the left renal vein \| \| Gonadal vein \| Generic term for a vein draining a reproductive organ; may be either an ovarian vein or a testicular vein, depending on the sex of the individual \| \| Phrenic vein \| Drains the diaphragm; the right phrenic vein flows into the inferior vena cava and the left phrenic vein empties into the left renal vein \| \| Hepatic vein \| Drains systemic blood from the liver and flows into the inferior vena cava \| Table 20.15 Veins Draining the Lower Limbs The superior surface of the foot drains into the digital veins, and the inferior surface drains into the plantar veins, which flow into a complex series of anastomoses in the feet and ankles, including the dorsal venous arch and the plantar venous arch (Figure 20.41). From the dorsal venous arch, blood supply drains into the anterior and posterior tibial veins. The anterior tibial vein drains the area near the tibialis anterior muscle and combines with the posterior tibial vein and the fibular vein to form the popliteal vein. The posterior tibial vein drains the posterior surface of the tibia and joins the popliteal vein. The fibular vein drains the muscles and integument in proximity to the fibula and also joins the popliteal vein. The small saphenous vein located on the lateral surface of the leg drains blood from the superficial regions of the lower leg and foot, and flows into to the popliteal vein. As the popliteal vein passes behind the knee in the popliteal region, it becomes the femoral vein. It is palpable in patients without excessive adipose tissue. Close to the body wall, the great saphenous vein, the deep femoral vein, and the femoral circumflex vein drain into the femoral vein. The great saphenous vein is a prominent surface vessel located on the medial surface of the leg and thigh that collects blood from the superficial portions of these areas. The deep femoral vein, as the name suggests, drains blood from the deeper portions of the thigh. The femoral circumflex vein forms a loop around the femur just inferior to the trochanters and drains blood from the areas in proximity to the head and neck of the femur. As the femoral vein penetrates the body wall from the femoral portion of the upper limb, it becomes the external iliac vein, a large vein that drains blood from the leg to the common iliac vein. The pelvic organs and integument drain into the internal iliac vein, which forms from several smaller veins in the region, including the umbilical veins that run on either side of the bladder. The external and internal iliac veins combine near the inferior portion of the sacroiliac joint to form the common iliac vein. In addition to blood supply from the external and internal iliac veins, the middle sacral vein drains the sacral region into the common iliac vein. Similar to the common iliac arteries, the common iliac veins come together at the level of L5 to form the inferior vena cava. Figure 20.42 is a flow chart of veins flowing into the lower limb. Table 20.16 summarizes the major veins of the lower limbs. Figure 20.41 Major Veins Serving the Lower Limbs Anterior and posterior views show the major veins that drain the lower limb into the inferior vena cava. Figure 20.42 Major Veins of the Lower Limb The flow chart summarizes venous flow from the lower limb. Veins of the Lower Limbs \| Vessel \| Description \| \|---\|---\| \| Plantar veins \| Drain the foot and flow into the plantar venous arch \| \| Dorsal venous arch \| Drains blood from digital veins and vessels on the superior surface of the foot \| \| Plantar venous arch \| Formed from the plantar veins; flows into the anterior and posterior tibial veins through anastomoses \| \| Anterior tibial vein \| Formed from the dorsal venous arch; drains the area near the tibialis anterior muscle and flows into the popliteal vein \| \| Posterior tibial vein \| Formed from the dorsal venous arch; drains the area near the posterior surface of the tibia and flows into the popliteal vein \| \| Fibular vein \| Drains the muscles and integument near the fibula and flows into the popliteal vein \| \| Small saphenous vein \| Located on the lateral surface of the leg; drains blood from the superficial regions of the lower leg and foot, and flows into the popliteal vein \| \| Popliteal vein \| Drains the region behind the knee and forms from the fusion of the fibular, anterior, and posterior tibial veins; flows into the femoral vein \| \| Great saphenous vein \| Prominent surface vessel located on the medial surface of the leg and thigh; drains the superficial portions of these areas and flows into the femoral vein \| \| Deep femoral vein \| Drains blood from the deeper portions of the thigh and flows into the femoral vein \| \| Femoral circumflex vein \| Forms a loop around the femur just inferior to the trochanters; drains blood from the areas around the head and neck of the femur; flows into the femoral vein \| \| Femoral vein \| Drains the upper leg; receives blood from the great saphenous vein, the deep femoral vein, and the femoral circumflex vein; becomes the external iliac vein when it crosses the body wall \| \| External iliac vein \| Formed when the femoral vein passes into the body cavity; drains the legs and flows into the common iliac vein \| \| Internal iliac vein \| Drains the pelvic organs and integument; formed from several smaller veins in the region; flows into the common iliac vein \| \| Middle sacral vein \| Drains the sacral region and flows into the left common iliac vein \| \| Common iliac vein \| Flows into the inferior vena cava at the level of L5; the left common iliac vein drains the sacral region; formed from the union of the external and internal iliac veins near the inferior portion of the sacroiliac joint \| Table 20.16 Hepatic Portal System The liver is a complex biochemical processing plant. It packages nutrients absorbed by the digestive system; produces plasma proteins, clotting factors, and bile; and disposes of worn-out cell components and waste products. Instead of entering the circulation directly, absorbed nutrients and certain wastes (for example, materials produced by the spleen) travel to the liver for processing. They do so via the hepatic portal system (Figure 20.43). Portal systems begin and end in capillaries. In this case, the initial capillaries from the stomach, small intestine, large intestine, and spleen lead to the hepatic portal vein and end in specialized capillaries within the liver, the hepatic sinusoids. You saw the only other portal system with the hypothalamic-hypophyseal portal vessel in the endocrine chapter. The hepatic portal system consists of the hepatic portal vein and the veins that drain into it. The hepatic portal vein itself is relatively short, beginning at the level of L2 with the confluence of the superior mesenteric and splenic veins. It also receives branches from the inferior mesenteric vein, plus the splenic veins and all their tributaries. The superior mesenteric vein receives blood from the small intestine, two-thirds of the large intestine, and the stomach. The inferior mesenteric vein drains the distal third of the large intestine, including the descending colon, the sigmoid colon, and the rectum. The splenic vein is formed from branches from the spleen, pancreas, and portions of the stomach, and the inferior mesenteric vein. After its formation, the hepatic portal vein also receives branches from the gastric veins of the stomach and cystic veins from the gall bladder. The hepatic portal vein delivers materials from these digestive and circulatory organs directly to the liver for processing. Because of the hepatic portal system, the liver receives its blood supply from two different sources: from normal systemic circulation via the hepatic artery and from the hepatic portal vein. The liver processes the blood from the portal system to remove certain wastes and excess nutrients, which are stored for later use. This processed blood, as well as the systemic blood that came from the hepatic artery, exits the liver via the right, left, and middle hepatic veins, and flows into the inferior vena cava. Overall systemic blood composition remains relatively stable, since the liver is able to metabolize the absorbed digestive components. Figure 20.43 Hepatic Portal System The liver receives blood from the normal systemic circulation via the hepatic artery. It also receives and processes blood from other organs, delivered via the veins of the hepatic portal system. All blood exits the liver via the hepatic vein, which delivers the blood to the inferior vena cava. (Different colors are used to help distinguish among the different vessels in the system.) Development of Blood Vessels and Fetal Circulation - Describe the development of blood vessels - Describe the fetal circulation In a developing embryo,the heart has developed enough by day 21 post-fertilization to begin beating. Circulation patterns are clearly established by the fourth week of embryonic life. It is critical to the survival of the developing human that the circulatory system forms early to supply the growing tissue with nutrients and gases, and to remove waste products. Blood cells and vessel production in structures outside the embryo proper called the yolk sac, chorion, and connecting stalk begin about 15 to 16 days following fertilization. Development of these circulatory elements within the embryo itself begins approximately 2 days later. You will learn more about the formation and function of these early structures when you study the chapter on development. During those first few weeks, blood vessels begin to form from the embryonic mesoderm. The precursor cells are known as hemangioblasts. These in turn differentiate into angioblasts, which give rise to the blood vessels and pluripotent stem cells, which differentiate into the formed elements of blood. (Seek additional content for more detail on fetal development and circulation.) Together, these cells form masses known as blood islands scattered throughout the embryonic disc. Spaces appear on the blood islands that develop into vessel lumens. The endothelial lining of the vessels arise from the angioblasts within these islands. Surrounding mesenchymal cells give rise to the smooth muscle and connective tissue layers of the vessels. While the vessels are developing, the pluripotent stem cells begin to form the blood. Vascular tubes also develop on the blood islands, and they eventually connect to one another as well as to the developing, tubular heart. Thus, the developmental pattern, rather than beginning from the formation of one central vessel and spreading outward, occurs in many regions simultaneously with vessels later joining together. This angiogenesis—the creation of new blood vessels from existing ones—continues as needed throughout life as we grow and develop. Blood vessel development often follows the same pattern as nerve development and travels to the same target tissues and organs. This occurs because the many factors directing growth of nerves also stimulate blood vessels to follow a similar pattern. Whether a given vessel develops into an artery or a vein is dependent upon local concentrations of signaling proteins. As the embryo grows within the mother’s uterus, its requirements for nutrients and gas exchange also grow. The placenta—a circulatory organ unique to pregnancy—develops jointly from the embryo and uterine wall structures to fill this need. Emerging from the placenta is the umbilical vein, which carries oxygen-rich blood from the mother to the fetal inferior vena cava via the ductus venosus to the heart that pumps it into fetal circulation. Two umbilical arteries carry oxygen-depleted fetal blood, including wastes and carbon dioxide, to the placenta. Remnants of the umbilical arteries remain in the adult. (Seek additional content for more information on the role of the placenta in fetal circulation.) There are three major shunts—alternate paths for blood flow—found in the circulatory system of the fetus. Two of these shunts divert blood from the pulmonary to the systemic circuit, whereas the third connects the umbilical vein to the inferior vena cava. The first two shunts are critical during fetal life, when the lungs are compressed, filled with amniotic fluid, and nonfunctional, and gas exchange is provided by the placenta. These shunts close shortly after birth, however, when the newborn begins to breathe. The third shunt persists a bit longer but becomes nonfunctional once the umbilical cord is severed. The three shunts are as follows (Figure 20.44): - The foramen ovale is an opening in the interatrial septum that allows blood to flow from the right atrium to the left atrium. A valve associated with this opening prevents backflow of blood during the fetal period. As the newborn begins to breathe and blood pressure in the atria increases, this shunt closes. The fossa ovalis remains in the interatrial septum after birth, marking the location of the former foramen ovale. - The ductus arteriosus is a short, muscular vessel that connects the pulmonary trunk to the aorta. Most of the blood pumped from the right ventricle into the pulmonary trunk is thereby diverted into the aorta. Only enough blood reaches the fetal lungs to maintain the developing lung tissue. When the newborn takes the first breath, pressure within the lungs drops dramatically, and both the lungs and the pulmonary vessels expand. As the amount of oxygen increases, the smooth muscles in the wall of the ductus arteriosus constrict, sealing off the passage. Eventually, the muscular and endothelial components of the ductus arteriosus degenerate, leaving only the connective tissue component of the ligamentum arteriosum. - The ductus venosus is a temporary blood vessel that branches from the umbilical vein, allowing much of the freshly oxygenated blood from the placenta—the organ of gas exchange between the mother and fetus—to bypass the fetal liver and go directly to the fetal heart. The ductus venosus closes slowly during the first weeks of infancy and degenerates to become the ligamentum venosum. Figure 20.44 Fetal Shunts The foramen ovale in the interatrial septum allows blood to flow from the right atrium to the left atrium. The ductus arteriosus is a temporary vessel, connecting the aorta to the pulmonary trunk. The ductus venosus links the umbilical vein to the inferior vena cava largely through the liver. Key Terms - abdominal aorta - portion of the aorta inferior to the aortic hiatus and superior to the common iliac arteries - adrenal artery - branch of the abdominal aorta; supplies blood to the adrenal (suprarenal) glands - adrenal vein - drains the adrenal or suprarenal glands that are immediately superior to the kidneys; the right adrenal vein enters the inferior vena cava directly and the left adrenal vein enters the left renal vein - anaphylactic shock - type of shock that follows a severe allergic reaction and results from massive vasodilation - angioblasts - stem cells that give rise to blood vessels - angiogenesis - development of new blood vessels from existing vessels - anterior cerebral artery - arises from the internal carotid artery; supplies the frontal lobe of the cerebrum - anterior communicating artery - anastomosis of the right and left internal carotid arteries; supplies blood to the brain - anterior tibial artery - branches from the popliteal artery; supplies blood to the anterior tibial region; becomes the dorsalis pedis artery - anterior tibial vein - forms from the dorsal venous arch; drains the area near the tibialis anterior muscle and leads to the popliteal vein - aorta - largest artery in the body, originating from the left ventricle and descending to the abdominal region where it bifurcates into the common iliac arteries at the level of the fourth lumbar vertebra; arteries originating from the aorta distribute blood to virtually all tissues of the body - aortic arch - arc that connects the ascending aorta to the descending aorta; ends at the intervertebral disk between the fourth and fifth thoracic vertebrae - aortic hiatus - opening in the diaphragm that allows passage of the thoracic aorta into the abdominal region where it becomes the abdominal aorta - aortic sinuses - small pockets in the ascending aorta near the aortic valve that are the locations of the baroreceptors (stretch receptors) and chemoreceptors that trigger a reflex that aids in the regulation of vascular homeostasis - arterial circle - (also, circle of Willis) anastomosis located at the base of the brain that ensures continual blood supply; formed from branches of the internal carotid and vertebral arteries; supplies blood to the brain - arteriole - (also, resistance vessel) very small artery that leads to a capillary - arteriovenous anastomosis - short vessel connecting an arteriole directly to a venule and bypassing the capillary beds - artery - blood vessel that conducts blood away from the heart; may be a conducting or distributing vessel - ascending aorta - initial portion of the aorta, rising from the left ventricle for a distance of approximately 5 cm - atrial reflex - mechanism for maintaining vascular homeostasis involving atrial baroreceptors: if blood is returning to the right atrium more rapidly than it is being ejected from the left ventricle, the atrial receptors will stimulate the cardiovascular centers to increase sympathetic firing and increase cardiac output until the situation is reversed; the opposite is also true - axillary artery - continuation of the subclavian artery as it penetrates the body wall and enters the axillary region; supplies blood to the region near the head of the humerus (humeral circumflex arteries); the majority of the vessel continues into the brachium and becomes the brachial artery - axillary vein - major vein in the axillary region; drains the upper limb and becomes the subclavian vein - azygos vein - originates in the lumbar region and passes through the diaphragm into the thoracic cavity on the right side of the vertebral column; drains blood from the intercostal veins, esophageal veins, bronchial veins, and other veins draining the mediastinal region; leads to the superior vena cava - basilar artery - formed from the fusion of the two vertebral arteries; sends branches to the cerebellum, brain stem, and the posterior cerebral arteries; the main blood supply to the brain stem - basilic vein - superficial vein of the arm that arises from the palmar venous arches, intersects with the median cubital vein, parallels the ulnar vein, and continues into the upper arm; along with the brachial vein, it leads to the axillary vein - blood colloidal osmotic pressure (BCOP) - pressure exerted by colloids suspended in blood within a vessel; a primary determinant is the presence of plasma proteins - blood flow - movement of blood through a vessel, tissue, or organ that is usually expressed in terms of volume per unit of time - blood hydrostatic pressure - force blood exerts against the walls of a blood vessel or heart chamber - blood islands - masses of developing blood vessels and formed elements from mesodermal cells scattered throughout the embryonic disc - blood pressure - force exerted by the blood against the wall of a vessel or heart chamber; can be described with the more generic term hydrostatic pressure - brachial artery - continuation of the axillary artery in the brachium; supplies blood to much of the brachial region; gives off several smaller branches that provide blood to the posterior surface of the arm in the region of the elbow; bifurcates into the radial and ulnar arteries at the coronoid fossa - brachial vein - deeper vein of the arm that forms from the radial and ulnar veins in the lower arm; leads to the axillary vein - brachiocephalic artery - single vessel located on the right side of the body; the first vessel branching from the aortic arch; gives rise to the right subclavian artery and the right common carotid artery; supplies blood to the head, neck, upper limb, and wall of the thoracic region - brachiocephalic vein - one of a pair of veins that form from a fusion of the external and internal jugular veins and the subclavian vein; subclavian, external and internal jugulars, vertebral, and internal thoracic veins lead to it; drains the upper thoracic region and flows into the superior vena cava - bronchial artery - systemic branch from the aorta that provides oxygenated blood to the lungs in addition to the pulmonary circuit - bronchial vein - drains the systemic circulation from the lungs and leads to the azygos vein - capacitance - ability of a vein to distend and store blood - capacitance vessels - veins - capillary - smallest of blood vessels where physical exchange occurs between the blood and tissue cells surrounded by interstitial fluid - capillary bed - network of 10–100 capillaries connecting arterioles to venules - capillary hydrostatic pressure (CHP) - force blood exerts against a capillary - cardiogenic shock - type of shock that results from the inability of the heart to maintain cardiac output - carotid sinuses - small pockets near the base of the internal carotid arteries that are the locations of the baroreceptors and chemoreceptors that trigger a reflex that aids in the regulation of vascular homeostasis - cavernous sinus - enlarged vein that receives blood from most of the other cerebral veins and the eye socket, and leads to the petrosal sinus - celiac trunk - (also, celiac artery) major branch of the abdominal aorta; gives rise to the left gastric artery, the splenic artery, and the common hepatic artery that forms the hepatic artery to the liver, the right gastric artery to the stomach, and the cystic artery to the gall bladder - cephalic vein - superficial vessel in the upper arm; leads to the axillary vein - cerebrovascular accident (CVA) - blockage of blood flow to the brain; also called a stroke - circle of Willis - (also, arterial circle) anastomosis located at the base of the brain that ensures continual blood supply; formed from branches of the internal carotid and vertebral arteries; supplies blood to the brain - circulatory shock - also simply called shock; a life-threatening medical condition in which the circulatory system is unable to supply enough blood flow to provide adequate oxygen and other nutrients to the tissues to maintain cellular metabolism - common carotid artery - right common carotid artery arises from the brachiocephalic artery, and the left common carotid arises from the aortic arch; gives rise to the external and internal carotid arteries; supplies the respective sides of the head and neck - common hepatic artery - branch of the celiac trunk that forms the hepatic artery, the right gastric artery, and the cystic artery - common iliac artery - branch of the aorta that leads to the internal and external iliac arteries - common iliac vein - one of a pair of veins that flows into the inferior vena cava at the level of L5; the left common iliac vein drains the sacral region; divides into external and internal iliac veins near the inferior portion of the sacroiliac joint - compliance - degree to which a blood vessel can stretch as opposed to being rigid - continuous capillary - most common type of capillary, found in virtually all tissues except epithelia and cartilage; contains very small gaps in the endothelial lining that permit exchange - cystic artery - branch of the common hepatic artery; supplies blood to the gall bladder - deep femoral artery - branch of the femoral artery; gives rise to the lateral circumflex arteries - deep femoral vein - drains blood from the deeper portions of the thigh and leads to the femoral vein - descending aorta - portion of the aorta that continues downward past the end of the aortic arch; subdivided into the thoracic aorta and the abdominal aorta - diastolic pressure - lower number recorded when measuring arterial blood pressure; represents the minimal value corresponding to the pressure that remains during ventricular relaxation - digital arteries - formed from the superficial and deep palmar arches; supply blood to the digits - digital veins - drain the digits and feed into the palmar arches of the hand and dorsal venous arch of the foot - dorsal arch - (also, arcuate arch) formed from the anastomosis of the dorsalis pedis artery and medial and plantar arteries; branches supply the distal portions of the foot and digits - dorsal venous arch - drains blood from digital veins and vessels on the superior surface of the foot - dorsalis pedis artery - forms from the anterior tibial artery; branches repeatedly to supply blood to the tarsal and dorsal regions of the foot - ductus arteriosus - shunt in the fetal pulmonary trunk that diverts oxygenated blood back to the aorta - ductus venosus - shunt that causes oxygenated blood to bypass the fetal liver on its way to the inferior vena cava - elastic artery - (also, conducting artery) artery with abundant elastic fibers located closer to the heart, which maintains the pressure gradient and conducts blood to smaller branches - esophageal artery - branch of the thoracic aorta; supplies blood to the esophagus - esophageal vein - drains the inferior portions of the esophagus and leads to the azygos vein - external carotid artery - arises from the common carotid artery; supplies blood to numerous structures within the face, lower jaw, neck, esophagus, and larynx - external elastic membrane - membrane composed of elastic fibers that separates the tunica media from the tunica externa; seen in larger arteries - external iliac artery - branch of the common iliac artery that leaves the body cavity and becomes a femoral artery; supplies blood to the lower limbs - external iliac vein - formed when the femoral vein passes into the body cavity; drains the legs and leads to the common iliac vein - external jugular vein - one of a pair of major veins located in the superficial neck region that drains blood from the more superficial portions of the head, scalp, and cranial regions, and leads to the subclavian vein - femoral artery - continuation of the external iliac artery after it passes through the body cavity; divides into several smaller branches, the lateral deep femoral artery, and the genicular artery; becomes the popliteal artery as it passes posterior to the knee - femoral circumflex vein - forms a loop around the femur just inferior to the trochanters; drains blood from the areas around the head and neck of the femur; leads to the femoral vein - femoral vein - drains the upper leg; receives blood from the great saphenous vein, the deep femoral vein, and the femoral circumflex vein; becomes the external iliac vein when it crosses the body wall - fenestrated capillary - type of capillary with pores or fenestrations in the endothelium that allow for rapid passage of certain small materials - fibular vein - drains the muscles and integument near the fibula and leads to the popliteal vein - filtration - in the cardiovascular system, the movement of material from a capillary into the interstitial fluid, moving from an area of higher pressure to lower pressure - foramen ovale - shunt that directly connects the right and left atria and helps to divert oxygenated blood from the fetal pulmonary circuit - genicular artery - branch of the femoral artery; supplies blood to the region of the knee - gonadal artery - branch of the abdominal aorta; supplies blood to the gonads or reproductive organs; also described as ovarian arteries or testicular arteries, depending upon the sex of the individual - gonadal vein - generic term for a vein draining a reproductive organ; may be either an ovarian vein or a testicular vein, depending on the sex of the individual - great cerebral vein - receives most of the smaller vessels from the inferior cerebral veins and leads to the straight sinus - great saphenous vein - prominent surface vessel located on the medial surface of the leg and thigh; drains the superficial portions of these areas and leads to the femoral vein - hemangioblasts - embryonic stem cells that appear in the mesoderm and give rise to both angioblasts and pluripotent stem cells - hemiazygos vein - smaller vein complementary to the azygos vein; drains the esophageal veins from the esophagus and the left intercostal veins, and leads to the brachiocephalic vein via the superior intercostal vein - hepatic artery proper - branch of the common hepatic artery; supplies systemic blood to the liver - hepatic portal system - specialized circulatory pathway that carries blood from digestive organs to the liver for processing before being sent to the systemic circulation - hepatic vein - drains systemic blood from the liver and flows into the inferior vena cava - hypertension - chronic and persistent blood pressure measurements of 140/90 mm Hg or above - hypervolemia - abnormally high levels of fluid and blood within the body - hypovolemia - abnormally low levels of fluid and blood within the body - hypovolemic shock - type of circulatory shock caused by excessive loss of blood volume due to hemorrhage or possibly dehydration - hypoxia - lack of oxygen supply to the tissues - inferior mesenteric artery - branch of the abdominal aorta; supplies blood to the distal segment of the large intestine and rectum - inferior phrenic artery - branch of the abdominal aorta; supplies blood to the inferior surface of the diaphragm - inferior vena cava - large systemic vein that drains blood from areas largely inferior to the diaphragm; empties into the right atrium - intercostal artery - branch of the thoracic aorta; supplies blood to the muscles of the thoracic cavity and vertebral column - intercostal vein - drains the muscles of the thoracic wall and leads to the azygos vein - internal carotid artery - arises from the common carotid artery and begins with the carotid sinus; goes through the carotid canal of the temporal bone to the base of the brain; combines with branches of the vertebral artery forming the arterial circle; supplies blood to the brain - internal elastic membrane - membrane composed of elastic fibers that separates the tunica intima from the tunica media; seen in larger arteries - internal iliac artery - branch from the common iliac arteries; supplies blood to the urinary bladder, walls of the pelvis, external genitalia, and the medial portion of the femoral region; in females, also provide blood to the uterus and vagina - internal iliac vein - drains the pelvic organs and integument; formed from several smaller veins in the region; leads to the common iliac vein - internal jugular vein - one of a pair of major veins located in the neck region that passes through the jugular foramen and canal, flows parallel to the common carotid artery that is more or less its counterpart; primarily drains blood from the brain, receives the superficial facial vein, and empties into the subclavian vein - internal thoracic artery - (also, mammary artery) arises from the subclavian artery; supplies blood to the thymus, pericardium of the heart, and the anterior chest wall - internal thoracic vein - (also, internal mammary vein) drains the anterior surface of the chest wall and leads to the brachiocephalic vein - interstitial fluid colloidal osmotic pressure (IFCOP) - pressure exerted by the colloids within the interstitial fluid - interstitial fluid hydrostatic pressure (IFHP) - force exerted by the fluid in the tissue spaces - ischemia - insufficient blood flow to the tissues - Korotkoff sounds - noises created by turbulent blood flow through the vessels - lateral circumflex artery - branch of the deep femoral artery; supplies blood to the deep muscles of the thigh and the ventral and lateral regions of the integument - lateral plantar artery - arises from the bifurcation of the posterior tibial arteries; supplies blood to the lateral plantar surfaces of the foot - left gastric artery - branch of the celiac trunk; supplies blood to the stomach - lumbar arteries - branches of the abdominal aorta; supply blood to the lumbar region, the abdominal wall, and spinal cord - lumbar veins - drain the lumbar portion of the abdominal wall and spinal cord; the superior lumbar veins drain into the azygos vein on the right or the hemiazygos vein on the left; blood from these vessels is returned to the superior vena cava rather than the inferior vena cava - lumen - interior of a tubular structure such as a blood vessel or a portion of the alimentary canal through which blood, chyme, or other substances travel - maxillary vein - drains blood from the maxillary region and leads to the external jugular vein - mean arterial pressure (MAP) - average driving force of blood to the tissues; approximated by taking diastolic pressure and adding 1/3 of pulse pressure - medial plantar artery - arises from the bifurcation of the posterior tibial arteries; supplies blood to the medial plantar surfaces of the foot - median antebrachial vein - vein that parallels the ulnar vein but is more medial in location; intertwines with the palmar venous arches - median cubital vein - superficial vessel located in the antecubital region that links the cephalic vein to the basilic vein in the form of a v; a frequent site for a blood draw - median sacral artery - continuation of the aorta into the sacrum - mediastinal artery - branch of the thoracic aorta; supplies blood to the mediastinum - metarteriole - short vessel arising from a terminal arteriole that branches to supply a capillary bed - microcirculation - blood flow through the capillaries - middle cerebral artery - another branch of the internal carotid artery; supplies blood to the temporal and parietal lobes of the cerebrum - middle sacral vein - drains the sacral region and leads to the left common iliac vein - muscular artery - (also, distributing artery) artery with abundant smooth muscle in the tunica media that branches to distribute blood to the arteriole network - myogenic response - constriction or dilation in the walls of arterioles in response to pressures related to blood flow; reduces high blood flow or increases low blood flow to help maintain consistent flow to the capillary network - nervi vasorum - small nerve fibers found in arteries and veins that trigger contraction of the smooth muscle in their walls - net filtration pressure (NFP) - force driving fluid out of the capillary and into the tissue spaces; equal to the difference of the capillary hydrostatic pressure and the blood colloidal osmotic pressure - neurogenic shock - type of shock that occurs with cranial or high spinal injuries that damage the cardiovascular centers in the medulla oblongata or the nervous fibers originating from this region - obstructive shock - type of shock that occurs when a significant portion of the vascular system is blocked - occipital sinus - enlarged vein that drains the occipital region near the falx cerebelli and flows into the left and right transverse sinuses, and also into the vertebral veins - ophthalmic artery - branch of the internal carotid artery; supplies blood to the eyes - ovarian artery - branch of the abdominal aorta; supplies blood to the ovary, uterine (Fallopian) tube, and uterus - ovarian vein - drains the ovary; the right ovarian vein leads to the inferior vena cava and the left ovarian vein leads to the left renal vein - palmar arches - superficial and deep arches formed from anastomoses of the radial and ulnar arteries; supply blood to the hand and digital arteries - palmar venous arches - drain the hand and digits, and feed into the radial and ulnar veins - parietal branches - (also, somatic branches) group of arterial branches of the thoracic aorta; includes those that supply blood to the thoracic cavity, vertebral column, and the superior surface of the diaphragm - perfusion - distribution of blood into the capillaries so the tissues can be supplied - pericardial artery - branch of the thoracic aorta; supplies blood to the pericardium - petrosal sinus - enlarged vein that receives blood from the cavernous sinus and flows into the internal jugular vein - phrenic vein - drains the diaphragm; the right phrenic vein flows into the inferior vena cava and the left phrenic vein leads to the left renal vein - plantar arch - formed from the anastomosis of the dorsalis pedis artery and medial and plantar arteries; branches supply the distal portions of the foot and digits - plantar veins - drain the foot and lead to the plantar venous arch - plantar venous arch - formed from the plantar veins; leads to the anterior and posterior tibial veins through anastomoses - popliteal artery - continuation of the femoral artery posterior to the knee; branches into the anterior and posterior tibial arteries - popliteal vein - continuation of the femoral vein behind the knee; drains the region behind the knee and forms from the fusion of the fibular and anterior and posterior tibial veins - posterior cerebral artery - branch of the basilar artery that forms a portion of the posterior segment of the arterial circle; supplies blood to the posterior portion of the cerebrum and brain stem - posterior communicating artery - branch of the posterior cerebral artery that forms part of the posterior portion of the arterial circle; supplies blood to the brain - posterior tibial artery - branch from the popliteal artery that gives rise to the fibular or peroneal artery; supplies blood to the posterior tibial region - posterior tibial vein - forms from the dorsal venous arch; drains the area near the posterior surface of the tibia and leads to the popliteal vein - precapillary sphincters - circular rings of smooth muscle that surround the entrance to a capillary and regulate blood flow into that capillary - pulmonary artery - one of two branches, left and right, that divides off from the pulmonary trunk and leads to smaller arterioles and eventually to the pulmonary capillaries - pulmonary circuit - system of blood vessels that provide gas exchange via a network of arteries, veins, and capillaries that run from the heart, through the body, and back to the lungs - pulmonary trunk - single large vessel exiting the right ventricle that divides to form the right and left pulmonary arteries - pulmonary veins - two sets of paired vessels, one pair on each side, that are formed from the small venules leading away from the pulmonary capillaries that flow into the left atrium - pulse - alternating expansion and recoil of an artery as blood moves through the vessel; an indicator of heart rate - pulse pressure - difference between the systolic and diastolic pressures - radial artery - formed at the bifurcation of the brachial artery; parallels the radius; gives off smaller branches until it reaches the carpal region where it fuses with the ulnar artery to form the superficial and deep palmar arches; supplies blood to the lower arm and carpal region - radial vein - parallels the radius and radial artery; arises from the palmar venous arches and leads to the brachial vein - reabsorption - in the cardiovascular system, the movement of material from the interstitial fluid into the capillaries - renal artery - branch of the abdominal aorta; supplies each kidney - renal vein - largest vein entering the inferior vena cava; drains the kidneys and leads to the inferior vena cava - resistance - any condition or parameter that slows or counteracts the flow of blood - respiratory pump - increase in the volume of the thorax during inhalation that decreases air pressure, enabling venous blood to flow into the thoracic region, then exhalation increases pressure, moving blood into the atria - right gastric artery - branch of the common hepatic artery; supplies blood to the stomach - sepsis - (also, septicemia) organismal-level inflammatory response to a massive infection - septic shock - (also, blood poisoning) type of shock that follows a massive infection resulting in organism-wide inflammation - sigmoid sinuses - enlarged veins that receive blood from the transverse sinuses; flow through the jugular foramen and into the internal jugular vein - sinusoid capillary - rarest type of capillary, which has extremely large intercellular gaps in the basement membrane in addition to clefts and fenestrations; found in areas such as the bone marrow and liver where passage of large molecules occurs - skeletal muscle pump - effect on increasing blood pressure within veins by compression of the vessel caused by the contraction of nearby skeletal muscle - small saphenous vein - located on the lateral surface of the leg; drains blood from the superficial regions of the lower leg and foot, and leads to the popliteal vein - sphygmomanometer - blood pressure cuff attached to a device that measures blood pressure - splenic artery - branch of the celiac trunk; supplies blood to the spleen - straight sinus - enlarged vein that drains blood from the brain; receives most of the blood from the great cerebral vein and flows into the left or right transverse sinus - subclavian artery - right subclavian arises from the brachiocephalic artery, whereas the left subclavian artery arises from the aortic arch; gives rise to the internal thoracic, vertebral, and thyrocervical arteries; supplies blood to the arms, chest, shoulders, back, and central nervous system - subclavian vein - located deep in the thoracic cavity; becomes the axillary vein as it enters the axillary region; drains the axillary and smaller local veins near the scapular region; leads to the brachiocephalic vein - subscapular vein - drains blood from the subscapular region and leads to the axillary vein - superior mesenteric artery - branch of the abdominal aorta; supplies blood to the small intestine (duodenum, jejunum, and ileum), the pancreas, and a majority of the large intestine - superior phrenic artery - branch of the thoracic aorta; supplies blood to the superior surface of the diaphragm - superior sagittal sinus - enlarged vein located midsagittally between the meningeal and periosteal layers of the dura mater within the falx cerebri; receives most of the blood drained from the superior surface of the cerebrum and leads to the inferior jugular vein and the vertebral vein - superior vena cava - large systemic vein; drains blood from most areas superior to the diaphragm; empties into the right atrium - systolic pressure - larger number recorded when measuring arterial blood pressure; represents the maximum value following ventricular contraction - temporal vein - drains blood from the temporal region and leads to the external jugular vein - testicular artery - branch of the abdominal aorta; will ultimately travel outside the body cavity to the testes and form one component of the spermatic cord - testicular vein - drains the testes and forms part of the spermatic cord; the right testicular vein empties directly into the inferior vena cava and the left testicular vein empties into the left renal vein - thoracic aorta - portion of the descending aorta superior to the aortic hiatus - thoroughfare channel - continuation of the metarteriole that enables blood to bypass a capillary bed and flow directly into a venule, creating a vascular shunt - thyrocervical artery - arises from the subclavian artery; supplies blood to the thyroid, the cervical region, the upper back, and shoulder - transient ischemic attack (TIA) - temporary loss of neurological function caused by a brief interruption in blood flow; also known as a mini-stroke - transverse sinuses - pair of enlarged veins near the lambdoid suture that drain the occipital, sagittal, and straight sinuses, and leads to the sigmoid sinuses - trunk - large vessel that gives rise to smaller vessels - tunica externa - (also, tunica adventitia) outermost layer or tunic of a vessel (except capillaries) - tunica intima - (also, tunica interna) innermost lining or tunic of a vessel - tunica media - middle layer or tunic of a vessel (except capillaries) - ulnar artery - formed at the bifurcation of the brachial artery; parallels the ulna; gives off smaller branches until it reaches the carpal region where it fuses with the radial artery to form the superficial and deep palmar arches; supplies blood to the lower arm and carpal region - ulnar vein - parallels the ulna and ulnar artery; arises from the palmar venous arches and leads to the brachial vein - umbilical arteries - pair of vessels that runs within the umbilical cord and carries fetal blood low in oxygen and high in waste to the placenta for exchange with maternal blood - umbilical vein - single vessel that originates in the placenta and runs within the umbilical cord, carrying oxygen- and nutrient-rich blood to the fetal heart - vasa vasorum - small blood vessels located within the walls or tunics of larger vessels that supply nourishment to and remove wastes from the cells of the vessels - vascular shock - type of shock that occurs when arterioles lose their normal muscular tone and dilate dramatically - vascular shunt - continuation of the metarteriole and thoroughfare channel that allows blood to bypass the capillary beds to flow directly from the arterial to the venous circulation - vascular tone - contractile state of smooth muscle in a blood vessel - vascular tubes - rudimentary blood vessels in a developing fetus - vasoconstriction - constriction of the smooth muscle of a blood vessel, resulting in a decreased vascular diameter - vasodilation - relaxation of the smooth muscle in the wall of a blood vessel, resulting in an increased vascular diameter - vasomotion - irregular, pulsating flow of blood through capillaries and related structures - vein - blood vessel that conducts blood toward the heart - venous reserve - volume of blood contained within systemic veins in the integument, bone marrow, and liver that can be returned to the heart for circulation, if needed - venule - small vessel leading from the capillaries to veins - vertebral artery - arises from the subclavian artery and passes through the vertebral foramen through the foramen magnum to the brain; joins with the internal carotid artery to form the arterial circle; supplies blood to the brain and spinal cord - vertebral vein - arises from the base of the brain and the cervical region of the spinal cord; passes through the intervertebral foramina in the cervical vertebrae; drains smaller veins from the cranium, spinal cord, and vertebrae, and leads to the brachiocephalic vein; counterpart of the vertebral artery - visceral branches - branches of the descending aorta that supply blood to the viscera Chapter Review 20.1 Structure and Function of Blood Vessels Blood pumped by the heart flows through a series of vessels known as arteries, arterioles, capillaries, venules, and veins before returning to the heart. Arteries transport blood away from the heart and branch into smaller vessels, forming arterioles. Arterioles distribute blood to capillary beds, the sites of exchange with the body tissues. Capillaries lead back to small vessels known as venules that flow into the larger veins and eventually back to the heart. The arterial system is a relatively high-pressure system, so arteries have thick walls that appear round in cross section. The venous system is a lower-pressure system, containing veins that have larger lumens and thinner walls. They often appear flattened. Arteries, arterioles, venules, and veins are composed of three tunics known as the tunica intima, tunica media, and tunica externa. Capillaries have only a tunica intima layer. The tunica intima is a thin layer composed of a simple squamous epithelium known as endothelium and a small amount of connective tissue. The tunica media is a thicker area composed of variable amounts of smooth muscle and connective tissue. It is the thickest layer in all but the largest arteries. The tunica externa is primarily a layer of connective tissue, although in veins, it also contains some smooth muscle. Blood flow through vessels can be dramatically influenced by vasoconstriction and vasodilation in their walls. 20.2 Blood Flow, Blood Pressure, and Resistance Blood flow is the movement of blood through a vessel, tissue, or organ. The slowing or blocking of blood flow is called resistance. Blood pressure is the force that blood exerts upon the walls of the blood vessels or chambers of the heart. The components of blood pressure include systolic pressure, which results from ventricular contraction, and diastolic pressure, which results from ventricular relaxation. Pulse pressure is the difference between systolic and diastolic measures, and mean arterial pressure is the “average” pressure of blood in the arterial system, driving blood into the tissues. Pulse, the expansion and recoiling of an artery, reflects the heartbeat. The variables affecting blood flow and blood pressure in the systemic circulation are cardiac output, compliance, blood volume, blood viscosity, and the length and diameter of the blood vessels. In the arterial system, vasodilation and vasoconstriction of the arterioles is a significant factor in systemic blood pressure: Slight vasodilation greatly decreases resistance and increases flow, whereas slight vasoconstriction greatly increases resistance and decreases flow. In the arterial system, as resistance increases, blood pressure increases and flow decreases. In the venous system, constriction increases blood pressure as it does in arteries; the increasing pressure helps to return blood to the heart. In addition, constriction causes the vessel lumen to become more rounded, decreasing resistance and increasing blood flow. Venoconstriction, while less important than arterial vasoconstriction, works with the skeletal muscle pump, the respiratory pump, and their valves to promote venous return to the heart. 20.3 Capillary Exchange Small molecules can cross into and out of capillaries via simple or facilitated diffusion. Some large molecules can cross in vesicles or through clefts, fenestrations, or gaps between cells in capillary walls. However, the bulk flow of capillary and tissue fluid occurs via filtration and reabsorption. Filtration, the movement of fluid out of the capillaries, is driven by the CHP. Reabsorption, the influx of tissue fluid into the capillaries, is driven by the BCOP. Filtration predominates in the arterial end of the capillary; in the middle section, the opposing pressures are virtually identical so there is no net exchange, whereas reabsorption predominates at the venule end of the capillary. The hydrostatic and colloid osmotic pressures in the interstitial fluid are negligible in healthy circumstances. 20.4 Homeostatic Regulation of the Vascular System Neural, endocrine, and autoregulatory mechanisms affect blood flow, blood pressure, and eventually perfusion of blood to body tissues. Neural mechanisms include the cardiovascular centers in the medulla oblongata, baroreceptors in the aorta and carotid arteries and right atrium, and associated chemoreceptors that monitor blood levels of oxygen, carbon dioxide, and hydrogen ions. Endocrine controls include epinephrine and norepinephrine, as well as ADH, the renin-angiotensin-aldosterone mechanism, ANH, and EPO. Autoregulation is the local control of vasodilation and constriction by chemical signals and the myogenic response. Exercise greatly improves cardiovascular function and reduces the risk of cardiovascular diseases, including hypertension, a leading cause of heart attacks and strokes. Significant hemorrhage can lead to a form of circulatory shock known as hypovolemic shock. Sepsis, obstruction, and widespread inflammation can also cause circulatory shock. 20.5 Circulatory Pathways The right ventricle pumps oxygen-depleted blood into the pulmonary trunk and right and left pulmonary arteries, which carry it to the right and left lungs for gas exchange. Oxygen-rich blood is transported by pulmonary veins to the left atrium. The left ventricle pumps this blood into the aorta. The main regions of the aorta are the ascending aorta, aortic arch, and descending aorta, which is further divided into the thoracic and abdominal aorta. The coronary arteries branch from the ascending aorta. After oxygenating tissues in the capillaries, systemic blood is returned to the right atrium from the venous system via the superior vena cava, which drains most of the veins superior to the diaphragm, the inferior vena cava, which drains most of the veins inferior to the diaphragm, and the coronary veins via the coronary sinus. The hepatic portal system carries blood to the liver for processing before it enters circulation. Review the figures provided in this section for circulation of blood through the blood vessels. 20.6 Development of Blood Vessels and Fetal Circulation Blood vessels begin to form from the embryonic mesoderm. The precursor hemangioblasts differentiate into angioblasts, which give rise to the blood vessels and pluripotent stem cells that differentiate into the formed elements of the blood. Together, these cells form blood islands scattered throughout the embryo. Extensions known as vascular tubes eventually connect the vascular network. As the embryo grows within the mother’s womb, the placenta develops to supply blood rich in oxygen and nutrients via the umbilical vein and to remove wastes in oxygen-depleted blood via the umbilical arteries. Three major shunts found in the fetus are the foramen ovale and ductus arteriosus, which divert blood from the pulmonary to the systemic circuit, and the ductus venosus, which carries freshly oxygenated blood high in nutrients to the fetal heart. Interactive Link Questions Watch this video to explore capillaries and how they function in the body. Capillaries are never more than 100 micrometers away. What is the main component of interstitial fluid? 2.Listen to this CDC podcast to learn about hypertension, often described as a “silent killer.” What steps can you take to reduce your risk of a heart attack or stroke? Review Questions The endothelium is found in the ________. - tunica intima - tunica media - tunica externa - lumen Nervi vasorum control ________. - vasoconstriction - vasodilation - capillary permeability - both vasoconstriction and vasodilation Closer to the heart, arteries would be expected to have a higher percentage of ________. - endothelium - smooth muscle fibers - elastic fibers - collagenous fibers Which of the following best describes veins? - thick walled, small lumens, low pressure, lack valves - thin walled, large lumens, low pressure, have valves - thin walled, small lumens, high pressure, have valves - thick walled, large lumens, high pressure, lack valves An especially leaky type of capillary found in the liver and certain other tissues is called a ________. - capillary bed - fenestrated capillary - sinusoid capillary - metarteriole In a blood pressure measurement of 110/70, the number 70 is the ________. - systolic pressure - diastolic pressure - pulse pressure - mean arterial pressure A healthy elastic artery ________. - is compliant - reduces blood flow - is a resistance artery - has a thin wall and irregular lumen Which of the following statements is true? - The longer the vessel, the lower the resistance and the greater the flow. - As blood volume decreases, blood pressure and blood flow also decrease. - Increased viscosity increases blood flow. - All of the above are true. Slight vasodilation in an arteriole prompts a ________. - slight increase in resistance - huge increase in resistance - slight decrease in resistance - huge decrease in resistance Venoconstriction increases which of the following? - blood pressure within the vein - blood flow within the vein - return of blood to the heart - all of the above Hydrostatic pressure is ________. - greater than colloid osmotic pressure at the venous end of the capillary bed - the pressure exerted by fluid in an enclosed space - about zero at the midpoint of a capillary bed - all of the above Net filtration pressure is calculated by ________. - adding the capillary hydrostatic pressure to the interstitial fluid hydrostatic pressure - subtracting the fluid drained by the lymphatic vessels from the total fluid in the interstitial fluid - adding the blood colloid osmotic pressure to the capillary hydrostatic pressure - subtracting the blood colloid osmotic pressure from the capillary hydrostatic pressure Which of the following statements is true? - In one day, more fluid exits the capillary through filtration than enters through reabsorption. - In one day, approximately 35 mm of blood are filtered and 7 mm are reabsorbed. - In one day, the capillaries of the lymphatic system absorb about 20.4 liters of fluid. - None of the above are true. Clusters of neurons in the medulla oblongata that regulate blood pressure are known collectively as ________. - baroreceptors - angioreceptors - the cardiomotor mechanism - the cardiovascular center In the renin-angiotensin-aldosterone mechanism, ________. - decreased blood pressure prompts the release of renin from the liver - aldosterone prompts increased urine output - aldosterone prompts the kidneys to reabsorb sodium - all of the above In the myogenic response, ________. - muscle contraction promotes venous return to the heart - ventricular contraction strength is decreased - vascular smooth muscle responds to stretch - endothelins dilate muscular arteries A form of circulatory shock common in young children with severe diarrhea or vomiting is ________. - hypovolemic shock - anaphylactic shock - obstructive shock - hemorrhagic shock The coronary arteries branch off of the ________. - aortic valve - ascending aorta - aortic arch - thoracic aorta Which of the following statements is true? - The left and right common carotid arteries both branch off of the brachiocephalic trunk. - The brachial artery is the distal branch of the axillary artery. - The radial and ulnar arteries join to form the palmar arch. - All of the above are true. Arteries serving the stomach, pancreas, and liver all branch from the ________. - superior mesenteric artery - inferior mesenteric artery - celiac trunk - splenic artery The right and left brachiocephalic veins ________. - drain blood from the right and left internal jugular veins - drain blood from the right and left subclavian veins - drain into the superior vena cava - all of the above are true The hepatic portal system delivers blood from the digestive organs to the ________. - liver - hypothalamus - spleen - left atrium Blood islands are ________. - clusters of blood-filtering cells in the placenta - masses of pluripotent stem cells scattered throughout the fetal bone marrow - vascular tubes that give rise to the embryonic tubular heart - masses of developing blood vessels and formed elements scattered throughout the embryonic disc Which of the following statements is true? - Two umbilical veins carry oxygen-depleted blood from the fetal circulation to the placenta. - One umbilical vein carries oxygen-rich blood from the placenta to the fetal heart. - Two umbilical arteries carry oxygen-depleted blood to the fetal lungs. - None of the above are true. The ductus venosus is a shunt that allows ________. - fetal blood to flow from the right atrium to the left atrium - fetal blood to flow from the right ventricle to the left ventricle - most freshly oxygenated blood to flow into the fetal heart - most oxygen-depleted fetal blood to flow directly into the fetal pulmonary trunk Critical Thinking Questions Arterioles are often referred to as resistance vessels. Why? 29.Cocaine use causes vasoconstriction. Is this likely to increase or decrease blood pressure, and why? 30.A blood vessel with a few smooth muscle fibers and connective tissue, and only a very thin tunica externa conducts blood toward the heart. What type of vessel is this? 31.You measure a patient’s blood pressure at 130/85. Calculate the patient’s pulse pressure and mean arterial pressure. Determine whether each pressure is low, normal, or high. 32.An obese patient comes to the clinic complaining of swollen feet and ankles, fatigue, shortness of breath, and often feeling “spaced out.” She is a cashier in a grocery store, a job that requires her to stand all day. Outside of work, she engages in no physical activity. She confesses that, because of her weight, she finds even walking uncomfortable. Explain how the skeletal muscle pump might play a role in this patient’s signs and symptoms. 33.A patient arrives at the emergency department with dangerously low blood pressure. The patient’s blood colloid osmotic pressure is normal. How would you expect this situation to affect the patient’s net filtration pressure? 34.True or false? The plasma proteins suspended in blood cross the capillary cell membrane and enter the tissue fluid via facilitated diffusion. Explain your thinking. 35.A patient arrives in the emergency department with a blood pressure of 70/45 confused and complaining of thirst. Why? 36.Nitric oxide is broken down very quickly after its release. Why? 37.Identify the ventricle of the heart that pumps oxygen-depleted blood and the arteries of the body that carry oxygen-depleted blood. 38.What organs do the gonadal veins drain? 39.What arteries play the leading roles in supplying blood to the brain? 40.All tissues, including malignant tumors, need a blood supply. Explain why drugs called angiogenesis inhibitors would be used in cancer treatment. 41.Explain the location and importance of the ductus arteriosus in fetal circulation.	oercommons	2025-03-18T00:37:01.120737	null	{ "license": "Creative Commons - Attribution - https://creativecommons.org/licenses/by/4.0/", "url": "https://oercommons.org/courseware/lesson/58766/overview", "title": "Anatomy and Physiology, Fluids and Transport", "author": null }
https://oercommons.org/courseware/lesson/58767/overview	The Lymphatic and Immune System Introduction Figure 21.1 The Worldwide AIDS Epidemic (a) As of 2008, more than 15 percent of adults were infected with HIV in certain African countries. This grim picture had changed little by 2012. (b) In this scanning electron micrograph, HIV virions (green particles) are budding off the surface of a macrophage (pink structure). (credit b: C. Goldsmith) CHAPTER OBJECTIVES After studying this chapter, you will be able to: - Identify the components and anatomy of the lymphatic system - Discuss the role of the innate immune response against pathogens - Describe the power of the adaptive immune response to cure disease - Explain immunological deficiencies and over-reactions of the immune system - Discuss the role of the immune response in transplantation and cancer - Describe the interaction of the immune and lymphatic systems with other body systems In June 1981, the Centers for Disease Control and Prevention (CDC), in Atlanta, Georgia, published a report of an unusual cluster of five patients in Los Angeles, California. All five were diagnosed with a rare pneumonia caused by a fungus called Pneumocystis jirovecii (formerly known as Pneumocystis carinii). Why was this unusual? Although commonly found in the lungs of healthy individuals, this fungus is an opportunistic pathogen that causes disease in individuals with suppressed or underdeveloped immune systems. The very young, whose immune systems have yet to mature, and the elderly, whose immune systems have declined with age, are particularly susceptible. The five patients from LA, though, were between 29 and 36 years of age and should have been in the prime of their lives, immunologically speaking. What could be going on? A few days later, a cluster of eight cases was reported in New York City, also involving young patients, this time exhibiting a rare form of skin cancer known as Kaposi’s sarcoma. This cancer of the cells that line the blood and lymphatic vessels was previously observed as a relatively innocuous disease of the elderly. The disease that doctors saw in 1981 was frighteningly more severe, with multiple, fast-growing lesions that spread to all parts of the body, including the trunk and face. Could the immune systems of these young patients have been compromised in some way? Indeed, when they were tested, they exhibited extremely low numbers of a specific type of white blood cell in their bloodstreams, indicating that they had somehow lost a major part of the immune system. Acquired immune deficiency syndrome, or AIDS, turned out to be a new disease caused by the previously unknown human immunodeficiency virus (HIV). Although nearly 100 percent fatal in those with active HIV infections in the early years, the development of anti-HIV drugs has transformed HIV infection into a chronic, manageable disease and not the certain death sentence it once was. One positive outcome resulting from the emergence of HIV disease was that the public’s attention became focused as never before on the importance of having a functional and healthy immune system. Anatomy of the Lymphatic and Immune Systems - Describe the structure and function of the lymphatic tissue (lymph fluid, vessels, ducts, and organs) - Describe the structure and function of the primary and secondary lymphatic organs - Discuss the cells of the immune system, how they function, and their relationship with the lymphatic system The immune system is the complex collection of cells and organs that destroys or neutralizes pathogens that would otherwise cause disease or death. The lymphatic system, for most people, is associated with the immune system to such a degree that the two systems are virtually indistinguishable. The lymphatic system is the system of vessels, cells, and organs that carries excess fluids to the bloodstream and filters pathogens from the blood. The swelling of lymph nodes during an infection and the transport of lymphocytes via the lymphatic vessels are but two examples of the many connections between these critical organ systems. Functions of the Lymphatic System A major function of the lymphatic system is to drain body fluids and return them to the bloodstream. Blood pressure causes leakage of fluid from the capillaries, resulting in the accumulation of fluid in the interstitial space—that is, spaces between individual cells in the tissues. In humans, 20 liters of plasma is released into the interstitial space of the tissues each day due to capillary filtration. Once this filtrate is out of the bloodstream and in the tissue spaces, it is referred to as interstitial fluid. Of this, 17 liters is reabsorbed directly by the blood vessels. But what happens to the remaining three liters? This is where the lymphatic system comes into play. It drains the excess fluid and empties it back into the bloodstream via a series of vessels, trunks, and ducts. Lymph is the term used to describe interstitial fluid once it has entered the lymphatic system. When the lymphatic system is damaged in some way, such as by being blocked by cancer cells or destroyed by injury, protein-rich interstitial fluid accumulates (sometimes “backs up” from the lymph vessels) in the tissue spaces. This inappropriate accumulation of fluid referred to as lymphedema may lead to serious medical consequences. As the vertebrate immune system evolved, the network of lymphatic vessels became convenient avenues for transporting the cells of the immune system. Additionally, the transport of dietary lipids and fat-soluble vitamins absorbed in the gut uses this system. Cells of the immune system not only use lymphatic vessels to make their way from interstitial spaces back into the circulation, but they also use lymph nodes as major staging areas for the development of critical immune responses. A lymph node is one of the small, bean-shaped organs located throughout the lymphatic system. INTERACTIVE LINK Visit this website for an overview of the lymphatic system. What are the three main components of the lymphatic system? Structure of the Lymphatic System The lymphatic vessels begin as as blind ending, or closed at one end, capillaries, which feed into larger and larger lymphatic vessels, and eventually empty into the bloodstream by a series of ducts. Along the way, the lymph travels through the lymph nodes, which are commonly found near the groin, armpits, neck, chest, and abdomen. Humans have about 500–600 lymph nodes throughout the body (Figure 21.2). Figure 21.2 Anatomy of the Lymphatic System Lymphatic vessels in the arms and legs convey lymph to the larger lymphatic vessels in the torso. A major distinction between the lymphatic and cardiovascular systems in humans is that lymph is not actively pumped by the heart, but is forced through the vessels by the movements of the body, the contraction of skeletal muscles during body movements, and breathing. One-way valves (semi-lunar valves) in lymphatic vessels keep the lymph moving toward the heart. Lymph flows from the lymphatic capillaries, through lymphatic vessels, and then is dumped into the circulatory system via the lymphatic ducts located at the junction of the jugular and subclavian veins in the neck. Lymphatic Capillaries Lymphatic capillaries, also called the terminal lymphatics, are vessels where interstitial fluid enters the lymphatic system to become lymph fluid. Located in almost every tissue in the body, these vessels are interlaced among the arterioles and venules of the circulatory system in the soft connective tissues of the body (Figure 21.3). Exceptions are the central nervous system, bone marrow, bones, teeth, and the cornea of the eye, which do not contain lymph vessels. Figure 21.3 Lymphatic Capillaries Lymphatic capillaries are interlaced with the arterioles and venules of the cardiovascular system. Collagen fibers anchor a lymphatic capillary in the tissue (inset). Interstitial fluid slips through spaces between the overlapping endothelial cells that compose the lymphatic capillary. Lymphatic capillaries are formed by a one cell-thick layer of endothelial cells and represent the open end of the system, allowing interstitial fluid to flow into them via overlapping cells (see Figure 21.3). When interstitial pressure is low, the endothelial flaps close to prevent “backflow.” As interstitial pressure increases, the spaces between the cells open up, allowing the fluid to enter. Entry of fluid into lymphatic capillaries is also enabled by the collagen filaments that anchor the capillaries to surrounding structures. As interstitial pressure increases, the filaments pull on the endothelial cell flaps, opening up them even further to allow easy entry of fluid. In the small intestine, lymphatic capillaries called lacteals are critical for the transport of dietary lipids and lipid-soluble vitamins to the bloodstream. In the small intestine, dietary triglycerides combine with other lipids and proteins, and enter the lacteals to form a milky fluid called chyle. The chyle then travels through the lymphatic system, eventually entering the bloodstream. Larger Lymphatic Vessels, Trunks, and Ducts The lymphatic capillaries empty into larger lymphatic vessels, which are similar to veins in terms of their three-tunic structure and the presence of valves. These one-way valves are located fairly close to one another, and each one causes a bulge in the lymphatic vessel, giving the vessels a beaded appearance (see Figure 21.3). The superficial and deep lymphatics eventually merge to form larger lymphatic vessels known as lymphatic trunks. On the right side of the body, the right sides of the head, thorax, and right upper limb drain lymph fluid into the right subclavian vein via the right lymphatic duct (Figure 21.4). On the left side of the body, the remaining portions of the body drain into the larger thoracic duct, which drains into the left subclavian vein. The thoracic duct itself begins just beneath the diaphragm in the cisterna chyli, a sac-like chamber that receives lymph from the lower abdomen, pelvis, and lower limbs by way of the left and right lumbar trunks and the intestinal trunk. Figure 21.4 Major Trunks and Ducts of the Lymphatic System The thoracic duct drains a much larger portion of the body than does the right lymphatic duct. The overall drainage system of the body is asymmetrical (see Figure 21.4). The right lymphatic duct receives lymph from only the upper right side of the body. The lymph from the rest of the body enters the bloodstream through the thoracic duct via all the remaining lymphatic trunks. In general, lymphatic vessels of the subcutaneous tissues of the skin, that is, the superficial lymphatics, follow the same routes as veins, whereas the deep lymphatic vessels of the viscera generally follow the paths of arteries. The Organization of Immune Function The immune system is a collection of barriers, cells, and soluble proteins that interact and communicate with each other in extraordinarily complex ways. The modern model of immune function is organized into three phases based on the timing of their effects. The three temporal phases consist of the following: - Barrier defenses such as the skin and mucous membranes, which act instantaneously to prevent pathogenic invasion into the body tissues - The rapid but nonspecific innate immune response, which consists of a variety of specialized cells and soluble factors - The slower but more specific and effective adaptive immune response, which involves many cell types and soluble factors, but is primarily controlled by white blood cells (leukocytes) known as lymphocytes, which help control immune responses The cells of the blood, including all those involved in the immune response, arise in the bone marrow via various differentiation pathways from hematopoietic stem cells (Figure 21.5). In contrast with embryonic stem cells, hematopoietic stem cells are present throughout adulthood and allow for the continuous differentiation of blood cells to replace those lost to age or function. These cells can be divided into three classes based on function: - Phagocytic cells, which ingest pathogens to destroy them - Lymphocytes, which specifically coordinate the activities of adaptive immunity - Cells containing cytoplasmic granules, which help mediate immune responses against parasites and intracellular pathogens such as viruses Figure 21.5 Hematopoietic System of the Bone Marrow All the cells of the immune response as well as of the blood arise by differentiation from hematopoietic stem cells. Platelets are cell fragments involved in the clotting of blood. Lymphocytes: B Cells, T Cells, Plasma Cells, and Natural Killer Cells As stated above, lymphocytes are the primary cells of adaptive immune responses (Table 21.1). The two basic types of lymphocytes, B cells and T cells, are identical morphologically with a large central nucleus surrounded by a thin layer of cytoplasm. They are distinguished from each other by their surface protein markers as well as by the molecules they secrete. While B cells mature in red bone marrow and T cells mature in the thymus, they both initially develop from bone marrow. T cells migrate from bone marrow to the thymus gland where they further mature. B cells and T cells are found in many parts of the body, circulating in the bloodstream and lymph, and residing in secondary lymphoid organs, including the spleen and lymph nodes, which will be described later in this section. The human body contains approximately 1012 lymphocytes. B Cells B cells are immune cells that function primarily by producing antibodies. An antibody is any of the group of proteins that binds specifically to pathogen-associated molecules known as antigens. An antigen is a chemical structure on the surface of a pathogen that binds to T or B lymphocyte antigen receptors. Once activated by binding to antigen, B cells differentiate into cells that secrete a soluble form of their surface antibodies. These activated B cells are known as plasma cells. T Cells The T cell, on the other hand, does not secrete antibody but performs a variety of functions in the adaptive immune response. Different T cell types have the ability to either secrete soluble factors that communicate with other cells of the adaptive immune response or destroy cells infected with intracellular pathogens. The roles of T and B lymphocytes in the adaptive immune response will be discussed further in this chapter. Plasma Cells Another type of lymphocyte of importance is the plasma cell. A plasma cell is a B cell that has differentiated in response to antigen binding, and has thereby gained the ability to secrete soluble antibodies. These cells differ in morphology from standard B and T cells in that they contain a large amount of cytoplasm packed with the protein-synthesizing machinery known as rough endoplasmic reticulum. Natural Killer Cells A fourth important lymphocyte is the natural killer cell, a participant in the innate immune response. A natural killer cell (NK) is a circulating blood cell that contains cytotoxic (cell-killing) granules in its extensive cytoplasm. It shares this mechanism with the cytotoxic T cells of the adaptive immune response. NK cells are among the body’s first lines of defense against viruses and certain types of cancer. Lymphocytes \| Type of lymphocyte \| Primary function \| \|---\|---\| \| B lymphocyte \| Generates diverse antibodies \| \| T lymphocyte \| Secretes chemical messengers \| \| Plasma cell \| Secretes antibodies \| \| NK cell \| Destroys virally infected cells \| Table 21.1 INTERACTIVE LINK Visit this website to learn about the many different cell types in the immune system and their very specialized jobs. What is the role of the dendritic cell in an HIV infection? Primary Lymphoid Organs and Lymphocyte Development Understanding the differentiation and development of B and T cells is critical to the understanding of the adaptive immune response. It is through this process that the body (ideally) learns to destroy only pathogens and leaves the body’s own cells relatively intact. The primary lymphoid organs are the bone marrow and thymus gland. The lymphoid organs are where lymphocytes mature, proliferate, and are selected, which enables them to attack pathogens without harming the cells of the body. Bone Marrow In the embryo, blood cells are made in the yolk sac. As development proceeds, this function is taken over by the spleen, lymph nodes, and liver. Later, the bone marrow takes over most hematopoietic functions, although the final stages of the differentiation of some cells may take place in other organs. The red bone marrow is a loose collection of cells where hematopoiesis occurs, and the yellow bone marrow is a site of energy storage, which consists largely of fat cells (Figure 21.6). The B cell undergoes nearly all of its development in the red bone marrow, whereas the immature T cell, called a thymocyte, leaves the bone marrow and matures largely in the thymus gland. Figure 21.6 Bone Marrow Red bone marrow fills the head of the femur, and a spot of yellow bone marrow is visible in the center. The white reference bar is 1 cm. Thymus The thymus gland is a bilobed organ found in the space between the sternum and the aorta of the heart (Figure 21.7). Connective tissue holds the lobes closely together but also separates them and forms a capsule. Figure 21.7 Location, Structure, and Histology of the Thymus The thymus lies above the heart. The trabeculae and lobules, including the darkly staining cortex and the lighter staining medulla of each lobule, are clearly visible in the light micrograph of the thymus of a newborn. LM × 100. (Micrograph provided by the Regents of the University of Michigan Medical School © 2012) INTERACTIVE LINK View the University of Michigan WebScope to explore the tissue sample in greater detail. The connective tissue capsule further divides the thymus into lobules via extensions called trabeculae. The outer region of the organ is known as the cortex and contains large numbers of thymocytes with some epithelial cells, macrophages, and dendritic cells (two types of phagocytic cells that are derived from monocytes). The cortex is densely packed so it stains more intensely than the rest of the thymus (see Figure 21.7). The medulla, where thymocytes migrate before leaving the thymus, contains a less dense collection of thymocytes, epithelial cells, and dendritic cells. AGING AND THE... Immune System By the year 2050, 25 percent of the population of the United States will be 60 years of age or older. The CDC estimates that 80 percent of those 60 years and older have one or more chronic disease associated with deficiencies of the immune systems. This loss of immune function with age is called immunosenescence. To treat this growing population, medical professionals must better understand the aging process. One major cause of age-related immune deficiencies is thymic involution, the shrinking of the thymus gland that begins at birth, at a rate of about three percent tissue loss per year, and continues until 35–45 years of age, when the rate declines to about one percent loss per year for the rest of one’s life. At that pace, the total loss of thymic epithelial tissue and thymocytes would occur at about 120 years of age. Thus, this age is a theoretical limit to a healthy human lifespan. Thymic involution has been observed in all vertebrate species that have a thymus gland. Animal studies have shown that transplanted thymic grafts between inbred strains of mice involuted according to the age of the donor and not of the recipient, implying the process is genetically programmed. There is evidence that the thymic microenvironment, so vital to the development of naïve T cells, loses thymic epithelial cells according to the decreasing expression of the FOXN1 gene with age. It is also known that thymic involution can be altered by hormone levels. Sex hormones such as estrogen and testosterone enhance involution, and the hormonal changes in pregnant women cause a temporary thymic involution that reverses itself, when the size of the thymus and its hormone levels return to normal, usually after lactation ceases. What does all this tell us? Can we reverse immunosenescence, or at least slow it down? The potential is there for using thymic transplants from younger donors to keep thymic output of naïve T cells high. Gene therapies that target gene expression are also seen as future possibilities. The more we learn through immunosenescence research, the more opportunities there will be to develop therapies, even though these therapies will likely take decades to develop. The ultimate goal is for everyone to live and be healthy longer, but there may be limits to immortality imposed by our genes and hormones. Secondary Lymphoid Organs and their Roles in Active Immune Responses Lymphocytes develop and mature in the primary lymphoid organs, but they mount immune responses from the secondary lymphoid organs. A naïve lymphocyte is one that has left the primary organ and entered a secondary lymphoid organ. Naïve lymphocytes are fully functional immunologically, but have yet to encounter an antigen to respond to. In addition to circulating in the blood and lymph, lymphocytes concentrate in secondary lymphoid organs, which include the lymph nodes, spleen, and lymphoid nodules. All of these tissues have many features in common, including the following: - The presence of lymphoid follicles, the sites of the formation of lymphocytes, with specific B cell-rich and T cell-rich areas - An internal structure of reticular fibers with associated fixed macrophages - Germinal centers, which are the sites of rapidly dividing and differentiating B lymphocytes - Specialized post-capillary vessels known as high endothelial venules; the cells lining these venules are thicker and more columnar than normal endothelial cells, which allow cells from the blood to directly enter these tissues Lymph Nodes Lymph nodes function to remove debris and pathogens from the lymph, and are thus sometimes referred to as the “filters of the lymph” (Figure 21.8). Any bacteria that infect the interstitial fluid are taken up by the lymphatic capillaries and transported to a regional lymph node. Dendritic cells and macrophages within this organ internalize and kill many of the pathogens that pass through, thereby removing them from the body. The lymph node is also the site of adaptive immune responses mediated by T cells, B cells, and accessory cells of the adaptive immune system. Like the thymus, the bean-shaped lymph nodes are surrounded by a tough capsule of connective tissue and are separated into compartments by trabeculae, the extensions of the capsule. In addition to the structure provided by the capsule and trabeculae, the structural support of the lymph node is provided by a series of reticular fibers laid down by fibroblasts. Figure 21.8 Structure and Histology of a Lymph Node Lymph nodes are masses of lymphatic tissue located along the larger lymph vessels. The micrograph of the lymph nodes shows a germinal center, which consists of rapidly dividing B cells surrounded by a layer of T cells and other accessory cells. LM × 128. (Micrograph provided by the Regents of the University of Michigan Medical School © 2012) INTERACTIVE LINK View the University of Michigan WebScope to explore the tissue sample in greater detail. The major routes into the lymph node are via afferent lymphatic vessels (see Figure 21.8). Cells and lymph fluid that leave the lymph node may do so by another set of vessels known as the efferent lymphatic vessels. Lymph enters the lymph node via the subcapsular sinus, which is occupied by dendritic cells, macrophages, and reticular fibers. Within the cortex of the lymph node are lymphoid follicles, which consist of germinal centers of rapidly dividing B cells surrounded by a layer of T cells and other accessory cells. As the lymph continues to flow through the node, it enters the medulla, which consists of medullary cords of B cells and plasma cells, and the medullary sinuses where the lymph collects before leaving the node via the efferent lymphatic vessels. Spleen In addition to the lymph nodes, the spleen is a major secondary lymphoid organ (Figure 21.9). It is about 12 cm (5 in) long and is attached to the lateral border of the stomach via the gastrosplenic ligament. The spleen is a fragile organ without a strong capsule, and is dark red due to its extensive vascularization. The spleen is sometimes called the “filter of the blood” because of its extensive vascularization and the presence of macrophages and dendritic cells that remove microbes and other materials from the blood, including dying red blood cells. The spleen also functions as the location of immune responses to blood-borne pathogens. Figure 21.9 Spleen (a) The spleen is attached to the stomach. (b) A micrograph of spleen tissue shows the germinal center. The marginal zone is the region between the red pulp and white pulp, which sequesters particulate antigens from the circulation and presents these antigens to lymphocytes in the white pulp. EM × 660. (Micrograph provided by the Regents of the University of Michigan Medical School © 2012) The spleen is also divided by trabeculae of connective tissue, and within each splenic nodule is an area of red pulp, consisting of mostly red blood cells, and white pulp, which resembles the lymphoid follicles of the lymph nodes. Upon entering the spleen, the splenic artery splits into several arterioles (surrounded by white pulp) and eventually into sinusoids. Blood from the capillaries subsequently collects in the venous sinuses and leaves via the splenic vein. The red pulp consists of reticular fibers with fixed macrophages attached, free macrophages, and all of the other cells typical of the blood, including some lymphocytes. The white pulp surrounds a central arteriole and consists of germinal centers of dividing B cells surrounded by T cells and accessory cells, including macrophages and dendritic cells. Thus, the red pulp primarily functions as a filtration system of the blood, using cells of the relatively nonspecific immune response, and white pulp is where adaptive T and B cell responses are mounted. Lymphoid Nodules The other lymphoid tissues, the lymphoid nodules, have a simpler architecture than the spleen and lymph nodes in that they consist of a dense cluster of lymphocytes without a surrounding fibrous capsule. These nodules are located in the respiratory and digestive tracts, areas routinely exposed to environmental pathogens. Tonsils are lymphoid nodules located along the inner surface of the pharynx and are important in developing immunity to oral pathogens (Figure 21.10). The tonsil located at the back of the throat, the pharyngeal tonsil, is sometimes referred to as the adenoid when swollen. Such swelling is an indication of an active immune response to infection. Histologically, tonsils do not contain a complete capsule, and the epithelial layer invaginates deeply into the interior of the tonsil to form tonsillar crypts. These structures, which accumulate all sorts of materials taken into the body through eating and breathing, actually “encourage” pathogens to penetrate deep into the tonsillar tissues where they are acted upon by numerous lymphoid follicles and eliminated. This seems to be the major function of tonsils—to help children’s bodies recognize, destroy, and develop immunity to common environmental pathogens so that they will be protected in their later lives. Tonsils are often removed in those children who have recurring throat infections, especially those involving the palatine tonsils on either side of the throat, whose swelling may interfere with their breathing and/or swallowing. Figure 21.10 Locations and Histology of the Tonsils (a) The pharyngeal tonsil is located on the roof of the posterior superior wall of the nasopharynx. The palatine tonsils lay on each side of the pharynx. (b) A micrograph shows the palatine tonsil tissue. LM × 40. (Micrograph provided by the Regents of the University of Michigan Medical School © 2012) INTERACTIVE LINK View the University of Michigan WebScope to explore the tissue sample in greater detail. Mucosa-associated lymphoid tissue (MALT) consists of an aggregate of lymphoid follicles directly associated with the mucous membrane epithelia. MALT makes up dome-shaped structures found underlying the mucosa of the gastrointestinal tract, breast tissue, lungs, and eyes. Peyer’s patches, a type of MALT in the small intestine, are especially important for immune responses against ingested substances (Figure 21.11). Peyer’s patches contain specialized endothelial cells called M (or microfold) cells that sample material from the intestinal lumen and transport it to nearby follicles so that adaptive immune responses to potential pathogens can be mounted. A similar process occurs involving MALT in the mucosa and submucosa of the appendix. A blockage of the lumen triggers these cells to elicit an inflammatory response that can lead to appendicitis. Figure 21.11 Mucosa-associated Lymphoid Tissue (MALT) Nodule LM × 40. (Micrograph provided by the Regents of the University of Michigan Medical School © 2012) Bronchus-associated lymphoid tissue (BALT) consists of lymphoid follicular structures with an overlying epithelial layer found along the bifurcations of the bronchi, and between bronchi and arteries. They also have the typically less-organized structure of other lymphoid nodules. These tissues, in addition to the tonsils, are effective against inhaled pathogens. Barrier Defenses and the Innate Immune Response - Describe the barrier defenses of the body - Show how the innate immune response is important and how it helps guide and prepare the body for adaptive immune responses - Describe various soluble factors that are part of the innate immune response - Explain the steps of inflammation and how they lead to destruction of a pathogen - Discuss early induced immune responses and their level of effectiveness The immune system can be divided into two overlapping mechanisms to destroy pathogens: the innate immune response, which is relatively rapid but nonspecific and thus not always effective, and the adaptive immune response, which is slower in its development during an initial infection with a pathogen, but is highly specific and effective at attacking a wide variety of pathogens (Figure 21.12). Figure 21.12 Cooperation between Innate and Adaptive Immune Responses The innate immune system enhances adaptive immune responses so they can be more effective. Any discussion of the innate immune response usually begins with the physical barriers that prevent pathogens from entering the body, destroy them after they enter, or flush them out before they can establish themselves in the hospitable environment of the body’s soft tissues. Barrier defenses are part of the body’s most basic defense mechanisms. The barrier defenses are not a response to infections, but they are continuously working to protect against a broad range of pathogens. The different modes of barrier defenses are associated with the external surfaces of the body, where pathogens may try to enter (Table 21.2). The primary barrier to the entrance of microorganisms into the body is the skin. Not only is the skin covered with a layer of dead, keratinized epithelium that is too dry for bacteria in which to grow, but as these cells are continuously sloughed off from the skin, they carry bacteria and other pathogens with them. Additionally, sweat and other skin secretions may lower pH, contain toxic lipids, and physically wash microbes away. Barrier Defenses \| Site \| Specific defense \| Protective aspect \| \|---\|---\|---\| \| Skin \| Epidermal surface \| Keratinized cells of surface, Langerhans cells \| \| Skin (sweat/secretions) \| Sweat glands, sebaceous glands \| Low pH, washing action \| \| Oral cavity \| Salivary glands \| Lysozyme \| \| Stomach \| Gastrointestinal tract \| Low pH \| \| Mucosal surfaces \| Mucosal epithelium \| Nonkeratinized epithelial cells \| \| Normal flora (nonpathogenic bacteria) \| Mucosal tissues \| Prevent pathogens from growing on mucosal surfaces \| Table 21.2 Another barrier is the saliva in the mouth, which is rich in lysozyme—an enzyme that destroys bacteria by digesting their cell walls. The acidic environment of the stomach, which is fatal to many pathogens, is also a barrier. Additionally, the mucus layer of the gastrointestinal tract, respiratory tract, reproductive tract, eyes, ears, and nose traps both microbes and debris, and facilitates their removal. In the case of the upper respiratory tract, ciliated epithelial cells move potentially contaminated mucus upwards to the mouth, where it is then swallowed into the digestive tract, ending up in the harsh acidic environment of the stomach. Considering how often you breathe compared to how often you eat or perform other activities that expose you to pathogens, it is not surprising that multiple barrier mechanisms have evolved to work in concert to protect this vital area. Cells of the Innate Immune Response A phagocyte is a cell that is able to surround and engulf a particle or cell, a process called phagocytosis. The phagocytes of the immune system engulf other particles or cells, either to clean an area of debris, old cells, or to kill pathogenic organisms such as bacteria. The phagocytes are the body’s fast acting, first line of immunological defense against organisms that have breached barrier defenses and have entered the vulnerable tissues of the body. Phagocytes: Macrophages and Neutrophils Many of the cells of the immune system have a phagocytic ability, at least at some point during their life cycles. Phagocytosis is an important and effective mechanism of destroying pathogens during innate immune responses. The phagocyte takes the organism inside itself as a phagosome, which subsequently fuses with a lysosome and its digestive enzymes, effectively killing many pathogens. On the other hand, some bacteria including Mycobacteria tuberculosis, the cause of tuberculosis, may be resistant to these enzymes and are therefore much more difficult to clear from the body. Macrophages, neutrophils, and dendritic cells are the major phagocytes of the immune system. A macrophage is an irregularly shaped phagocyte that is amoeboid in nature and is the most versatile of the phagocytes in the body. Macrophages move through tissues and squeeze through capillary walls using pseudopodia. They not only participate in innate immune responses but have also evolved to cooperate with lymphocytes as part of the adaptive immune response. Macrophages exist in many tissues of the body, either freely roaming through connective tissues or fixed to reticular fibers within specific tissues such as lymph nodes. When pathogens breach the body’s barrier defenses, macrophages are the first line of defense (Table 21.3). They are called different names, depending on the tissue: Kupffer cells in the liver, histiocytes in connective tissue, and alveolar macrophages in the lungs. A neutrophil is a phagocytic cell that is attracted via chemotaxis from the bloodstream to infected tissues. These spherical cells are granulocytes. A granulocyte contains cytoplasmic granules, which in turn contain a variety of vasoactive mediators such as histamine. In contrast, macrophages are agranulocytes. An agranulocyte has few or no cytoplasmic granules. Whereas macrophages act like sentries, always on guard against infection, neutrophils can be thought of as military reinforcements that are called into a battle to hasten the destruction of the enemy. Although, usually thought of as the primary pathogen-killing cell of the inflammatory process of the innate immune response, new research has suggested that neutrophils play a role in the adaptive immune response as well, just as macrophages do. A monocyte is a circulating precursor cell that differentiates into either a macrophage or dendritic cell, which can be rapidly attracted to areas of infection by signal molecules of inflammation. Phagocytic Cells of the Innate Immune System \| Cell \| Cell type \| Primary location \| Function in the innate immune response \| \|---\|---\|---\|---\| \| Macrophage \| Agranulocyte \| Body cavities/organs \| Phagocytosis \| \| Neutrophil \| Granulocyte \| Blood \| Phagocytosis \| \| Monocyte \| Agranulocyte \| Blood \| Precursor of macrophage/dendritic cell \| Table 21.3 Natural Killer Cells NK cells are a type of lymphocyte that have the ability to induce apoptosis, that is, programmed cell death, in cells infected with intracellular pathogens such as obligate intracellular bacteria and viruses. NK cells recognize these cells by mechanisms that are still not well understood, but that presumably involve their surface receptors. NK cells can induce apoptosis, in which a cascade of events inside the cell causes its own death by either of two mechanisms: 1) NK cells are able to respond to chemical signals and express the fas ligand. The fas ligand is a surface molecule that binds to the fas molecule on the surface of the infected cell, sending it apoptotic signals, thus killing the cell and the pathogen within it; or 2) The granules of the NK cells release perforins and granzymes. A perforin is a protein that forms pores in the membranes of infected cells. A granzyme is a protein-digesting enzyme that enters the cell via the perforin pores and triggers apoptosis intracellularly. Both mechanisms are especially effective against virally infected cells. If apoptosis is induced before the virus has the ability to synthesize and assemble all its components, no infectious virus will be released from the cell, thus preventing further infection. Recognition of Pathogens Cells of the innate immune response, the phagocytic cells, and the cytotoxic NK cells recognize patterns of pathogen-specific molecules, such as bacterial cell wall components or bacterial flagellar proteins, using pattern recognition receptors. A pattern recognition receptor (PRR) is a membrane-bound receptor that recognizes characteristic features of a pathogen and molecules released by stressed or damaged cells. These receptors, which are thought to have evolved prior to the adaptive immune response, are present on the cell surface whether they are needed or not. Their variety, however, is limited by two factors. First, the fact that each receptor type must be encoded by a specific gene requires the cell to allocate most or all of its DNA to make receptors able to recognize all pathogens. Secondly, the variety of receptors is limited by the finite surface area of the cell membrane. Thus, the innate immune system must “get by” using only a limited number of receptors that are active against as wide a variety of pathogens as possible. This strategy is in stark contrast to the approach used by the adaptive immune system, which uses large numbers of different receptors, each highly specific to a particular pathogen. Should the cells of the innate immune system come into contact with a species of pathogen they recognize, the cell will bind to the pathogen and initiate phagocytosis (or cellular apoptosis in the case of an intracellular pathogen) in an effort to destroy the offending microbe. Receptors vary somewhat according to cell type, but they usually include receptors for bacterial components and for complement, discussed below. Soluble Mediators of the Innate Immune Response The previous discussions have alluded to chemical signals that can induce cells to change various physiological characteristics, such as the expression of a particular receptor. These soluble factors are secreted during innate or early induced responses, and later during adaptive immune responses. Cytokines and Chemokines A cytokine is signaling molecule that allows cells to communicate with each other over short distances. Cytokines are secreted into the intercellular space, and the action of the cytokine induces the receiving cell to change its physiology. A chemokine is a soluble chemical mediator similar to cytokines except that its function is to attract cells (chemotaxis) from longer distances. INTERACTIVE LINK Visit this website to learn about phagocyte chemotaxis. Phagocyte chemotaxis is the movement of phagocytes according to the secretion of chemical messengers in the form of interleukins and other chemokines. By what means does a phagocyte destroy a bacterium that it has ingested? Early induced Proteins Early induced proteins are those that are not constitutively present in the body, but are made as they are needed early during the innate immune response. Interferons are an example of early induced proteins. Cells infected with viruses secrete interferons that travel to adjacent cells and induce them to make antiviral proteins. Thus, even though the initial cell is sacrificed, the surrounding cells are protected. Other early induced proteins specific for bacterial cell wall components are mannose-binding protein and C-reactive protein, made in the liver, which bind specifically to polysaccharide components of the bacterial cell wall. Phagocytes such as macrophages have receptors for these proteins, and they are thus able to recognize them as they are bound to the bacteria. This brings the phagocyte and bacterium into close proximity and enhances the phagocytosis of the bacterium by the process known as opsonization. Opsonization is the tagging of a pathogen for phagocytosis by the binding of an antibody or an antimicrobial protein. Complement System The complement system is a series of proteins constitutively found in the blood plasma. As such, these proteins are not considered part of the early induced immune response, even though they share features with some of the antibacterial proteins of this class. Made in the liver, they have a variety of functions in the innate immune response, using what is known as the “alternate pathway” of complement activation. Additionally, complement functions in the adaptive immune response as well, in what is called the classical pathway. The complement system consists of several proteins that enzymatically alter and fragment later proteins in a series, which is why it is termed cascade. Once activated, the series of reactions is irreversible, and releases fragments that have the following actions: - Bind to the cell membrane of the pathogen that activates it, labeling it for phagocytosis (opsonization) - Diffuse away from the pathogen and act as chemotactic agents to attract phagocytic cells to the site of inflammation - Form damaging pores in the plasma membrane of the pathogen Figure 21.13 shows the classical pathway, which requires antibodies of the adaptive immune response. The alternate pathway does not require an antibody to become activated. Figure 21.13 Complement Cascade and Function The classical pathway, used during adaptive immune responses, occurs when C1 reacts with antibodies that have bound an antigen. The splitting of the C3 protein is the common step to both pathways. In the alternate pathway, C3 is activated spontaneously and, after reacting with the molecules factor P, factor B, and factor D, splits apart. The larger fragment, C3b, binds to the surface of the pathogen and C3a, the smaller fragment, diffuses outward from the site of activation and attracts phagocytes to the site of infection. Surface-bound C3b then activates the rest of the cascade, with the last five proteins, C5–C9, forming the membrane-attack complex (MAC). The MAC can kill certain pathogens by disrupting their osmotic balance. The MAC is especially effective against a broad range of bacteria. The classical pathway is similar, except the early stages of activation require the presence of antibody bound to antigen, and thus is dependent on the adaptive immune response. The earlier fragments of the cascade also have important functions. Phagocytic cells such as macrophages and neutrophils are attracted to an infection site by chemotactic attraction to smaller complement fragments. Additionally, once they arrive, their receptors for surface-bound C3b opsonize the pathogen for phagocytosis and destruction. Inflammatory Response The hallmark of the innate immune response is inflammation. Inflammation is something everyone has experienced. Stub a toe, cut a finger, or do any activity that causes tissue damage and inflammation will result, with its four characteristics: heat, redness, pain, and swelling (“loss of function” is sometimes mentioned as a fifth characteristic). It is important to note that inflammation does not have to be initiated by an infection, but can also be caused by tissue injuries. The release of damaged cellular contents into the site of injury is enough to stimulate the response, even in the absence of breaks in physical barriers that would allow pathogens to enter (by hitting your thumb with a hammer, for example). The inflammatory reaction brings in phagocytic cells to the damaged area to clear cellular debris and to set the stage for wound repair (Figure 21.14). Figure 21.14 This reaction also brings in the cells of the innate immune system, allowing them to get rid of the sources of a possible infection. Inflammation is part of a very basic form of immune response. The process not only brings fluid and cells into the site to destroy the pathogen and remove it and debris from the site, but also helps to isolate the site, limiting the spread of the pathogen. Acute inflammation is a short-term inflammatory response to an insult to the body. If the cause of the inflammation is not resolved, however, it can lead to chronic inflammation, which is associated with major tissue destruction and fibrosis. Chronic inflammationis ongoing inflammation. It can be caused by foreign bodies, persistent pathogens, and autoimmune diseases such as rheumatoid arthritis. There are four important parts to the inflammatory response: - Tissue Injury. The released contents of injured cells stimulate the release of mast cell granules and their potent inflammatory mediators such as histamine, leukotrienes, and prostaglandins. Histamine increases the diameter of local blood vessels (vasodilation), causing an increase in blood flow. Histamine also increases the permeability of local capillaries, causing plasma to leak out and form interstitial fluid. This causes the swelling associated with inflammation. Additionally, injured cells, phagocytes, and basophils are sources of inflammatory mediators, including prostaglandins and leukotrienes. Leukotrienes attract neutrophils from the blood by chemotaxis and increase vascular permeability. Prostaglandins cause vasodilation by relaxing vascular smooth muscle and are a major cause of the pain associated with inflammation. Nonsteroidal anti-inflammatory drugs such as aspirin and ibuprofen relieve pain by inhibiting prostaglandin production. - Vasodilation. Many inflammatory mediators such as histamine are vasodilators that increase the diameters of local capillaries. This causes increased blood flow and is responsible for the heat and redness of inflamed tissue. It allows greater access of the blood to the site of inflammation. - Increased Vascular Permeability. At the same time, inflammatory mediators increase the permeability of the local vasculature, causing leakage of fluid into the interstitial space, resulting in the swelling, or edema, associated with inflammation. - Recruitment of Phagocytes. Leukotrienes are particularly good at attracting neutrophils from the blood to the site of infection by chemotaxis. Following an early neutrophil infiltrate stimulated by macrophage cytokines, more macrophages are recruited to clean up the debris left over at the site. When local infections are severe, neutrophils are attracted to the sites of infections in large numbers, and as they phagocytose the pathogens and subsequently die, their accumulated cellular remains are visible as pus at the infection site. Overall, inflammation is valuable for many reasons. Not only are the pathogens killed and debris removed, but the increase in vascular permeability encourages the entry of clotting factors, the first step towards wound repair. Inflammation also facilitates the transport of antigen to lymph nodes by dendritic cells for the development of the adaptive immune response. The Adaptive Immune Response: T lymphocytes and Their Functional Types - Explain the advantages of the adaptive immune response over the innate immune response - List the various characteristics of an antigen - Describe the types of T cell antigen receptors - Outline the steps of T cell development - Describe the major T cell types and their functions Innate immune responses (and early induced responses) are in many cases ineffective at completely controlling pathogen growth. However, they slow pathogen growth and allow time for the adaptive immune response to strengthen and either control or eliminate the pathogen. The innate immune system also sends signals to the cells of the adaptive immune system, guiding them in how to attack the pathogen. Thus, these are the two important arms of the immune response. The Benefits of the Adaptive Immune Response The specificity of the adaptive immune response—its ability to specifically recognize and make a response against a wide variety of pathogens—is its great strength. Antigens, the small chemical groups often associated with pathogens, are recognized by receptors on the surface of B and T lymphocytes. The adaptive immune response to these antigens is so versatile that it can respond to nearly any pathogen. This increase in specificity comes because the adaptive immune response has a unique way to develop as many as 1011, or 100 trillion, different receptors to recognize nearly every conceivable pathogen. How could so many different types of antibodies be encoded? And what about the many specificities of T cells? There is not nearly enough DNA in a cell to have a separate gene for each specificity. The mechanism was finally worked out in the 1970s and 1980s using the new tools of molecular genetics Primary Disease and Immunological Memory The immune system’s first exposure to a pathogen is called a primary adaptive response. Symptoms of a first infection, called primary disease, are always relatively severe because it takes time for an initial adaptive immune response to a pathogen to become effective. Upon re-exposure to the same pathogen, a secondary adaptive immune response is generated, which is stronger and faster that the primary response. The secondary adaptive response often eliminates a pathogen before it can cause significant tissue damage or any symptoms. Without symptoms, there is no disease, and the individual is not even aware of the infection. This secondary response is the basis of immunological memory, which protects us from getting diseases repeatedly from the same pathogen. By this mechanism, an individual’s exposure to pathogens early in life spares the person from these diseases later in life. Self Recognition A third important feature of the adaptive immune response is its ability to distinguish between self-antigens, those that are normally present in the body, and foreign antigens, those that might be on a potential pathogen. As T and B cells mature, there are mechanisms in place that prevent them from recognizing self-antigen, preventing a damaging immune response against the body. These mechanisms are not 100 percent effective, however, and their breakdown leads to autoimmune diseases, which will be discussed later in this chapter. T Cell-Mediated Immune Responses The primary cells that control the adaptive immune response are the lymphocytes, the T and B cells. T cells are particularly important, as they not only control a multitude of immune responses directly, but also control B cell immune responses in many cases as well. Thus, many of the decisions about how to attack a pathogen are made at the T cell level, and knowledge of their functional types is crucial to understanding the functioning and regulation of adaptive immune responses as a whole. T lymphocytes recognize antigens based on a two-chain protein receptor. The most common and important of these are the alpha-beta T cell receptors (Figure 21.15). Figure 21.15 Alpha-beta T Cell Receptor Notice the constant and variable regions of each chain, anchored by the transmembrane region. There are two chains in the T cell receptor, and each chain consists of two domains. The variable region domain is furthest away from the T cell membrane and is so named because its amino acid sequence varies between receptors. In contrast, the constant region domain has less variation. The differences in the amino acid sequences of the variable domains are the molecular basis of the diversity of antigens the receptor can recognize. Thus, the antigen-binding site of the receptor consists of the terminal ends of both receptor chains, and the amino acid sequences of those two areas combine to determine its antigenic specificity. Each T cell produces only one type of receptor and thus is specific for a single particular antigen. Antigens Antigens on pathogens are usually large and complex, and consist of many antigenic determinants. An antigenic determinant(epitope) is one of the small regions within an antigen to which a receptor can bind, and antigenic determinants are limited by the size of the receptor itself. They usually consist of six or fewer amino acid residues in a protein, or one or two sugar moieties in a carbohydrate antigen. Antigenic determinants on a carbohydrate antigen are usually less diverse than on a protein antigen. Carbohydrate antigens are found on bacterial cell walls and on red blood cells (the ABO blood group antigens). Protein antigens are complex because of the variety of three-dimensional shapes that proteins can assume, and are especially important for the immune responses to viruses and worm parasites. It is the interaction of the shape of the antigen and the complementary shape of the amino acids of the antigen-binding site that accounts for the chemical basis of specificity (Figure 21.16). Figure 21.16 Antigenic Determinants A typical protein antigen has multiple antigenic determinants, shown by the ability of T cells with three different specificities to bind to different parts of the same antigen. Antigen Processing and Presentation Although Figure 21.16 shows T cell receptors interacting with antigenic determinants directly, the mechanism that T cells use to recognize antigens is, in reality, much more complex. T cells do not recognize free-floating or cell-bound antigens as they appear on the surface of the pathogen. They only recognize antigen on the surface of specialized cells called antigen-presenting cells. Antigens are internalized by these cells. Antigen processing is a mechanism that enzymatically cleaves the antigen into smaller pieces. The antigen fragments are then brought to the cell’s surface and associated with a specialized type of antigen-presenting protein known as a major histocompatibility complex (MHC) molecule. The MHC is the cluster of genes that encode these antigen-presenting molecules. The association of the antigen fragments with an MHC molecule on the surface of a cell is known as antigen presentation and results in the recognition of antigen by a T cell. This association of antigen and MHC occurs inside the cell, and it is the complex of the two that is brought to the surface. The peptide-binding cleft is a small indentation at the end of the MHC molecule that is furthest away from the cell membrane; it is here that the processed fragment of antigen sits. MHC molecules are capable of presenting a variety of antigens, depending on the amino acid sequence, in their peptide-binding clefts. It is the combination of the MHC molecule and the fragment of the original peptide or carbohydrate that is actually physically recognized by the T cell receptor (Figure 21.17). Figure 21.17 Antigen Processing and Presentation Two distinct types of MHC molecules, MHC class I and MHC class II, play roles in antigen presentation. Although produced from different genes, they both have similar functions. They bring processed antigen to the surface of the cell via a transport vesicle and present the antigen to the T cell and its receptor. Antigens from different classes of pathogens, however, use different MHC classes and take different routes through the cell to get to the surface for presentation. The basic mechanism, though, is the same. Antigens are processed by digestion, are brought into the endomembrane system of the cell, and then are expressed on the surface of the antigen-presenting cell for antigen recognition by a T cell. Intracellular antigens are typical of viruses, which replicate inside the cell, and certain other intracellular parasites and bacteria. These antigens are processed in the cytosol by an enzyme complex known as the proteasome and are then brought into the endoplasmic reticulum by the transporter associated with antigen processing (TAP) system, where they interact with class I MHC molecules and are eventually transported to the cell surface by a transport vesicle. Extracellular antigens, characteristic of many bacteria, parasites, and fungi that do not replicate inside the cell’s cytoplasm, are brought into the endomembrane system of the cell by receptor-mediated endocytosis. The resulting vesicle fuses with vesicles from the Golgi complex, which contain pre-formed MHC class II molecules. After fusion of these two vesicles and the association of antigen and MHC, the new vesicle makes its way to the cell surface. Professional Antigen-presenting Cells Many cell types express class I molecules for the presentation of intracellular antigens. These MHC molecules may then stimulate a cytotoxic T cell immune response, eventually destroying the cell and the pathogen within. This is especially important when it comes to the most common class of intracellular pathogens, the virus. Viruses infect nearly every tissue of the body, so all these tissues must necessarily be able to express class I MHC or no T cell response can be made. On the other hand, class II MHC molecules are expressed only on the cells of the immune system, specifically cells that affect other arms of the immune response. Thus, these cells are called “professional” antigen-presenting cells to distinguish them from those that bear class I MHC. The three types of professional antigen presenters are macrophages, dendritic cells, and B cells (Table 21.4). Macrophages stimulate T cells to release cytokines that enhance phagocytosis. Dendritic cells also kill pathogens by phagocytosis (see Figure 21.17), but their major function is to bring antigens to regional draining lymph nodes. The lymph nodes are the locations in which most T cell responses against pathogens of the interstitial tissues are mounted. Macrophages are found in the skin and in the lining of mucosal surfaces, such as the nasopharynx, stomach, lungs, and intestines. B cells may also present antigens to T cells, which are necessary for certain types of antibody responses, to be covered later in this chapter. Classes of Antigen-presenting Cells \| MHC \| Cell type \| Phagocytic? \| Function \| \|---\|---\|---\|---\| \| Class I \| Many \| No \| Stimulates cytotoxic T cell immune response \| \| Class II \| Macrophage \| Yes \| Stimulates phagocytosis and presentation at primary infection site \| \| Class II \| Dendritic \| Yes, in tissues \| Brings antigens to regional lymph nodes \| \| Class II \| B cell \| Yes, internalizes surface Ig and antigen \| Stimulates antibody secretion by B cells \| Table 21.4 T Cell Development and Differentiation The process of eliminating T cells that might attack the cells of one’s own body is referred to as T cell tolerance. While thymocytes are in the cortex of the thymus, they are referred to as “double negatives,” meaning that they do not bear the CD4 or CD8 molecules that you can use to follow their pathways of differentiation (Figure 21.18). In the cortex of the thymus, they are exposed to cortical epithelial cells. In a process known as positive selection, double-negative thymocytes bind to the MHC molecules they observe on the thymic epithelia, and the MHC molecules of “self” are selected. This mechanism kills many thymocytes during T cell differentiation. In fact, only two percent of the thymocytes that enter the thymus leave it as mature, functional T cells. Figure 21.18 Differentiation of T Cells within the Thymus Thymocytes enter the thymus and go through a series of developmental stages that ensures both function and tolerance before they leave and become functional components of the adaptive immune response. Later, the cells become double positives that express both CD4 and CD8 markers and move from the cortex to the junction between the cortex and medulla. It is here that negative selection takes place. In negative selection, self-antigens are brought into the thymus from other parts of the body by professional antigen-presenting cells. The T cells that bind to these self-antigens are selected for negatively and are killed by apoptosis. In summary, the only T cells left are those that can bind to MHC molecules of the body with foreign antigens presented on their binding clefts, preventing an attack on one’s own body tissues, at least under normal circumstances. Tolerance can be broken, however, by the development of an autoimmune response, to be discussed later in this chapter. The cells that leave the thymus become single positives, expressing either CD4 or CD8, but not both (see Figure 21.18). The CD4+ T cells will bind to class II MHC and the CD8+ cells will bind to class I MHC. The discussion that follows explains the functions of these molecules and how they can be used to differentiate between the different T cell functional types. Mechanisms of T Cell-mediated Immune Responses Mature T cells become activated by recognizing processed foreign antigen in association with a self-MHC molecule and begin dividing rapidly by mitosis. This proliferation of T cells is called clonal expansion and is necessary to make the immune response strong enough to effectively control a pathogen. How does the body select only those T cells that are needed against a specific pathogen? Again, the specificity of a T cell is based on the amino acid sequence and the three-dimensional shape of the antigen-binding site formed by the variable regions of the two chains of the T cell receptor (Figure 21.19). Clonal selection is the process of antigen binding only to those T cells that have receptors specific to that antigen. Each T cell that is activated has a specific receptor “hard-wired” into its DNA, and all of its progeny will have identical DNA and T cell receptors, forming clones of the original T cell. Figure 21.19 Clonal Selection and Expansion of T Lymphocytes Stem cells differentiate into T cells with specific receptors, called clones. The clones with receptors specific for antigens on the pathogen are selected for and expanded. Clonal Selection and Expansion The clonal selection theory was proposed by Frank Burnet in the 1950s. However, the term clonal selection is not a complete description of the theory, as clonal expansion goes hand in glove with the selection process. The main tenet of the theory is that a typical individual has a multitude (1011) of different types of T cell clones based on their receptors. In this use, a clone is a group of lymphocytes that share the same antigen receptor. Each clone is necessarily present in the body in low numbers. Otherwise, the body would not have room for lymphocytes with so many specificities. Only those clones of lymphocytes whose receptors are activated by the antigen are stimulated to proliferate. Keep in mind that most antigens have multiple antigenic determinants, so a T cell response to a typical antigen involves a polyclonal response. A polyclonal response is the stimulation of multiple T cell clones. Once activated, the selected clones increase in number and make many copies of each cell type, each clone with its unique receptor. By the time this process is complete, the body will have large numbers of specific lymphocytes available to fight the infection (see Figure 21.19). The Cellular Basis of Immunological Memory As already discussed, one of the major features of an adaptive immune response is the development of immunological memory. During a primary adaptive immune response, both memory T cells and effector T cells are generated. Memory T cells are long-lived and can even persist for a lifetime. Memory cells are primed to act rapidly. Thus, any subsequent exposure to the pathogen will elicit a very rapid T cell response. This rapid, secondary adaptive response generates large numbers of effector T cells so fast that the pathogen is often overwhelmed before it can cause any symptoms of disease. This is what is meant by immunity to a disease. The same pattern of primary and secondary immune responses occurs in B cells and the antibody response, as will be discussed later in the chapter. T Cell Types and their Functions In the discussion of T cell development, you saw that mature T cells express either the CD4 marker or the CD8 marker, but not both. These markers are cell adhesion molecules that keep the T cell in close contact with the antigen-presenting cell by directly binding to the MHC molecule (to a different part of the molecule than does the antigen). Thus, T cells and antigen-presenting cells are held together in two ways: by CD4 or CD8 attaching to MHC and by the T cell receptor binding to antigen (Figure 21.20). Figure 21.20 Pathogen Presentation (a) CD4 is associated with helper and regulatory T cells. An extracellular pathogen is processed and presented in the binding cleft of a class II MHC molecule, and this interaction is strengthened by the CD4 molecule. (b) CD8 is associated with cytotoxic T cells. An intracellular pathogen is presented by a class I MHC molecule, and CD8 interacts with it. Although the correlation is not 100 percent, CD4-bearing T cells are associated with helper functions and CD8-bearing T cells are associated with cytotoxicity. These functional distinctions based on CD4 and CD8 markers are useful in defining the function of each type. Helper T Cells and their Cytokines Helper T cells (Th), bearing the CD4 molecule, function by secreting cytokines that act to enhance other immune responses. There are two classes of Th cells, and they act on different components of the immune response. These cells are not distinguished by their surface molecules but by the characteristic set of cytokines they secrete (Table 21.5). Th1 cells are a type of helper T cell that secretes cytokines that regulate the immunological activity and development of a variety of cells, including macrophages and other types of T cells. Th2 cells, on the other hand, are cytokine-secreting cells that act on B cells to drive their differentiation into plasma cells that make antibody. In fact, T cell help is required for antibody responses to most protein antigens, and these are called T cell-dependent antigens. Cytotoxic T cells Cytotoxic T cells (Tc) are T cells that kill target cells by inducing apoptosis using the same mechanism as NK cells. They either express Fas ligand, which binds to the fas molecule on the target cell, or act by using perforins and granzymes contained in their cytoplasmic granules. As was discussed earlier with NK cells, killing a virally infected cell before the virus can complete its replication cycle results in the production of no infectious particles. As more Tc cells are developed during an immune response, they overwhelm the ability of the virus to cause disease. In addition, each Tc cell can kill more than one target cell, making them especially effective. Tc cells are so important in the antiviral immune response that some speculate that this was the main reason the adaptive immune response evolved in the first place. Regulatory T Cells Regulatory T cells (Treg), or suppressor T cells, are the most recently discovered of the types listed here, so less is understood about them. In addition to CD4, they bear the molecules CD25 and FOXP3. Exactly how they function is still under investigation, but it is known that they suppress other T cell immune responses. This is an important feature of the immune response, because if clonal expansion during immune responses were allowed to continue uncontrolled, these responses could lead to autoimmune diseases and other medical issues. Not only do T cells directly destroy pathogens, but they regulate nearly all other types of the adaptive immune response as well, as evidenced by the functions of the T cell types, their surface markers, the cells they work on, and the types of pathogens they work against (see Table 21.5). Functions of T Cell Types and Their Cytokines \| T cell \| Main target \| Function \| Pathogen \| Surface marker \| MHC \| Cytokines or mediators \| \|---\|---\|---\|---\|---\|---\|---\| \| Tc \| Infected cells \| Cytotoxicity \| Intracellular \| CD8 \| Class I \| Perforins, granzymes, and fas ligand \| \| Th1 \| Macrophage \| Helper inducer \| Extracellular \| CD4 \| Class II \| Interferon-γ and TGF-β \| \| Th2 \| B cell \| Helper inducer \| Extracellular \| CD4 \| Class II \| IL-4, IL-6, IL-10, and others \| \| Treg \| Th cell \| Suppressor \| None \| CD4, CD25 \| ? \| TGF-β and IL-10 \| Table 21.5 The Adaptive Immune Response: B-lymphocytes and Antibodies - Explain how B cells mature and how B cell tolerance develops - Discuss how B cells are activated and differentiate into plasma cells - Describe the structure of the antibody classes and their functions Antibodies were the first component of the adaptive immune response to be characterized by scientists working on the immune system. It was already known that individuals who survived a bacterial infection were immune to re-infection with the same pathogen. Early microbiologists took serum from an immune patient and mixed it with a fresh culture of the same type of bacteria, then observed the bacteria under a microscope. The bacteria became clumped in a process called agglutination. When a different bacterial species was used, the agglutination did not happen. Thus, there was something in the serum of immune individuals that could specifically bind to and agglutinate bacteria. Scientists now know the cause of the agglutination is an antibody molecule, also called an immunoglobulin. What is an antibody? An antibody protein is essentially a secreted form of a B cell receptor. (In fact, surface immunoglobulin is another name for the B cell receptor.) Not surprisingly, the same genes encode both the secreted antibodies and the surface immunoglobulins. One minor difference in the way these proteins are synthesized distinguishes a naïve B cell with antibody on its surface from an antibody-secreting plasma cell with no antibodies on its surface. The antibodies of the plasma cell have the exact same antigen-binding site and specificity as their B cell precursors. There are five different classes of antibody found in humans: IgM, IgD, IgG, IgA, and IgE. Each of these has specific functions in the immune response, so by learning about them, researchers can learn about the great variety of antibody functions critical to many adaptive immune responses. B cells do not recognize antigen in the complex fashion of T cells. B cells can recognize native, unprocessed antigen and do not require the participation of MHC molecules and antigen-presenting cells. B Cell Differentiation and Activation B cells differentiate in the bone marrow. During the process of maturation, up to 100 trillion different clones of B cells are generated, which is similar to the diversity of antigen receptors seen in T cells. B cell differentiation and the development of tolerance are not quite as well understood as it is in T cells. Central tolerance is the destruction or inactivation of B cells that recognize self-antigens in the bone marrow, and its role is critical and well established. In the process of clonal deletion, immature B cells that bind strongly to self-antigens expressed on tissues are signaled to commit suicide by apoptosis, removing them from the population. In the process of clonal anergy, however, B cells exposed to soluble antigen in the bone marrow are not physically deleted, but become unable to function. Another mechanism called peripheral tolerance is a direct result of T cell tolerance. In peripheral tolerance, functional, mature B cells leave the bone marrow but have yet to be exposed to self-antigen. Most protein antigens require signals from helper T cells (Th2) to proceed to make antibody. When a B cell binds to a self-antigen but receives no signals from a nearby Th2 cell to produce antibody, the cell is signaled to undergo apoptosis and is destroyed. This is yet another example of the control that T cells have over the adaptive immune response. After B cells are activated by their binding to antigen, they differentiate into plasma cells. Plasma cells often leave the secondary lymphoid organs, where the response is generated, and migrate back to the bone marrow, where the whole differentiation process started. After secreting antibodies for a specific period, they die, as most of their energy is devoted to making antibodies and not to maintaining themselves. Thus, plasma cells are said to be terminally differentiated. The final B cell of interest is the memory B cell, which results from the clonal expansion of an activated B cell. Memory B cells function in a way similar to memory T cells. They lead to a stronger and faster secondary response when compared to the primary response, as illustrated below. Antibody Structure Antibodies are glycoproteins consisting of two types of polypeptide chains with attached carbohydrates. The heavy chain and the light chain are the two polypeptides that form the antibody. The main differences between the classes of antibodies are in the differences between their heavy chains, but as you shall see, the light chains have an important role, forming part of the antigen-binding site on the antibody molecules. Four-chain Models of Antibody Structures All antibody molecules have two identical heavy chains and two identical light chains. (Some antibodies contain multiple units of this four-chain structure.) The Fc region of the antibody is formed by the two heavy chains coming together, usually linked by disulfide bonds (Figure 21.21). The Fc portion of the antibody is important in that many effector cells of the immune system have Fc receptors. Cells having these receptors can then bind to antibody-coated pathogens, greatly increasing the specificity of the effector cells. At the other end of the molecule are two identical antigen-binding sites. Figure 21.21 Antibody and IgG2 Structures The typical four chain structure of a generic antibody (a) and the corresponding three-dimensional structure of the antibody IgG2 (b). (credit b: modification of work by Tim Vickers) Five Classes of Antibodies and their Functions In general, antibodies have two basic functions. They can act as the B cell antigen receptor or they can be secreted, circulate, and bind to a pathogen, often labeling it for identification by other forms of the immune response. Of the five antibody classes, notice that only two can function as the antigen receptor for naïve B cells: IgM and IgD (Figure 21.22). Mature B cells that leave the bone marrow express both IgM and IgD, but both antibodies have the same antigen specificity. Only IgM is secreted, however, and no other nonreceptor function for IgD has been discovered. Figure 21.22 Five Classes of Antibodies IgM consists of five four-chain structures (20 total chains with 10 identical antigen-binding sites) and is thus the largest of the antibody molecules. IgM is usually the first antibody made during a primary response. Its 10 antigen-binding sites and large shape allow it to bind well to many bacterial surfaces. It is excellent at binding complement proteins and activating the complement cascade, consistent with its role in promoting chemotaxis, opsonization, and cell lysis. Thus, it is a very effective antibody against bacteria at early stages of a primary antibody response. As the primary response proceeds, the antibody produced in a B cell can change to IgG, IgA, or IgE by the process known as class switching. Class switching is the change of one antibody class to another. While the class of antibody changes, the specificity and the antigen-binding sites do not. Thus, the antibodies made are still specific to the pathogen that stimulated the initial IgM response. IgG is a major antibody of late primary responses and the main antibody of secondary responses in the blood. This is because class switching occurs during primary responses. IgG is a monomeric antibody that clears pathogens from the blood and can activate complement proteins (although not as well as IgM), taking advantage of its antibacterial activities. Furthermore, this class of antibody is the one that crosses the placenta to protect the developing fetus from disease exits the blood to the interstitial fluid to fight extracellular pathogens. IgA exists in two forms, a four-chain monomer in the blood and an eight-chain structure, or dimer, in exocrine gland secretions of the mucous membranes, including mucus, saliva, and tears. Thus, dimeric IgA is the only antibody to leave the interior of the body to protect body surfaces. IgA is also of importance to newborns, because this antibody is present in mother’s breast milk (colostrum), which serves to protect the infant from disease. IgE is usually associated with allergies and anaphylaxis. It is present in the lowest concentration in the blood, because its Fc region binds strongly to an IgE-specific Fc receptor on the surfaces of mast cells. IgE makes mast cell degranulation very specific, such that if a person is allergic to peanuts, there will be peanut-specific IgE bound to his or her mast cells. In this person, eating peanuts will cause the mast cells to degranulate, sometimes causing severe allergic reactions, including anaphylaxis, a severe, systemic allergic response that can cause death. Clonal Selection of B Cells Clonal selection and expansion work much the same way in B cells as in T cells. Only B cells with appropriate antigen specificity are selected for and expanded (Figure 21.23). Eventually, the plasma cells secrete antibodies with antigenic specificity identical to those that were on the surfaces of the selected B cells. Notice in the figure that both plasma cells and memory B cells are generated simultaneously. Figure 21.23 Clonal Selection of B Cells During a primary B cell immune response, both antibody-secreting plasma cells and memory B cells are produced. These memory cells lead to the differentiation of more plasma cells and memory B cells during secondary responses. Primary versus Secondary B Cell Responses Primary and secondary responses as they relate to T cells were discussed earlier. This section will look at these responses with B cells and antibody production. Because antibodies are easily obtained from blood samples, they are easy to follow and graph (Figure 21.24). As you will see from the figure, the primary response to an antigen (representing a pathogen) is delayed by several days. This is the time it takes for the B cell clones to expand and differentiate into plasma cells. The level of antibody produced is low, but it is sufficient for immune protection. The second time a person encounters the same antigen, there is no time delay, and the amount of antibody made is much higher. Thus, the secondary antibody response overwhelms the pathogens quickly and, in most situations, no symptoms are felt. When a different antigen is used, another primary response is made with its low antibody levels and time delay. Figure 21.24 Primary and Secondary Antibody Responses Antigen A is given once to generate a primary response and later to generate a secondary response. When a different antigen is given for the first time, a new primary response is made. Active versus Passive Immunity Immunity to pathogens, and the ability to control pathogen growth so that damage to the tissues of the body is limited, can be acquired by (1) the active development of an immune response in the infected individual or (2) the passive transfer of immune components from an immune individual to a nonimmune one. Both active and passive immunity have examples in the natural world and as part of medicine. Active immunity is the resistance to pathogens acquired during an adaptive immune response within an individual (Table 21.6). Naturally acquired active immunity, the response to a pathogen, is the focus of this chapter. Artificially acquired active immunity involves the use of vaccines. A vaccine is a killed or weakened pathogen or its components that, when administered to a healthy individual, leads to the development of immunological memory (a weakened primary immune response) without causing much in the way of symptoms. Thus, with the use of vaccines, one can avoid the damage from disease that results from the first exposure to the pathogen, yet reap the benefits of protection from immunological memory. The advent of vaccines was one of the major medical advances of the twentieth century and led to the eradication of smallpox and the control of many infectious diseases, including polio, measles, and whooping cough. Active versus Passive Immunity \| Natural \| Artificial \| \| \|---\|---\|---\| \| Active \| Adaptive immune response \| Vaccine response \| \| Passive \| Trans-placental antibodies/breastfeeding \| Immune globulin injections \| Table 21.6 Passive immunity arises from the transfer of antibodies to an individual without requiring them to mount their own active immune response. Naturally acquired passive immunity is seen during fetal development. IgG is transferred from the maternal circulation to the fetus via the placenta, protecting the fetus from infection and protecting the newborn for the first few months of its life. As already stated, a newborn benefits from the IgA antibodies it obtains from milk during breastfeeding. The fetus and newborn thus benefit from the immunological memory of the mother to the pathogens to which she has been exposed. In medicine, artificially acquired passive immunity usually involves injections of immunoglobulins, taken from animals previously exposed to a specific pathogen. This treatment is a fast-acting method of temporarily protecting an individual who was possibly exposed to a pathogen. The downside to both types of passive immunity is the lack of the development of immunological memory. Once the antibodies are transferred, they are effective for only a limited time before they degrade. INTERACTIVE LINK Immunity can be acquired in an active or passive way, and it can be natural or artificial. Watch this video to see an animated discussion of passive and active immunity. What is an example of natural immunity acquired passively? T cell-dependent versus T cell-independent Antigens As discussed previously, Th2 cells secrete cytokines that drive the production of antibodies in a B cell, responding to complex antigens such as those made by proteins. On the other hand, some antigens are T cell independent. A T cell-independent antigenusually is in the form of repeated carbohydrate moieties found on the cell walls of bacteria. Each antibody on the B cell surface has two binding sites, and the repeated nature of T cell-independent antigen leads to crosslinking of the surface antibodies on the B cell. The crosslinking is enough to activate it in the absence of T cell cytokines. A T cell-dependent antigen, on the other hand, usually is not repeated to the same degree on the pathogen and thus does not crosslink surface antibody with the same efficiency. To elicit a response to such antigens, the B and T cells must come close together (Figure 21.25). The B cell must receive two signals to become activated. Its surface immunoglobulin must recognize native antigen. Some of this antigen is internalized, processed, and presented to the Th2 cells on a class II MHC molecule. The T cell then binds using its antigen receptor and is activated to secrete cytokines that diffuse to the B cell, finally activating it completely. Thus, the B cell receives signals from both its surface antibody and the T cell via its cytokines, and acts as a professional antigen-presenting cell in the process. Figure 21.25 T and B Cell Binding To elicit a response to a T cell-dependent antigen, the B and T cells must come close together. To become fully activated, the B cell must receive two signals from the native antigen and the T cell’s cytokines. The Immune Response against Pathogens - Explain the development of immunological competence - Describe the mucosal immune response - Discuss immune responses against bacterial, viral, fungal, and animal pathogens - Describe different ways pathogens evade immune responses Now that you understand the development of mature, naïve B cells and T cells, and some of their major functions, how do all of these various cells, proteins, and cytokines come together to actually resolve an infection? Ideally, the immune response will rid the body of a pathogen entirely. The adaptive immune response, with its rapid clonal expansion, is well suited to this purpose. Think of a primary infection as a race between the pathogen and the immune system. The pathogen bypasses barrier defenses and starts multiplying in the host’s body. During the first 4 to 5 days, the innate immune response will partially control, but not stop, pathogen growth. As the adaptive immune response gears up, however, it will begin to clear the pathogen from the body, while at the same time becoming stronger and stronger. When following antibody responses in patients with a particular disease such as a virus, this clearance is referred to as seroconversion (sero- = “serum”). Seroconversion is the reciprocal relationship between virus levels in the blood and antibody levels. As the antibody levels rise, the virus levels decline, and this is a sign that the immune response is being at least partially effective (partially, because in many diseases, seroconversion does not necessarily mean a patient is getting well). An excellent example of this is seroconversion during HIV disease (Figure 21.26). Notice that antibodies are made early in this disease, and the increase in anti-HIV antibodies correlates with a decrease in detectable virus in the blood. Although these antibodies are an important marker for diagnosing the disease, they are not sufficient to completely clear the virus. Several years later, the vast majority of these individuals, if untreated, will lose their entire adaptive immune response, including the ability to make antibodies, during the final stages of AIDS. Figure 21.26 HIV Disease Progression Seroconversion, the rise of anti-HIV antibody levels and the concomitant decline in measurable virus levels, happens during the first several months of HIV disease. Unfortunately, this antibody response is ineffective at controlling the disease, as seen by the progression of the disease towards AIDS, in which all adaptive immune responses are compromised. EVERYDAY CONNECTION Disinfectants: Fighting the Good Fight? “Wash your hands!” Parents have been telling their children this for generations. Dirty hands can spread disease. But is it possible to get rid of enough pathogens that children will never get sick? Are children who avoid exposure to pathogens better off? The answers to both these questions appears to be no. Antibacterial wipes, soaps, gels, and even toys with antibacterial substances embedded in their plastic are ubiquitous in our society. Still, these products do not rid the skin and gastrointestinal tract of bacteria, and it would be harmful to our health if they did. We need these nonpathogenic bacteria on and within our bodies to keep the pathogenic ones from growing. The urge to keep children perfectly clean is thus probably misguided. Children will get sick anyway, and the later benefits of immunological memory far outweigh the minor discomforts of most childhood diseases. In fact, getting diseases such as chickenpox or measles later in life is much harder on the adult and are associated with symptoms significantly worse than those seen in the childhood illnesses. Of course, vaccinations help children avoid some illnesses, but there are so many pathogens, we will never be immune to them all. Could over-cleanliness be the reason that allergies are increasing in more developed countries? Some scientists think so. Allergies are based on an IgE antibody response. Many scientists think the system evolved to help the body rid itself of worm parasites. The hygiene theory is the idea that the immune system is geared to respond to antigens, and if pathogens are not present, it will respond instead to inappropriate antigens such as allergens and self-antigens. This is one explanation for the rising incidence of allergies in developed countries, where the response to nonpathogens like pollen, shrimp, and cat dander cause allergic responses while not serving any protective function. The Mucosal Immune Response Mucosal tissues are major barriers to the entry of pathogens into the body. The IgA (and sometimes IgM) antibodies in mucus and other secretions can bind to the pathogen, and in the cases of many viruses and bacteria, neutralize them. Neutralization is the process of coating a pathogen with antibodies, making it physically impossible for the pathogen to bind to receptors. Neutralization, which occurs in the blood, lymph, and other body fluids and secretions, protects the body constantly. Neutralizing antibodies are the basis for the disease protection offered by vaccines. Vaccinations for diseases that commonly enter the body via mucous membranes, such as influenza, are usually formulated to enhance IgA production. Immune responses in some mucosal tissues such as the Peyer’s patches (see Figure 21.11) in the small intestine take up particulate antigens by specialized cells known as microfold or M cells (Figure 21.27). These cells allow the body to sample potential pathogens from the intestinal lumen. Dendritic cells then take the antigen to the regional lymph nodes, where an immune response is mounted. Figure 21.27 IgA Immunity The nasal-associated lymphoid tissue and Peyer’s patches of the small intestine generate IgA immunity. Both use M cells to transport antigen inside the body so that immune responses can be mounted. Defenses against Bacteria and Fungi The body fights bacterial pathogens with a wide variety of immunological mechanisms, essentially trying to find one that is effective. Bacteria such as Mycobacterium leprae, the cause of leprosy, are resistant to lysosomal enzymes and can persist in macrophage organelles or escape into the cytosol. In such situations, infected macrophages receiving cytokine signals from Th1 cells turn on special metabolic pathways. Macrophage oxidative metabolism is hostile to intracellular bacteria, often relying on the production of nitric oxide to kill the bacteria inside the macrophage. Fungal infections, such as those from Aspergillus, Candida, and Pneumocystis, are largely opportunistic infections that take advantage of suppressed immune responses. Most of the same immune mechanisms effective against bacteria have similar effects on fungi, both of which have characteristic cell wall structures that protect their cells. Defenses against Parasites Worm parasites such as helminths are seen as the primary reason why the mucosal immune response, IgE-mediated allergy and asthma, and eosinophils evolved. These parasites were at one time very common in human society. When infecting a human, often via contaminated food, some worms take up residence in the gastrointestinal tract. Eosinophils are attracted to the site by T cell cytokines, which release their granule contents upon their arrival. Mast cell degranulation also occurs, and the fluid leakage caused by the increase in local vascular permeability is thought to have a flushing action on the parasite, expelling its larvae from the body. Furthermore, if IgE labels the parasite, the eosinophils can bind to it by its Fc receptor. Defenses against Viruses The primary mechanisms against viruses are NK cells, interferons, and cytotoxic T cells. Antibodies are effective against viruses mostly during protection, where an immune individual can neutralize them based on a previous exposure. Antibodies have no effect on viruses or other intracellular pathogens once they enter the cell, since antibodies are not able to penetrate the plasma membrane of the cell. Many cells respond to viral infections by downregulating their expression of MHC class I molecules. This is to the advantage of the virus, because without class I expression, cytotoxic T cells have no activity. NK cells, however, can recognize virally infected class I-negative cells and destroy them. Thus, NK and cytotoxic T cells have complementary activities against virally infected cells. Interferons have activity in slowing viral replication and are used in the treatment of certain viral diseases, such as hepatitis B and C, but their ability to eliminate the virus completely is limited. The cytotoxic T cell response, though, is key, as it eventually overwhelms the virus and kills infected cells before the virus can complete its replicative cycle. Clonal expansion and the ability of cytotoxic T cells to kill more than one target cell make these cells especially effective against viruses. In fact, without cytotoxic T cells, it is likely that humans would all die at some point from a viral infection (if no vaccine were available). Evasion of the Immune System by Pathogens It is important to keep in mind that although the immune system has evolved to be able to control many pathogens, pathogens themselves have evolved ways to evade the immune response. An example already mentioned is in Mycobactrium tuberculosis, which has evolved a complex cell wall that is resistant to the digestive enzymes of the macrophages that ingest them, and thus persists in the host, causing the chronic disease tuberculosis. This section briefly summarizes other ways in which pathogens can “outwit” immune responses. But keep in mind, although it seems as if pathogens have a will of their own, they do not. All of these evasive “strategies” arose strictly by evolution, driven by selection. Bacteria sometimes evade immune responses because they exist in multiple strains, such as different groups of Staphylococcus aureus. S. aureus is commonly found in minor skin infections, such as boils, and some healthy people harbor it in their nose. One small group of strains of this bacterium, however, called methicillin-resistant Staphylococcus aureus, has become resistant to multiple antibiotics and is essentially untreatable. Different bacterial strains differ in the antigens on their surfaces. The immune response against one strain (antigen) does not affect the other; thus, the species survives. Another method of immune evasion is mutation. Because viruses’ surface molecules mutate continuously, viruses like influenza change enough each year that the flu vaccine for one year may not protect against the flu common to the next. New vaccine formulations must be derived for each flu season. Genetic recombination—the combining of gene segments from two different pathogens—is an efficient form of immune evasion. For example, the influenza virus contains gene segments that can recombine when two different viruses infect the same cell. Recombination between human and pig influenza viruses led to the 2010 H1N1 swine flu outbreak. Pathogens can produce immunosuppressive molecules that impair immune function, and there are several different types. Viruses are especially good at evading the immune response in this way, and many types of viruses have been shown to suppress the host immune response in ways much more subtle than the wholesale destruction caused by HIV. Diseases Associated with Depressed or Overactive Immune Responses - Discuss inherited and acquired immunodeficiencies - Explain the four types of hypersensitivity and how they differ - Give an example of how autoimmune disease breaks tolerance This section is about how the immune system goes wrong. When it goes haywire, and becomes too weak or too strong, it leads to a state of disease. The factors that maintain immunological homeostasis are complex and incompletely understood. Immunodeficiencies As you have seen, the immune system is quite complex. It has many pathways using many cell types and signals. Because it is so complex, there are many ways for it to go wrong. Inherited immunodeficiencies arise from gene mutations that affect specific components of the immune response. There are also acquired immunodeficiencies with potentially devastating effects on the immune system, such as HIV. Inherited Immunodeficiencies A list of all inherited immunodeficiencies is well beyond the scope of this book. The list is almost as long as the list of cells, proteins, and signaling molecules of the immune system itself. Some deficiencies, such as those for complement, cause only a higher susceptibility to some Gram-negative bacteria. Others are more severe in their consequences. Certainly, the most serious of the inherited immunodeficiencies is severe combined immunodeficiency disease (SCID). This disease is complex because it is caused by many different genetic defects. What groups them together is the fact that both the B cell and T cell arms of the adaptive immune response are affected. Children with this disease usually die of opportunistic infections within their first year of life unless they receive a bone marrow transplant. Such a procedure had not yet been perfected for David Vetter, the “boy in the bubble,” who was treated for SCID by having to live almost his entire life in a sterile plastic cocoon for the 12 years before his death from infection in 1984. One of the features that make bone marrow transplants work as well as they do is the proliferative capability of hematopoietic stem cells of the bone marrow. Only a small amount of bone marrow from a healthy donor is given intravenously to the recipient. It finds its own way to the bone where it populates it, eventually reconstituting the patient’s immune system, which is usually destroyed beforehand by treatment with radiation or chemotherapeutic drugs. New treatments for SCID using gene therapy, inserting nondefective genes into cells taken from the patient and giving them back, have the advantage of not needing the tissue match required for standard transplants. Although not a standard treatment, this approach holds promise, especially for those in whom standard bone marrow transplantation has failed. Human Immunodeficiency Virus/AIDS Although many viruses cause suppression of the immune system, only one wipes it out completely, and that is the previously mentioned HIV. It is worth discussing the biology of this virus, which can lead to the well-known AIDS, so that its full effects on the immune system can be understood. The virus is transmitted through semen, vaginal fluids, and blood, and can be caught by risky sexual behaviors and the sharing of needles by intravenous drug users. There are sometimes, but not always, flu-like symptoms in the first 1 to 2 weeks after infection. This is later followed by seroconversion. The anti-HIV antibodies formed during seroconversion are the basis for most initial HIV screening done in the United States. Because seroconversion takes different lengths of time in different individuals, multiple AIDS tests are given months apart to confirm or eliminate the possibility of infection. After seroconversion, the amount of virus circulating in the blood drops and stays at a low level for several years. During this time, the levels of CD4+ cells, especially helper T cells, decline steadily, until at some point, the immune response is so weak that opportunistic disease and eventually death result. HIV uses CD4 as the receptor to get inside cells, but it also needs a co-receptor, such as CCR5 or CXCR4. These co-receptors, which usually bind to chemokines, present another target for anti-HIV drug development. Although other antigen-presenting cells are infected with HIV, given that CD4+ helper T cells play an important role in T cell immune responses and antibody responses, it should be no surprise that both types of immune responses are eventually seriously compromised. Treatment for the disease consists of drugs that target virally encoded proteins that are necessary for viral replication but are absent from normal human cells. By targeting the virus itself and sparing the cells, this approach has been successful in significantly prolonging the lives of HIV-positive individuals. On the other hand, an HIV vaccine has been 30 years in development and is still years away. Because the virus mutates rapidly to evade the immune system, scientists have been looking for parts of the virus that do not change and thus would be good targets for a vaccine candidate. Hypersensitivities The word “hypersensitivity” simply means sensitive beyond normal levels of activation. Allergies and inflammatory responses to nonpathogenic environmental substances have been observed since the dawn of history. Hypersensitivity is a medical term describing symptoms that are now known to be caused by unrelated mechanisms of immunity. Still, it is useful for this discussion to use the four types of hypersensitivities as a guide to understand these mechanisms (Figure 21.28). Figure 21.28 Immune Hypersensitivity Components of the immune system cause four types of hypersensitivity. Notice that types I–III are B cell mediated, whereas type IV hypersensitivity is exclusively a T cell phenomenon. Immediate (Type I) Hypersensitivity Antigens that cause allergic responses are often referred to as allergens. The specificity of the immediate hypersensitivityresponse is predicated on the binding of allergen-specific IgE to the mast cell surface. The process of producing allergen-specific IgE is called sensitization, and is a necessary prerequisite for the symptoms of immediate hypersensitivity to occur. Allergies and allergic asthma are mediated by mast cell degranulation that is caused by the crosslinking of the antigen-specific IgE molecules on the mast cell surface. The mediators released have various vasoactive effects already discussed, but the major symptoms of inhaled allergens are the nasal edema and runny nose caused by the increased vascular permeability and increased blood flow of nasal blood vessels. As these mediators are released with mast cell degranulation, type I hypersensitivity reactions are usually rapid and occur within just a few minutes, hence the term immediate hypersensitivity. Most allergens are in themselves nonpathogenic and therefore innocuous. Some individuals develop mild allergies, which are usually treated with antihistamines. Others develop severe allergies that may cause anaphylactic shock, which can potentially be fatal within 20 to 30 minutes if untreated. This drop in blood pressure (shock) with accompanying contractions of bronchial smooth muscle is caused by systemic mast cell degranulation when an allergen is eaten (for example, shellfish and peanuts), injected (by a bee sting or being administered penicillin), or inhaled (asthma). Because epinephrine raises blood pressure and relaxes bronchial smooth muscle, it is routinely used to counteract the effects of anaphylaxis and can be lifesaving. Patients with known severe allergies are encouraged to keep automatic epinephrine injectors with them at all times, especially when away from easy access to hospitals. Allergists use skin testing to identify allergens in type I hypersensitivity. In skin testing, allergen extracts are injected into the epidermis, and a positive result of a soft, pale swelling at the site surrounded by a red zone (called the wheal and flare response), caused by the release of histamine and the granule mediators, usually occurs within 30 minutes. The soft center is due to fluid leaking from the blood vessels and the redness is caused by the increased blood flow to the area that results from the dilation of local blood vessels at the site. Type II and Type III Hypersensitivities Type II hypersensitivity, which involves IgG-mediated lysis of cells by complement proteins, occurs during mismatched blood transfusions and blood compatibility diseases such as erythroblastosis fetalis (see section on transplantation). Type III hypersensitivity occurs with diseases such as systemic lupus erythematosus, where soluble antigens, mostly DNA and other material from the nucleus, and antibodies accumulate in the blood to the point that the antigen and antibody precipitate along blood vessel linings. These immune complexes often lodge in the kidneys, joints, and other organs where they can activate complement proteins and cause inflammation. Delayed (Type IV) Hypersensitivity Delayed hypersensitivity, or type IV hypersensitivity, is basically a standard cellular immune response. In delayed hypersensitivity, the first exposure to an antigen is called sensitization, such that on re-exposure, a secondary cellular response results, secreting cytokines that recruit macrophages and other phagocytes to the site. These sensitized T cells, of the Th1 class, will also activate cytotoxic T cells. The time it takes for this reaction to occur accounts for the 24- to 72-hour delay in development. The classical test for delayed hypersensitivity is the tuberculin test for tuberculosis, where bacterial proteins from M. tuberculosisare injected into the skin. A couple of days later, a positive test is indicated by a raised red area that is hard to the touch, called an induration, which is a consequence of the cellular infiltrate, an accumulation of activated macrophages. A positive tuberculin test means that the patient has been exposed to the bacteria and exhibits a cellular immune response to it. Another type of delayed hypersensitivity is contact sensitivity, where substances such as the metal nickel cause a red and swollen area upon contact with the skin. The individual must have been previously sensitized to the metal. A much more severe case of contact sensitivity is poison ivy, but many of the harshest symptoms of the reaction are associated with the toxicity of its oils and are not T cell mediated. Autoimmune Responses The worst cases of the immune system over-reacting are autoimmune diseases. Somehow, tolerance breaks down and the immune systems in individuals with these diseases begin to attack their own bodies, causing significant damage. The trigger for these diseases is, more often than not, unknown, and the treatments are usually based on resolving the symptoms using immunosuppressive and anti-inflammatory drugs such as steroids. These diseases can be localized and crippling, as in rheumatoid arthritis, or diffuse in the body with multiple symptoms that differ in different individuals, as is the case with systemic lupus erythematosus (Figure 21.29). Figure 21.29 Autoimmune Disorders: Rheumatoid Arthritis and Lupus (a) Extensive damage to the right hand of a rheumatoid arthritis sufferer is shown in the x-ray. (b) The diagram shows a variety of possible symptoms of systemic lupus erythematosus. Environmental triggers seem to play large roles in autoimmune responses. One explanation for the breakdown of tolerance is that, after certain bacterial infections, an immune response to a component of the bacterium cross-reacts with a self-antigen. This mechanism is seen in rheumatic fever, a result of infection with Streptococcus bacteria, which causes strep throat. The antibodies to this pathogen’s M protein cross-react with an antigenic component of heart myosin, a major contractile protein of the heart that is critical to its normal function. The antibody binds to these molecules and activates complement proteins, causing damage to the heart, especially to the heart valves. On the other hand, some theories propose that having multiple common infectious diseases actually prevents autoimmune responses. The fact that autoimmune diseases are rare in countries that have a high incidence of infectious diseases supports this idea, another example of the hygiene hypothesis discussed earlier in this chapter. There are genetic factors in autoimmune diseases as well. Some diseases are associated with the MHC genes that an individual expresses. The reason for this association is likely because if one’s MHC molecules are not able to present a certain self-antigen, then that particular autoimmune disease cannot occur. Overall, there are more than 80 different autoimmune diseases, which are a significant health problem in the elderly. Table 21.7 lists several of the most common autoimmune diseases, the antigens that are targeted, and the segment of the adaptive immune response that causes the damage. Autoimmune Diseases \| Disease \| Autoantigen \| Symptoms \| \|---\|---\|---\| \| Celiac disease \| Tissue transglutaminase \| Damage to small intestine \| \| Diabetes mellitus type I \| Beta cells of pancreas \| Low insulin production; inability to regulate serum glucose \| \| Graves’ disease \| Thyroid-stimulating hormone receptor (antibody blocks receptor) \| Hyperthyroidism \| \| Hashimoto’s thyroiditis \| Thyroid-stimulating hormone receptor (antibody mimics hormone and stimulates receptor) \| Hypothyroidism \| \| Lupus erythematosus \| Nuclear DNA and proteins \| Damage of many body systems \| \| Myasthenia gravis \| Acetylcholine receptor in neuromuscular junctions \| Debilitating muscle weakness \| \| Rheumatoid arthritis \| Joint capsule antigens \| Chronic inflammation of joints \| Table 21.7 Transplantation and Cancer Immunology - Explain why blood typing is important and what happens when mismatched blood is used in a transfusion - Describe how tissue typing is done during organ transplantation and the role of transplant anti-rejection drugs - Show how the immune response is able to control some cancers and how this immune response might be enhanced by cancer vaccines The immune responses to transplanted organs and to cancer cells are both important medical issues. With the use of tissue typing and anti-rejection drugs, transplantation of organs and the control of the anti-transplant immune response have made huge strides in the past 50 years. Today, these procedures are commonplace. Tissue typing is the determination of MHC molecules in the tissue to be transplanted to better match the donor to the recipient. The immune response to cancer, on the other hand, has been more difficult to understand and control. Although it is clear that the immune system can recognize some cancers and control them, others seem to be resistant to immune mechanisms. The Rh Factor Red blood cells can be typed based on their surface antigens. ABO blood type, in which individuals are type A, B, AB, or O according to their genetics, is one example. A separate antigen system seen on red blood cells is the Rh antigen. When someone is “A positive” for example, the positive refers to the presence of the Rh antigen, whereas someone who is “A negative” would lack this molecule. An interesting consequence of Rh factor expression is seen in erythroblastosis fetalis, a hemolytic disease of the newborn (Figure 21.30). This disease occurs when mothers negative for Rh antigen have multiple Rh-positive children. During the birth of a first Rh-positive child, the mother makes a primary anti-Rh antibody response to the fetal blood cells that enter the maternal bloodstream. If the mother has a second Rh-positive child, IgG antibodies against Rh-positive blood mounted during this secondary response cross the placenta and attack the fetal blood, causing anemia. This is a consequence of the fact that the fetus is not genetically identical to the mother, and thus the mother is capable of mounting an immune response against it. This disease is treated with antibodies specific for Rh factor. These are given to the mother during the first and subsequent births, destroying any fetal blood that might enter her system and preventing the immune response. Figure 21.30 Erythroblastosis Fetalis Erythroblastosis fetalis (hemolytic disease of the newborn) is the result of an immune response in an Rh-negative mother who has multiple children with an Rh-positive father. During the first birth, fetal blood enters the mother’s circulatory system, and anti-Rh antibodies are made. During the gestation of the second child, these antibodies cross the placenta and attack the blood of the fetus. The treatment for this disease is to give the mother anti-Rh antibodies (RhoGAM) during the first pregnancy to destroy Rh-positive fetal red blood cells from entering her system and causing the anti-Rh antibody response in the first place. Tissue Transplantation Tissue transplantation is more complicated than blood transfusions because of two characteristics of MHC molecules. These molecules are the major cause of transplant rejection (hence the name “histocompatibility”). MHC polygeny refers to the multiple MHC proteins on cells, and MHC polymorphism refers to the multiple alleles for each individual MHC locus. Thus, there are many alleles in the human population that can be expressed (Table 21.8 and Table 21.9). When a donor organ expresses MHC molecules that are different from the recipient, the latter will often mount a cytotoxic T cell response to the organ and reject it. Histologically, if a biopsy of a transplanted organ exhibits massive infiltration of T lymphocytes within the first weeks after transplant, it is a sign that the transplant is likely to fail. The response is a classical, and very specific, primary T cell immune response. As far as medicine is concerned, the immune response in this scenario does the patient no good at all and causes significant harm. Partial Table of Alleles of the Human MHC (Class I) \| Gene \| # of alleles \| # of possible MHC I protein components \| \|---\|---\|---\| \| A \| 2132 \| 1527 \| \| B \| 2798 \| 2110 \| \| C \| 1672 \| 1200 \| \| E \| 11 \| 3 \| \| F \| 22 \| 4 \| \| G \| 50 \| 16 \| Table 21.8 Partial Table of Alleles of the Human MHC (Class II) \| Gene \| # of alleles \| # of possible MHC II protein components \| \|---\|---\|---\| \| DRA \| 7 \| 2 \| \| DRB \| 1297 \| 958 \| \| DQA1 \| 49 \| 31 \| \| DQB1 \| 179 \| 128 \| \| DPA1 \| 36 \| 18 \| \| DPB1 \| 158 \| 136 \| \| DMA \| 7 \| 4 \| \| DMB \| 13 \| 7 \| \| DOA \| 12 \| 3 \| \| DOB \| 13 \| 5 \| Table 21.9 Immunosuppressive drugs such as cyclosporine A have made transplants more successful, but matching the MHC molecules is still key. In humans, there are six MHC molecules that show the most polymorphisms, three class I molecules (A, B, and C) and three class II molecules called DP, DQ, and DR. A successful transplant usually requires a match between at least 3–4 of these molecules, with more matches associated with greater success. Family members, since they share a similar genetic background, are much more likely to share MHC molecules than unrelated individuals do. In fact, due to the extensive polymorphisms in these MHC molecules, unrelated donors are found only through a worldwide database. The system is not foolproof however, as there are not enough individuals in the system to provide the organs necessary to treat all patients needing them. One disease of transplantation occurs with bone marrow transplants, which are used to treat various diseases, including SCID and leukemia. Because the bone marrow cells being transplanted contain lymphocytes capable of mounting an immune response, and because the recipient’s immune response has been destroyed before receiving the transplant, the donor cells may attack the recipient tissues, causing graft-versus-host disease. Symptoms of this disease, which usually include a rash and damage to the liver and mucosa, are variable, and attempts have been made to moderate the disease by first removing mature T cells from the donor bone marrow before transplanting it. Immune Responses Against Cancer It is clear that with some cancers, for example Kaposi’s sarcoma, a healthy immune system does a good job at controlling them (Figure 21.31). This disease, which is caused by the human herpesvirus, is almost never observed in individuals with strong immune systems, such as the young and immunocompetent. Other examples of cancers caused by viruses include liver cancer caused by the hepatitis B virus and cervical cancer caused by the human papilloma virus. As these last two viruses have vaccines available for them, getting vaccinated can help prevent these two types of cancer by stimulating the immune response. Figure 21.31 Karposi’s Sarcoma Lesions (credit: National Cancer Institute) On the other hand, as cancer cells are often able to divide and mutate rapidly, they may escape the immune response, just as certain pathogens such as HIV do. There are three stages in the immune response to many cancers: elimination, equilibrium, and escape. Elimination occurs when the immune response first develops toward tumor-specific antigens specific to the cancer and actively kills most cancer cells, followed by a period of controlled equilibrium during which the remaining cancer cells are held in check. Unfortunately, many cancers mutate, so they no longer express any specific antigens for the immune system to respond to, and a subpopulation of cancer cells escapes the immune response, continuing the disease process. This fact has led to extensive research in trying to develop ways to enhance the early immune response to completely eliminate the early cancer and thus prevent a later escape. One method that has shown some success is the use of cancer vaccines, which differ from viral and bacterial vaccines in that they are directed against the cells of one’s own body. Treated cancer cells are injected into cancer patients to enhance their anti-cancer immune response and thereby prolong survival. The immune system has the capability to detect these cancer cells and proliferate faster than the cancer cells do, overwhelming the cancer in a similar way as they do for viruses. Cancer vaccines have been developed for malignant melanoma, a highly fatal skin cancer, and renal (kidney) cell carcinoma. These vaccines are still in the development stages, but some positive and encouraging results have been obtained clinically. It is tempting to focus on the complexity of the immune system and the problems it causes as a negative. The upside to immunity, however, is so much greater: The benefit of staying alive far outweighs the negatives caused when the system does sometimes go awry. Working on “autopilot,” the immune system helps to maintain your health and kill pathogens. The only time you really miss the immune response is when it is not being effective and illness results, or, as in the extreme case of HIV disease, the immune system is gone completely. EVERYDAY CONNECTION How Stress Affects the Immune Response: The Connections between the Immune, Nervous, and Endocrine Systems of the Body The immune system cannot exist in isolation. After all, it has to protect the entire body from infection. Therefore, the immune system is required to interact with other organ systems, sometimes in complex ways. Thirty years of research focusing on the connections between the immune system, the central nervous system, and the endocrine system have led to a new science with the unwieldy name of called psychoneuroimmunology. The physical connections between these systems have been known for centuries: All primary and secondary organs are connected to sympathetic nerves. What is more complex, though, is the interaction of neurotransmitters, hormones, cytokines, and other soluble signaling molecules, and the mechanism of “crosstalk” between the systems. For example, white blood cells, including lymphocytes and phagocytes, have receptors for various neurotransmitters released by associated neurons. Additionally, hormones such as cortisol (naturally produced by the adrenal cortex) and prednisone (synthetic) are well known for their abilities to suppress T cell immune mechanisms, hence, their prominent use in medicine as long-term, anti-inflammatory drugs. One well-established interaction of the immune, nervous, and endocrine systems is the effect of stress on immune health. In the human vertebrate evolutionary past, stress was associated with the fight-or-flight response, largely mediated by the central nervous system and the adrenal medulla. This stress was necessary for survival. The physical action of fighting or running, whichever the animal decides, usually resolves the problem in one way or another. On the other hand, there are no physical actions to resolve most modern day stresses, including short-term stressors like taking examinations and long-term stressors such as being unemployed or losing a spouse. The effect of stress can be felt by nearly every organ system, and the immune system is no exception (Table 21.10). Effects of Stress on Body Systems \| System \| Stress-related illness \| \|---\|---\| \| Integumentary system \| Acne, skin rashes, irritation \| \| Nervous system \| Headaches, depression, anxiety, irritability, loss of appetite, lack of motivation, reduced mental performance \| \| Muscular and skeletal systems \| Muscle and joint pain, neck and shoulder pain \| \| Circulatory system \| Increased heart rate, hypertension, increased probability of heart attacks \| \| Digestive system \| Indigestion, heartburn, stomach pain, nausea, diarrhea, constipation, weight gain or loss \| \| Immune system \| Depressed ability to fight infections \| \| Male reproductive system \| Lowered sperm production, impotence, reduced sexual desire \| \| Female reproductive system \| Irregular menstrual cycle, reduced sexual desire \| Table 21.10 At one time, it was assumed that all types of stress reduced all aspects of the immune response, but the last few decades of research have painted a different picture. First, most short-term stress does not impair the immune system in healthy individuals enough to lead to a greater incidence of diseases. However, older individuals and those with suppressed immune responses due to disease or immunosuppressive drugs may respond even to short-term stressors by getting sicker more often. It has been found that short-term stress diverts the body’s resources towards enhancing innate immune responses, which have the ability to act fast and would seem to help the body prepare better for possible infections associated with the trauma that may result from a fight-or-flight exchange. The diverting of resources away from the adaptive immune response, however, causes its own share of problems in fighting disease. Chronic stress, unlike short-term stress, may inhibit immune responses even in otherwise healthy adults. The suppression of both innate and adaptive immune responses is clearly associated with increases in some diseases, as seen when individuals lose a spouse or have other long-term stresses, such as taking care of a spouse with a fatal disease or dementia. The new science of psychoneuroimmunology, while still in its relative infancy, has great potential to make exciting advances in our understanding of how the nervous, endocrine, and immune systems have evolved together and communicate with each other. Key Terms - active immunity - immunity developed from an individual’s own immune system - acute inflammation - inflammation occurring for a limited time period; rapidly developing - adaptive immune response - relatively slow but very specific and effective immune response controlled by lymphocytes - afferent lymphatic vessels - lead into a lymph node - antibody - antigen-specific protein secreted by plasma cells; immunoglobulin - antigen - molecule recognized by the receptors of B and T lymphocytes - antigen presentation - binding of processed antigen to the protein-binding cleft of a major histocompatibility complex molecule - antigen processing - internalization and digestion of antigen in an antigen-presenting cell - antigen receptor - two-chain receptor by which lymphocytes recognize antigen - antigenic determinant - (also, epitope) one of the chemical groups recognized by a single type of lymphocyte antigen receptor - B cells - lymphocytes that act by differentiating into an antibody-secreting plasma cell - barrier defenses - antipathogen defenses deriving from a barrier that physically prevents pathogens from entering the body to establish an infection - bone marrow - tissue found inside bones; the site of all blood cell differentiation and maturation of B lymphocytes - bronchus-associated lymphoid tissue (BALT) - lymphoid nodule associated with the respiratory tract - central tolerance - B cell tolerance induced in immature B cells of the bone marrow - chemokine - soluble, long-range, cell-to-cell communication molecule - chronic inflammation - inflammation occurring for long periods of time - chyle - lipid-rich lymph inside the lymphatic capillaries of the small intestine - cisterna chyli - bag-like vessel that forms the beginning of the thoracic duct - class switching - ability of B cells to change the class of antibody they produce without altering the specificity for antigen - clonal anergy - process whereby B cells that react to soluble antigens in bone marrow are made nonfunctional - clonal deletion - removal of self-reactive B cells by inducing apoptosis - clonal expansion - growth of a clone of selected lymphocytes - clonal selection - stimulating growth of lymphocytes that have specific receptors - clone - group of lymphocytes sharing the same antigen receptor - complement - enzymatic cascade of constitutive blood proteins that have antipathogen effects, including the direct killing of bacteria - constant region domain - part of a lymphocyte antigen receptor that does not vary much between different receptor types - cytokine - soluble, short-range, cell-to-cell communication molecule - cytotoxic T cells (Tc) - T lymphocytes with the ability to induce apoptosis in target cells - delayed hypersensitivity - (type IV) T cell-mediated immune response against pathogens infiltrating interstitial tissues, causing cellular infiltrate - early induced immune response - includes antimicrobial proteins stimulated during the first several days of an infection - effector T cells - immune cells with a direct, adverse effect on a pathogen - efferent lymphatic vessels - lead out of a lymph node - erythroblastosis fetalis - disease of Rh factor-positive newborns in Rh-negative mothers with multiple Rh-positive children; resulting from the action of maternal antibodies against fetal blood - fas ligand - molecule expressed on cytotoxic T cells and NK cells that binds to the fas molecule on a target cell and induces it do undergo apoptosis - Fc region - in an antibody molecule, the site where the two termini of the heavy chains come together; many cells have receptors for this portion of the antibody, adding functionality to these molecules - germinal centers - clusters of rapidly proliferating B cells found in secondary lymphoid tissues - graft-versus-host disease - in bone marrow transplants; occurs when the transplanted cells mount an immune response against the recipient - granzyme - apoptosis-inducing substance contained in granules of NK cells and cytotoxic T cells - heavy chain - larger protein chain of an antibody - helper T cells (Th) - T cells that secrete cytokines to enhance other immune responses, involved in activation of both B and T cell lymphocytes - high endothelial venules - vessels containing unique endothelial cells specialized to allow migration of lymphocytes from the blood to the lymph node - histamine - vasoactive mediator in granules of mast cells and is the primary cause of allergies and anaphylactic shock - IgA - antibody whose dimer is secreted by exocrine glands, is especially effective against digestive and respiratory pathogens, and can pass immunity to an infant through breastfeeding - IgD - class of antibody whose only known function is as a receptor on naive B cells; important in B cell activation - IgE - antibody that binds to mast cells and causes antigen-specific degranulation during an allergic response - IgG - main blood antibody of late primary and early secondary responses; passed from mother to unborn child via placenta - IgM - antibody whose monomer is a surface receptor of naive B cells; the pentamer is the first antibody made blood plasma during primary responses - immediate hypersensitivity - (type I) IgE-mediated mast cell degranulation caused by crosslinking of surface IgE by antigen - immune system - series of barriers, cells, and soluble mediators that combine to response to infections of the body with pathogenic organisms - immunoglobulin - protein antibody; occurs as one of five main classes - immunological memory - ability of the adaptive immune response to mount a stronger and faster immune response upon re-exposure to a pathogen - inflammation - basic innate immune response characterized by heat, redness, pain, and swelling - innate immune response - rapid but relatively nonspecific immune response - interferons - early induced proteins made in virally infected cells that cause nearby cells to make antiviral proteins - light chain - small protein chain of an antibody - lymph - fluid contained within the lymphatic system - lymph node - one of the bean-shaped organs found associated with the lymphatic vessels - lymphatic capillaries - smallest of the lymphatic vessels and the origin of lymph flow - lymphatic system - network of lymphatic vessels, lymph nodes, and ducts that carries lymph from the tissues and back to the bloodstream. - lymphatic trunks - large lymphatics that collect lymph from smaller lymphatic vessels and empties into the blood via lymphatic ducts - lymphocytes - white blood cells characterized by a large nucleus and small rim of cytoplasm - lymphoid nodules - unencapsulated patches of lymphoid tissue found throughout the body - macrophage - ameboid phagocyte found in several tissues throughout the body - macrophage oxidative metabolism - metabolism turned on in macrophages by T cell signals that help destroy intracellular bacteria - major histocompatibility complex (MHC) - gene cluster whose proteins present antigens to T cells - mast cell - cell found in the skin and the lining of body cells that contains cytoplasmic granules with vasoactive mediators such as histamine - memory T cells - long-lived immune cell reserved for future exposure to an pathogen - MHC class I - found on most cells of the body, it binds to the CD8 molecule on T cells - MHC class II - found on macrophages, dendritic cells, and B cells, it binds to CD4 molecules on T cells - MHC polygeny - multiple MHC genes and their proteins found in body cells - MHC polymorphism - multiple alleles for each individual MHC locus - monocyte - precursor to macrophages and dendritic cells seen in the blood - mucosa-associated lymphoid tissue (MALT) - lymphoid nodule associated with the mucosa - naïve lymphocyte - mature B or T cell that has not yet encountered antigen for the first time - natural killer cell (NK) - cytotoxic lymphocyte of innate immune response - negative selection - selection against thymocytes in the thymus that react with self-antigen - neutralization - inactivation of a virus by the binding of specific antibody - neutrophil - phagocytic white blood cell recruited from the bloodstream to the site of infection via the bloodstream - opsonization - enhancement of phagocytosis by the binding of antibody or antimicrobial protein - passive immunity - transfer of immunity to a pathogen to an individual that lacks immunity to this pathogen usually by the injection of antibodies - pattern recognition receptor (PRR) - leukocyte receptor that binds to specific cell wall components of different bacterial species - perforin - molecule in NK cell and cytotoxic T cell granules that form pores in the membrane of a target cell - peripheral tolerance - mature B cell made tolerant by lack of T cell help - phagocytosis - movement of material from the outside to the inside of the cells via vesicles made from invaginations of the plasma membrane - plasma cell - differentiated B cell that is actively secreting antibody - polyclonal response - response by multiple clones to a complex antigen with many determinants - positive selection - selection of thymocytes within the thymus that interact with self, but not non-self, MHC molecules - primary adaptive response - immune system’s response to the first exposure to a pathogen - primary lymphoid organ - site where lymphocytes mature and proliferate; red bone marrow and thymus gland - psychoneuroimmunology - study of the connections between the immune, nervous, and endocrine systems - regulatory T cells (Treg) - (also, suppressor T cells) class of CD4 T cells that regulates other T cell responses - right lymphatic duct - drains lymph fluid from the upper right side of body into the right subclavian vein - secondary adaptive response - immune response observed upon re-exposure to a pathogen, which is stronger and faster than a primary response - secondary lymphoid organs - sites where lymphocytes mount adaptive immune responses; examples include lymph nodes and spleen - sensitization - first exposure to an antigen - seroconversion - clearance of pathogen in the serum and the simultaneous rise of serum antibody - severe combined immunodeficiency disease (SCID) - genetic mutation that affects both T cell and B cell arms of the immune response - spleen - secondary lymphoid organ that filters pathogens from the blood (white pulp) and removes degenerating or damaged blood cells (red pulp) - T cell - lymphocyte that acts by secreting molecules that regulate the immune system or by causing the destruction of foreign cells, viruses, and cancer cells - T cell tolerance - process during T cell differentiation where most T cells that recognize antigens from one’s own body are destroyed - T cell-dependent antigen - antigen that binds to B cells, which requires signals from T cells to make antibody - T cell-independent antigen - binds to B cells, which do not require signals from T cells to make antibody - Th1 cells - cells that secrete cytokines that enhance the activity of macrophages and other cells - Th2 cells - cells that secrete cytokines that induce B cells to differentiate into antibody-secreting plasma cells - thoracic duct - large duct that drains lymph from the lower limbs, left thorax, left upper limb, and the left side of the head - thymocyte - immature T cell found in the thymus - thymus - primary lymphoid organ; where T lymphocytes proliferate and mature - tissue typing - typing of MHC molecules between a recipient and donor for use in a potential transplantation procedure - tonsils - lymphoid nodules associated with the nasopharynx - type I hypersensitivity - immediate response mediated by mast cell degranulation caused by the crosslinking of the antigen-specific IgE molecules on the mast cell surface - type II hypersensitivity - cell damage caused by the binding of antibody and the activation of complement, usually against red blood cells - type III hypersensitivity - damage to tissues caused by the deposition of antibody-antigen (immune) complexes followed by the activation of complement - variable region domain - part of a lymphocyte antigen receptor that varies considerably between different receptor types Chapter Review 21.1 Anatomy of the Lymphatic and Immune Systems The lymphatic system is a series of vessels, ducts, and trunks that remove interstitial fluid from the tissues and return it the blood. The lymphatics are also used to transport dietary lipids and cells of the immune system. Cells of the immune system all come from the hematopoietic system of the bone marrow. Primary lymphoid organs, the bone marrow and thymus gland, are the locations where lymphocytes of the adaptive immune system proliferate and mature. Secondary lymphoid organs are site in which mature lymphocytes congregate to mount immune responses. Many immune system cells use the lymphatic and circulatory systems for transport throughout the body to search for and then protect against pathogens. 21.2 Barrier Defenses and the Innate Immune Response Innate immune responses are critical to the early control of infections. Whereas barrier defenses are the body’s first line of physical defense against pathogens, innate immune responses are the first line of physiological defense. Innate responses occur rapidly, but with less specificity and effectiveness than the adaptive immune response. Innate responses can be caused by a variety of cells, mediators, and antibacterial proteins such as complement. Within the first few days of an infection, another series of antibacterial proteins are induced, each with activities against certain bacteria, including opsonization of certain species. Additionally, interferons are induced that protect cells from viruses in their vicinity. Finally, the innate immune response does not stop when the adaptive immune response is developed. In fact, both can cooperate and one can influence the other in their responses against pathogens. 21.3 The Adaptive Immune Response: T lymphocytes and Their Functional Types T cells recognize antigens with their antigen receptor, a complex of two protein chains on their surface. They do not recognize self-antigens, however, but only processed antigen presented on their surfaces in a binding groove of a major histocompatibility complex molecule. T cells develop in the thymus, where they learn to use self-MHC molecules to recognize only foreign antigens, thus making them tolerant to self-antigens. There are several functional types of T lymphocytes, the major ones being helper, regulatory, and cytotoxic T cells. 21.4 The Adaptive Immune Response: B-lymphocytes and Antibodies B cells, which develop within the bone marrow, are responsible for making five different classes of antibodies, each with its own functions. B cells have their own mechanisms for tolerance, but in peripheral tolerance, the B cells that leave the bone marrow remain inactive due to T cell tolerance. Some B cells do not need T cell cytokines to make antibody, and they bypass this need by the crosslinking of their surface immunoglobulin by repeated carbohydrate residues found in the cell walls of many bacterial species. Others require T cells to become activated. 21.5 The Immune Response against Pathogens Early childhood is a time when the body develops much of its immunological memory that protects it from diseases in adulthood. The components of the immune response that have the maximum effectiveness against a pathogen are often associated with the class of pathogen involved. Bacteria and fungi are especially susceptible to damage by complement proteins, whereas viruses are taken care of by interferons and cytotoxic T cells. Worms are attacked by eosinophils. Pathogens have shown the ability, however, to evade the body’s immune responses, some leading to chronic infections or even death. The immune system and pathogens are in a slow, evolutionary race to see who stays on top. Modern medicine, hopefully, will keep the results skewed in humans’ favor. 21.6 Diseases Associated with Depressed or Overactive Immune Responses The immune response can be under-reactive or over-reactive. Suppressed immunity can result from inherited genetic defects or by acquiring viruses. Over-reactive immune responses include the hypersensitivities: B cell- and T cell-mediated immune responses designed to control pathogens, but that lead to symptoms or medical complications. The worst cases of over-reactive immune responses are autoimmune diseases, where an individual’s immune system attacks his or her own body because of the breakdown of immunological tolerance. These diseases are more common in the aged, so treating them will be a challenge in the future as the aged population in the world increases. 21.7 Transplantation and Cancer Immunology Blood transfusion and organ transplantation both require an understanding of the immune response to prevent medical complications. Blood needs to be typed so that natural antibodies against mismatched blood will not destroy it, causing more harm than good to the recipient. Transplanted organs must be matched by their MHC molecules and, with the use of immunosuppressive drugs, can be successful even if an exact tissue match cannot be made. Another aspect to the immune response is its ability to control and eradicate cancer. Although this has been shown to occur with some rare cancers and those caused by known viruses, the normal immune response to most cancers is not sufficient to control cancer growth. Thus, cancer vaccines designed to enhance these immune responses show promise for certain types of cancer. Interactive Link Questions Visit this website for an overview of the lymphatic system. What are the three main components of the lymphatic system? 2.Visit this website to learn about the many different cell types in the immune system and their very specialized jobs. What is the role of the dendritic cell in infection by HIV? 3.Visit this website to learn about phagocyte chemotaxis. Phagocyte chemotaxis is the movement of phagocytes according to the secretion of chemical messengers in the form of interleukins and other chemokines. By what means does a phagocyte destroy a bacterium that it has ingested? 4.Immunity can be acquired in an active or passive way, and it can be natural or artificial. Watch this video to see an animated discussion of passive and active immunity. What is an example of natural immunity acquired passively? Review Questions Which of the following cells is phagocytic? - plasma cell - macrophage - B cell - NK cell Which structure allows lymph from the lower right limb to enter the bloodstream? - thoracic duct - right lymphatic duct - right lymphatic trunk - left lymphatic trunk Which of the following cells is important in the innate immune response? - B cells - T cells - macrophages - plasma cells Which of the following cells would be most active in early, antiviral immune responses the first time one is exposed to pathogen? - macrophage - T cell - neutrophil - natural killer cell Which of the lymphoid nodules is most likely to see food antigens first? - tonsils - Peyer’s patches - bronchus-associated lymphoid tissue - mucosa-associated lymphoid tissue Which of the following signs is not characteristic of inflammation? - redness - pain - cold - swelling Which of the following is not important in the antiviral innate immune response? - interferons - natural killer cells - complement - microphages Enhanced phagocytosis of a cell by the binding of a specific protein is called ________. - endocytosis - opsonization - anaphylaxis - complement activation Which of the following leads to the redness of inflammation? - increased vascular permeability - anaphylactic shock - increased blood flow - complement activation T cells that secrete cytokines that help antibody responses are called ________. - Th1 - Th2 - regulatory T cells - thymocytes The taking in of antigen and digesting it for later presentation is called ________. - antigen presentation - antigen processing - endocytosis - exocytosis Why is clonal expansion so important? - to select for specific cells - to secrete cytokines - to kill target cells - to increase the numbers of specific cells The elimination of self-reactive thymocytes is called ________. - positive selection. - negative selection. - tolerance. - clonal selection. Which type of T cell is most effective against viruses? - Th1 - Th2 - cytotoxic T cells - regulatory T cells Removing functionality from a B cell without killing it is called ________. - clonal selection - clonal expansion - clonal deletion - clonal anergy Which class of antibody crosses the placenta in pregnant women? - IgM - IgA - IgE - IgG Which class of antibody has no known function other than as an antigen receptor? - IgM - IgA - IgE - IgD When does class switching occur? - primary response - secondary response - tolerance - memory response Which class of antibody is found in mucus? - IgM - IgA - IgE - IgD Which enzymes in macrophages are important for clearing intracellular bacteria? - metabolic - mitochondrial - nuclear - lysosomal What type of chronic lung disease is caused by a Mycobacterium? - asthma - emphysema - tuberculosis - leprosy Which type of immune response is most directly effective against bacteria? - natural killer cells - complement - cytotoxic T cells - helper T cells What is the reason that you have to be immunized with a new influenza vaccine each year? - the vaccine is only protective for a year - mutation - macrophage oxidative metabolism - memory response Which type of immune response works in concert with cytotoxic T cells against virally infected cells? - natural killer cells - complement - antibodies - memory Which type of hypersensitivity involves soluble antigen-antibody complexes? - type I - type II - type III - type IV What causes the delay in delayed hypersensitivity? - inflammation - cytokine release - recruitment of immune cells - histamine release Which of the following is a critical feature of immediate hypersensitivity? - inflammation - cytotoxic T cells - recruitment of immune cells - histamine release Which of the following is an autoimmune disease of the heart? - rheumatoid arthritis - lupus - rheumatic fever - Hashimoto’s thyroiditis What drug is used to counteract the effects of anaphylactic shock? - epinephrine - antihistamines - antibiotics - aspirin Which of the following terms means “many genes”? - polymorphism - polygeny - polypeptide - multiple alleles Why do we have natural antibodies? - We don’t know why. - immunity to environmental bacteria - immunity to transplants - from clonal selection Which type of cancer is associated with HIV disease? - Kaposi’s sarcoma - melanoma - lymphoma - renal cell carcinoma How does cyclosporine A work? - suppresses antibodies - suppresses T cells - suppresses macrophages - suppresses neutrophils What disease is associated with bone marrow transplants? - diabetes mellitus type I - melanoma - headache - graft-versus-host disease Critical Thinking Questions Describe the flow of lymph from its origins in interstitial fluid to its emptying into the venous bloodstream. 40.Describe the process of inflammation in an area that has been traumatized, but not infected. 41.Describe two early induced responses and what pathogens they affect. 42.Describe the processing and presentation of an intracellular antigen. 43.Describe clonal selection and expansion. 44.Describe how secondary B cell responses are developed. 45.Describe the role of IgM in immunity. 46.Describe how seroconversion works in HIV disease. 47.Describe tuberculosis and the innocent bystander effect. 48.Describe anaphylactic shock in someone sensitive to peanuts? 49.Describe rheumatic fever and how tolerance is broken. 50.Describe how stress affects immune responses.	oercommons	2025-03-18T00:37:01.281709	null	{ "license": "Creative Commons - Attribution - https://creativecommons.org/licenses/by/4.0/", "url": "https://oercommons.org/courseware/lesson/58767/overview", "title": "Anatomy and Physiology, Fluids and Transport", "author": null }
https://oercommons.org/courseware/lesson/56375/overview	The Nervous System and Nervous Tissue Introduction Figure 12.1 Robotic Arms Playing Foosball As the neural circuitry of the nervous system has become more fully understood and robotics more sophisticated, it is now possible to integrate technology with the body and restore abilities following traumatic events. At some point in the future, will this type of technology lead to the ability to augment our nervous systems? (credit: U.S. Army/Wikimedia Commons) CHAPTER OBJECTIVES After studying this chapter, you will be able to: - Name the major divisions of the nervous system, both anatomical and functional - Describe the functional and structural differences between gray matter and white matter structures - Name the parts of the multipolar neuron in order of polarity - List the types of glial cells and assign each to the proper division of the nervous system, along with their function(s) - Distinguish the major functions of the nervous system: sensation, integration, and response - Describe the components of the membrane that establish the resting membrane potential - Describe the changes that occur to the membrane that result in the action potential - Explain the differences between types of graded potentials - Categorize the major neurotransmitters by chemical type and effect The nervous system is a very complex organ system. In Peter D. Kramer’s book Listening to Prozac, a pharmaceutical researcher is quoted as saying, “If the human brain were simple enough for us to understand, we would be too simple to understand it” (1994). That quote is from the early 1990s; in the two decades since, progress has continued at an amazing rate within the scientific disciplines of neuroscience. It is an interesting conundrum to consider that the complexity of the nervous system may be too complex for it (that is, for us) to completely unravel. But our current level of understanding is probably nowhere close to that limit. One easy way to begin to understand the structure of the nervous system is to start with the large divisions and work through to a more in-depth understanding. In other chapters, the finer details of the nervous system will be explained, but first looking at an overview of the system will allow you to begin to understand how its parts work together. The focus of this chapter is on nervous (neural) tissue, both its structure and its function. But before you learn about that, you will see a big picture of the system—actually, a few big pictures. 12.1 Basic Structure and Function of the Nervous System - Identify the anatomical and functional divisions of the nervous system - Relate the functional and structural differences between gray matter and white matter structures of the nervous system to the structure of neurons - List the basic functions of the nervous system The picture you have in your mind of the nervous system probably includes the brain, the nervous tissue contained within the cranium, and the spinal cord, the extension of nervous tissue within the vertebral column. That suggests it is made of two organs—and you may not even think of the spinal cord as an organ—but the nervous system is a very complex structure. Within the brain, many different and separate regions are responsible for many different and separate functions. It is as if the nervous system is composed of many organs that all look similar and can only be differentiated using tools such as the microscope or electrophysiology. In comparison, it is easy to see that the stomach is different than the esophagus or the liver, so you can imagine the digestive system as a collection of specific organs. The Central and Peripheral Nervous Systems The nervous system can be divided into two major regions: the central and peripheral nervous systems. The central nervous system (CNS) is the brain and spinal cord, and the peripheral nervous system (PNS) is everything else (Figure 12.2). The brain is contained within the cranial cavity of the skull, and the spinal cord is contained within the vertebral cavity of the vertebral column. It is a bit of an oversimplification to say that the CNS is what is inside these two cavities and the peripheral nervous system is outside of them, but that is one way to start to think about it. In actuality, there are some elements of the peripheral nervous system that are within the cranial or vertebral cavities. The peripheral nervous system is so named because it is on the periphery—meaning beyond the brain and spinal cord. Depending on different aspects of the nervous system, the dividing line between central and peripheral is not necessarily universal. Figure 12.2 Central and Peripheral Nervous System The structures of the PNS are referred to as ganglia and nerves, which can be seen as distinct structures. The equivalent structures in the CNS are not obvious from this overall perspective and are best examined in prepared tissue under the microscope. Nervous tissue, present in both the CNS and PNS, contains two basic types of cells: neurons and glial cells. A glial cell is one of a variety of cells that provide a framework of tissue that supports the neurons and their activities. The neuron is the more functionally important of the two, in terms of the communicative function of the nervous system. To describe the functional divisions of the nervous system, it is important to understand the structure of a neuron. Neurons are cells and therefore have a soma, or cell body, but they also have extensions of the cell; each extension is generally referred to as a process. There is one important process that every neuron has called an axon, which is the fiber that connects a neuron with its target. Another type of process that branches off from the soma is the dendrite. Dendrites are responsible for receiving most of the input from other neurons. Looking at nervous tissue, there are regions that predominantly contain cell bodies and regions that are largely composed of just axons. These two regions within nervous system structures are often referred to as gray matter (the regions with many cell bodies and dendrites) or white matter (the regions with many axons). Figure 12.3 demonstrates the appearance of these regions in the brain and spinal cord. The colors ascribed to these regions are what would be seen in “fresh,” or unstained, nervous tissue. Gray matter is not necessarily gray. It can be pinkish because of blood content, or even slightly tan, depending on how long the tissue has been preserved. But white matter is white because axons are insulated by a lipid-rich substance called myelin. Lipids can appear as white (“fatty”) material, much like the fat on a raw piece of chicken or beef. Actually, gray matter may have that color ascribed to it because next to the white matter, it is just darker—hence, gray. The distinction between gray matter and white matter is most often applied to central nervous tissue, which has large regions that can be seen with the unaided eye. When looking at peripheral structures, often a microscope is used and the tissue is stained with artificial colors. That is not to say that central nervous tissue cannot be stained and viewed under a microscope, but unstained tissue is most likely from the CNS—for example, a frontal section of the brain or cross section of the spinal cord. Figure 12.3 Gray Matter and White Matter A brain removed during an autopsy, with a partial section removed, shows white matter surrounded by gray matter. Gray matter makes up the outer cortex of the brain. (credit: modification of work by “Suseno”/Wikimedia Commons) Regardless of the appearance of stained or unstained tissue, the cell bodies of neurons or axons can be located in discrete anatomical structures that need to be named. Those names are specific to whether the structure is central or peripheral. A localized collection of neuron cell bodies in the CNS is referred to as a nucleus. In the PNS, a cluster of neuron cell bodies is referred to as a ganglion. Figure 12.4 indicates how the term nucleus has a few different meanings within anatomy and physiology. It is the center of an atom, where protons and neutrons are found; it is the center of a cell, where the DNA is found; and it is a center of some function in the CNS. There is also a potentially confusing use of the word ganglion (plural = ganglia) that has a historical explanation. In the central nervous system, there is a group of nuclei that are connected together and were once called the basal ganglia before “ganglion” became accepted as a description for a peripheral structure. Some sources refer to this group of nuclei as the “basal nuclei” to avoid confusion. Figure 12.4 What Is a Nucleus? (a) The nucleus of an atom contains its protons and neutrons. (b) The nucleus of a cell is the organelle that contains DNA. (c) A nucleus in the CNS is a localized center of function with the cell bodies of several neurons, shown here circled in red. (credit c: “Was a bee”/Wikimedia Commons) Terminology applied to bundles of axons also differs depending on location. A bundle of axons, or fibers, found in the CNS is called a tract whereas the same thing in the PNS would be called a nerve. There is an important point to make about these terms, which is that they can both be used to refer to the same bundle of axons. When those axons are in the PNS, the term is nerve, but if they are CNS, the term is tract. The most obvious example of this is the axons that project from the retina into the brain. Those axons are called the optic nerve as they leave the eye, but when they are inside the cranium, they are referred to as the optic tract. There is a specific place where the name changes, which is the optic chiasm, but they are still the same axons (Figure 12.5). A similar situation outside of science can be described for some roads. Imagine a road called “Broad Street” in a town called “Anyville.” The road leaves Anyville and goes to the next town over, called “Hometown.” When the road crosses the line between the two towns and is in Hometown, its name changes to “Main Street.” That is the idea behind the naming of the retinal axons. In the PNS, they are called the optic nerve, and in the CNS, they are the optic tract. Table 12.1 helps to clarify which of these terms apply to the central or peripheral nervous systems. Figure 12.5 Optic Nerve Versus Optic Tract This drawing of the connections of the eye to the brain shows the optic nerve extending from the eye to the chiasm, where the structure continues as the optic tract. The same axons extend from the eye to the brain through these two bundles of fibers, but the chiasm represents the border between peripheral and central. INTERACTIVE LINK In 2003, the Nobel Prize in Physiology or Medicine was awarded to Paul C. Lauterbur and Sir Peter Mansfield for discoveries related to magnetic resonance imaging (MRI). This is a tool to see the structures of the body (not just the nervous system) that depends on magnetic fields associated with certain atomic nuclei. The utility of this technique in the nervous system is that fat tissue and water appear as different shades between black and white. Because white matter is fatty (from myelin) and gray matter is not, they can be easily distinguished in MRI images. Try this PhET simulation that demonstrates the use of this technology and compares it with other types of imaging technologies. Also, the results from an MRI session are compared with images obtained from X-ray or computed tomography. How do the imaging techniques shown in this game indicate the separation of white and gray matter compared with the freshly dissected tissue shown earlier? Structures of the CNS and PNS \| CNS \| PNS \| \| \|---\|---\|---\| \| Group of Neuron Cell Bodies (i.e., gray matter) \| Nucleus \| Ganglion \| \| Bundle of Axons (i.e., white matter) \| Tract \| Nerve \| Table12.1 Functional Divisions of the Nervous System The nervous system can also be divided on the basis of its functions, but anatomical divisions and functional divisions are different. The CNS and the PNS both contribute to the same functions, but those functions can be attributed to different regions of the brain (such as the cerebral cortex or the hypothalamus) or to different ganglia in the periphery. The problem with trying to fit functional differences into anatomical divisions is that sometimes the same structure can be part of several functions. For example, the optic nerve carries signals from the retina that are either used for the conscious perception of visual stimuli, which takes place in the cerebral cortex, or for the reflexive responses of smooth muscle tissue that are processed through the hypothalamus. There are two ways to consider how the nervous system is divided functionally. First, the basic functions of the nervous system are sensation, integration, and response. Secondly, control of the body can be somatic or autonomic—divisions that are largely defined by the structures that are involved in the response. There is also a region of the peripheral nervous system that is called the enteric nervous system that is responsible for a specific set of the functions within the realm of autonomic control related to gastrointestinal functions. Basic Functions The nervous system is involved in receiving information about the environment around us (sensation) and generating responses to that information (motor responses). The nervous system can be divided into regions that are responsible for sensation (sensory functions) and for the response (motor functions). But there is a third function that needs to be included. Sensory input needs to be integrated with other sensations, as well as with memories, emotional state, or learning (cognition). Some regions of the nervous system are termed integration or association areas. The process of integration combines sensory perceptions and higher cognitive functions such as memories, learning, and emotion to produce a response. Sensation. The first major function of the nervous system is sensation—receiving information about the environment to gain input about what is happening outside the body (or, sometimes, within the body). The sensory functions of the nervous system register the presence of a change from homeostasis or a particular event in the environment, known as a stimulus. The senses we think of most are the “big five”: taste, smell, touch, sight, and hearing. The stimuli for taste and smell are both chemical substances (molecules, compounds, ions, etc.), touch is physical or mechanical stimuli that interact with the skin, sight is light stimuli, and hearing is the perception of sound, which is a physical stimulus similar to some aspects of touch. There are actually more senses than just those, but that list represents the major senses. Those five are all senses that receive stimuli from the outside world, and of which there is conscious perception. Additional sensory stimuli might be from the internal environment (inside the body), such as the stretch of an organ wall or the concentration of certain ions in the blood. Response. The nervous system produces a response on the basis of the stimuli perceived by sensory structures. An obvious response would be the movement of muscles, such as withdrawing a hand from a hot stove, but there are broader uses of the term. The nervous system can cause the contraction of all three types of muscle tissue. For example, skeletal muscle contracts to move the skeleton, cardiac muscle is influenced as heart rate increases during exercise, and smooth muscle contracts as the digestive system moves food along the digestive tract. Responses also include the neural control of glands in the body as well, such as the production and secretion of sweat by the eccrine and merocrine sweat glands found in the skin to lower body temperature. Responses can be divided into those that are voluntary or conscious (contraction of skeletal muscle) and those that are involuntary (contraction of smooth muscles, regulation of cardiac muscle, activation of glands). Voluntary responses are governed by the somatic nervous system and involuntary responses are governed by the autonomic nervous system, which are discussed in the next section. Integration. Stimuli that are received by sensory structures are communicated to the nervous system where that information is processed. This is called integration. Stimuli are compared with, or integrated with, other stimuli, memories of previous stimuli, or the state of a person at a particular time. This leads to the specific response that will be generated. Seeing a baseball pitched to a batter will not automatically cause the batter to swing. The trajectory of the ball and its speed will need to be considered. Maybe the count is three balls and one strike, and the batter wants to let this pitch go by in the hope of getting a walk to first base. Or maybe the batter’s team is so far ahead, it would be fun to just swing away. Controlling the Body The nervous system can be divided into two parts mostly on the basis of a functional difference in responses. The somatic nervous system (SNS) is responsible for conscious perception and voluntary motor responses. Voluntary motor response means the contraction of skeletal muscle, but those contractions are not always voluntary in the sense that you have to want to perform them. Some somatic motor responses are reflexes, and often happen without a conscious decision to perform them. If your friend jumps out from behind a corner and yells “Boo!” you will be startled and you might scream or leap back. You didn’t decide to do that, and you may not have wanted to give your friend a reason to laugh at your expense, but it is a reflex involving skeletal muscle contractions. Other motor responses become automatic (in other words, unconscious) as a person learns motor skills (referred to as “habit learning” or “procedural memory”). The autonomic nervous system (ANS) is responsible for involuntary control of the body, usually for the sake of homeostasis (regulation of the internal environment). Sensory input for autonomic functions can be from sensory structures tuned to external or internal environmental stimuli. The motor output extends to smooth and cardiac muscle as well as glandular tissue. The role of the autonomic system is to regulate the organ systems of the body, which usually means to control homeostasis. Sweat glands, for example, are controlled by the autonomic system. When you are hot, sweating helps cool your body down. That is a homeostatic mechanism. But when you are nervous, you might start sweating also. That is not homeostatic, it is the physiological response to an emotional state. There is another division of the nervous system that describes functional responses. The enteric nervous system (ENS) is responsible for controlling the smooth muscle and glandular tissue in your digestive system. It is a large part of the PNS, and is not dependent on the CNS. It is sometimes valid, however, to consider the enteric system to be a part of the autonomic system because the neural structures that make up the enteric system are a component of the autonomic output that regulates digestion. There are some differences between the two, but for our purposes here there will be a good bit of overlap. See Figure 12.6 for examples of where these divisions of the nervous system can be found. Figure 12.6 Somatic, Autonomic, and Enteric Structures of the Nervous System Somatic structures include the spinal nerves, both motor and sensory fibers, as well as the sensory ganglia (posterior root ganglia and cranial nerve ganglia). Autonomic structures are found in the nerves also, but include the sympathetic and parasympathetic ganglia. The enteric nervous system includes the nervous tissue within the organs of the digestive tract. INTERACTIVE LINK Visit this site to read about a woman that notices that her daughter is having trouble walking up the stairs. This leads to the discovery of a hereditary condition that affects the brain and spinal cord. The electromyography and MRI tests indicated deficiencies in the spinal cord and cerebellum, both of which are responsible for controlling coordinated movements. To what functional division of the nervous system would these structures belong? EVERYDAY CONNECTION How Much of Your Brain Do You Use? Have you ever heard the claim that humans only use 10 percent of their brains? Maybe you have seen an advertisement on a website saying that there is a secret to unlocking the full potential of your mind—as if there were 90 percent of your brain sitting idle, just waiting for you to use it. If you see an ad like that, don’t click. It isn’t true. An easy way to see how much of the brain a person uses is to take measurements of brain activity while performing a task. An example of this kind of measurement is functional magnetic resonance imaging (fMRI), which generates a map of the most active areas and can be generated and presented in three dimensions (Figure 12.7). This procedure is different from the standard MRI technique because it is measuring changes in the tissue in time with an experimental condition or event. Figure 12.7 fMRI This fMRI shows activation of the visual cortex in response to visual stimuli. (credit: “Superborsuk”/Wikimedia Commons) The underlying assumption is that active nervous tissue will have greater blood flow. By having the subject perform a visual task, activity all over the brain can be measured. Consider this possible experiment: the subject is told to look at a screen with a black dot in the middle (a fixation point). A photograph of a face is projected on the screen away from the center. The subject has to look at the photograph and decipher what it is. The subject has been instructed to push a button if the photograph is of someone they recognize. The photograph might be of a celebrity, so the subject would press the button, or it might be of a random person unknown to the subject, so the subject would not press the button. In this task, visual sensory areas would be active, integrating areas would be active, motor areas responsible for moving the eyes would be active, and motor areas for pressing the button with a finger would be active. Those areas are distributed all around the brain and the fMRI images would show activity in more than just 10 percent of the brain (some evidence suggests that about 80 percent of the brain is using energy—based on blood flow to the tissue—during well-defined tasks similar to the one suggested above). This task does not even include all of the functions the brain performs. There is no language response, the body is mostly lying still in the MRI machine, and it does not consider the autonomic functions that would be ongoing in the background. Nervous Tissue - Describe the basic structure of a neuron - Identify the different types of neurons on the basis of polarity - List the glial cells of the CNS and describe their function - List the glial cells of the PNS and describe their function Nervous tissue is composed of two types of cells, neurons and glial cells. Neurons are the primary type of cell that most anyone associates with the nervous system. They are responsible for the computation and communication that the nervous system provides. They are electrically active and release chemical signals to target cells. Glial cells, or glia, are known to play a supporting role for nervous tissue. Ongoing research pursues an expanded role that glial cells might play in signaling, but neurons are still considered the basis of this function. Neurons are important, but without glial support they would not be able to perform their function. Neurons Neurons are the cells considered to be the basis of nervous tissue. They are responsible for the electrical signals that communicate information about sensations, and that produce movements in response to those stimuli, along with inducing thought processes within the brain. An important part of the function of neurons is in their structure, or shape. The three-dimensional shape of these cells makes the immense numbers of connections within the nervous system possible. Parts of a Neuron As you learned in the first section, the main part of a neuron is the cell body, which is also known as the soma (soma = “body”). The cell body contains the nucleus and most of the major organelles. But what makes neurons special is that they have many extensions of their cell membranes, which are generally referred to as processes. Neurons are usually described as having one, and only one, axon—a fiber that emerges from the cell body and projects to target cells. That single axon can branch repeatedly to communicate with many target cells. It is the axon that propagates the nerve impulse, which is communicated to one or more cells. The other processes of the neuron are dendrites, which receive information from other neurons at specialized areas of contact called synapses. The dendrites are usually highly branched processes, providing locations for other neurons to communicate with the cell body. Information flows through a neuron from the dendrites, across the cell body, and down the axon. This gives the neuron a polarity—meaning that information flows in this one direction. Figure 12.8 shows the relationship of these parts to one another. Figure 12.8 Parts of a Neuron The major parts of the neuron are labeled on a multipolar neuron from the CNS. Where the axon emerges from the cell body, there is a special region referred to as the axon hillock. This is a tapering of the cell body toward the axon fiber. Within the axon hillock, the cytoplasm changes to a solution of limited components called axoplasm. Because the axon hillock represents the beginning of the axon, it is also referred to as the initial segment. Many axons are wrapped by an insulating substance called myelin, which is actually made from glial cells. Myelin acts as insulation much like the plastic or rubber that is used to insulate electrical wires. A key difference between myelin and the insulation on a wire is that there are gaps in the myelin covering of an axon. Each gap is called a node of Ranvier and is important to the way that electrical signals travel down the axon. The length of the axon between each gap, which is wrapped in myelin, is referred to as an axon segment. At the end of the axon is the axon terminal, where there are usually several branches extending toward the target cell, each of which ends in an enlargement called a synaptic end bulb. These bulbs are what make the connection with the target cell at the synapse. INTERACTIVE LINK Visit this site to learn about how nervous tissue is composed of neurons and glial cells. Neurons are dynamic cells with the ability to make a vast number of connections, to respond incredibly quickly to stimuli, and to initiate movements on the basis of those stimuli. They are the focus of intense research because failures in physiology can lead to devastating illnesses. Why are neurons only found in animals? Based on what this article says about neuron function, why wouldn't they be helpful for plants or microorganisms? Types of Neurons There are many neurons in the nervous system—a number in the trillions. And there are many different types of neurons. They can be classified by many different criteria. The first way to classify them is by the number of processes attached to the cell body. Using the standard model of neurons, one of these processes is the axon, and the rest are dendrites. Because information flows through the neuron from dendrites or cell bodies toward the axon, these names are based on the neuron's polarity (Figure 12.9). Figure 12.9 Neuron Classification by Shape Unipolar cells have one process that includes both the axon and dendrite. Bipolar cells have two processes, the axon and a dendrite. Multipolar cells have more than two processes, the axon and two or more dendrites. Unipolar cells have only one process emerging from the cell. True unipolar cells are only found in invertebrate animals, so the unipolar cells in humans are more appropriately called “pseudo-unipolar” cells. Invertebrate unipolar cells do not have dendrites. Human unipolar cells have an axon that emerges from the cell body, but it splits so that the axon can extend along a very long distance. At one end of the axon are dendrites, and at the other end, the axon forms synaptic connections with a target. Unipolar cells are exclusively sensory neurons and have two unique characteristics. First, their dendrites are receiving sensory information, sometimes directly from the stimulus itself. Secondly, the cell bodies of unipolar neurons are always found in ganglia. Sensory reception is a peripheral function (those dendrites are in the periphery, perhaps in the skin) so the cell body is in the periphery, though closer to the CNS in a ganglion. The axon projects from the dendrite endings, past the cell body in a ganglion, and into the central nervous system. Bipolar cells have two processes, which extend from each end of the cell body, opposite to each other. One is the axon and one the dendrite. Bipolar cells are not very common. They are found mainly in the olfactory epithelium (where smell stimuli are sensed), and as part of the retina. Multipolar neurons are all of the neurons that are not unipolar or bipolar. They have one axon and two or more dendrites (usually many more). With the exception of the unipolar sensory ganglion cells, and the two specific bipolar cells mentioned above, all other neurons are multipolar. Some cutting edge research suggests that certain neurons in the CNS do not conform to the standard model of “one, and only one” axon. Some sources describe a fourth type of neuron, called an anaxonic neuron. The name suggests that it has no axon (an- = “without”), but this is not accurate. Anaxonic neurons are very small, and if you look through a microscope at the standard resolution used in histology (approximately 400X to 1000X total magnification), you will not be able to distinguish any process specifically as an axon or a dendrite. Any of those processes can function as an axon depending on the conditions at any given time. Nevertheless, even if they cannot be easily seen, and one specific process is definitively the axon, these neurons have multiple processes and are therefore multipolar. Neurons can also be classified on the basis of where they are found, who found them, what they do, or even what chemicals they use to communicate with each other. Some neurons referred to in this section on the nervous system are named on the basis of those sorts of classifications (Figure 12.10). For example, a multipolar neuron that has a very important role to play in a part of the brain called the cerebellum is known as a Purkinje (commonly pronounced per-KIN-gee) cell. It is named after the anatomist who discovered it (Jan Evangilista Purkinje, 1787–1869). Figure 12.10 Other Neuron Classifications Three examples of neurons that are classified on the basis of other criteria. (a) The pyramidal cell is a multipolar cell with a cell body that is shaped something like a pyramid. (b) The Purkinje cell in the cerebellum was named after the scientist who originally described it. (c) Olfactory neurons are named for the functional group with which they belong. Glial Cells Glial cells, or neuroglia or simply glia, are the other type of cell found in nervous tissue. They are considered to be supporting cells, and many functions are directed at helping neurons complete their function for communication. The name glia comes from the Greek word that means “glue,” and was coined by the German pathologist Rudolph Virchow, who wrote in 1856: “This connective substance, which is in the brain, the spinal cord, and the special sense nerves, is a kind of glue (neuroglia) in which the nervous elements are planted.” Today, research into nervous tissue has shown that there are many deeper roles that these cells play. And research may find much more about them in the future. There are six types of glial cells. Four of them are found in the CNS and two are found in the PNS. Table 12.2 outlines some common characteristics and functions. Glial Cell Types by Location and Basic Function \| CNS glia \| PNS glia \| Basic function \| \|---\|---\|---\| \| Astrocyte \| Satellite cell \| Support \| \| Oligodendrocyte \| Schwann cell \| Insulation, myelination \| \| Microglia \| - \| Immune surveillance and phagocytosis \| \| Ependymal cell \| - \| Creating CSF \| Table12.2 Glial Cells of the CNS One cell providing support to neurons of the CNS is the astrocyte, so named because it appears to be star-shaped under the microscope (astro- = “star”). Astrocytes have many processes extending from their main cell body (not axons or dendrites like neurons, just cell extensions). Those processes extend to interact with neurons, blood vessels, or the connective tissue covering the CNS that is called the pia mater (Figure 12.11). Generally, they are supporting cells for the neurons in the central nervous system. Some ways in which they support neurons in the central nervous system are by maintaining the concentration of chemicals in the extracellular space, removing excess signaling molecules, reacting to tissue damage, and contributing to the blood-brain barrier (BBB). The blood-brain barrier is a physiological barrier that keeps many substances that circulate in the rest of the body from getting into the central nervous system, restricting what can cross from circulating blood into the CNS. Nutrient molecules, such as glucose or amino acids, can pass through the BBB, but other molecules cannot. This actually causes problems with drug delivery to the CNS. Pharmaceutical companies are challenged to design drugs that can cross the BBB as well as have an effect on the nervous system. Figure 12.11 Glial Cells of the CNS The CNS has astrocytes, oligodendrocytes, microglia, and ependymal cells that support the neurons of the CNS in several ways. Like a few other parts of the body, the brain has a privileged blood supply. Very little can pass through by diffusion. Most substances that cross the wall of a blood vessel into the CNS must do so through an active transport process. Because of this, only specific types of molecules can enter the CNS. Glucose—the primary energy source—is allowed, as are amino acids. Water and some other small particles, like gases and ions, can enter. But most everything else cannot, including white blood cells, which are one of the body’s main lines of defense. While this barrier protects the CNS from exposure to toxic or pathogenic substances, it also keeps out the cells that could protect the brain and spinal cord from disease and damage. The BBB also makes it harder for pharmaceuticals to be developed that can affect the nervous system. Aside from finding efficacious substances, the means of delivery is also crucial. Also found in CNS tissue is the oligodendrocyte, sometimes called just “oligo,” which is the glial cell type that insulates axons in the CNS. The name means “cell of a few branches” (oligo- = “few”; dendro- = “branches”; -cyte = “cell”). There are a few processes that extend from the cell body. Each one reaches out and surrounds an axon to insulate it in myelin. One oligodendrocyte will provide the myelin for multiple axon segments, either for the same axon or for separate axons. The function of myelin will be discussed below. Microglia are, as the name implies, smaller than most of the other glial cells. Ongoing research into these cells, although not entirely conclusive, suggests that they may originate as white blood cells, called macrophages, that become part of the CNS during early development. While their origin is not conclusively determined, their function is related to what macrophages do in the rest of the body. When macrophages encounter diseased or damaged cells in the rest of the body, they ingest and digest those cells or the pathogens that cause disease. Microglia are the cells in the CNS that can do this in normal, healthy tissue, and they are therefore also referred to as CNS-resident macrophages. The ependymal cell is a glial cell that filters blood to make cerebrospinal fluid (CSF), the fluid that circulates through the CNS. Because of the privileged blood supply inherent in the BBB, the extracellular space in nervous tissue does not easily exchange components with the blood. Ependymal cells line each ventricle, one of four central cavities that are remnants of the hollow center of the neural tube formed during the embryonic development of the brain. The choroid plexus is a specialized structure in the ventricles where ependymal cells come in contact with blood vessels and filter and absorb components of the blood to produce cerebrospinal fluid. Because of this, ependymal cells can be considered a component of the BBB, or a place where the BBB breaks down. These glial cells appear similar to epithelial cells, making a single layer of cells with little intracellular space and tight connections between adjacent cells. They also have cilia on their apical surface to help move the CSF through the ventricular space. The relationship of these glial cells to the structure of the CNS is seen in Figure 12.11. Glial Cells of the PNS One of the two types of glial cells found in the PNS is the satellite cell. Satellite cells are found in sensory and autonomic ganglia, where they surround the cell bodies of neurons. This accounts for the name, based on their appearance under the microscope. They provide support, performing similar functions in the periphery as astrocytes do in the CNS—except, of course, for establishing the BBB. The second type of glial cell is the Schwann cell, which insulate axons with myelin in the periphery. Schwann cells are different than oligodendrocytes, in that a Schwann cell wraps around a portion of only one axon segment and no others. Oligodendrocytes have processes that reach out to multiple axon segments, whereas the entire Schwann cell surrounds just one axon segment. The nucleus and cytoplasm of the Schwann cell are on the edge of the myelin sheath. The relationship of these two types of glial cells to ganglia and nerves in the PNS is seen in Figure 12.12. Figure 12.12 Glial Cells of the PNS The PNS has satellite cells and Schwann cells. Myelin The insulation for axons in the nervous system is provided by glial cells, oligodendrocytes in the CNS, and Schwann cells in the PNS. Whereas the manner in which either cell is associated with the axon segment, or segments, that it insulates is different, the means of myelinating an axon segment is mostly the same in the two situations. Myelin is a lipid-rich sheath that surrounds the axon and by doing so creates a myelin sheath that facilitates the transmission of electrical signals along the axon. The lipids are essentially the phospholipids of the glial cell membrane. Myelin, however, is more than just the membrane of the glial cell. It also includes important proteins that are integral to that membrane. Some of the proteins help to hold the layers of the glial cell membrane closely together. The appearance of the myelin sheath can be thought of as similar to the pastry wrapped around a hot dog for “pigs in a blanket” or a similar food. The glial cell is wrapped around the axon several times with little to no cytoplasm between the glial cell layers. For oligodendrocytes, the rest of the cell is separate from the myelin sheath as a cell process extends back toward the cell body. A few other processes provide the same insulation for other axon segments in the area. For Schwann cells, the outermost layer of the cell membrane contains cytoplasm and the nucleus of the cell as a bulge on one side of the myelin sheath. During development, the glial cell is loosely or incompletely wrapped around the axon (Figure 12.13a). The edges of this loose enclosure extend toward each other, and one end tucks under the other. The inner edge wraps around the axon, creating several layers, and the other edge closes around the outside so that the axon is completely enclosed. INTERACTIVE LINK View the University of Michigan WebScope to see an electron micrograph of a cross-section of a myelinated nerve fiber. The axon contains microtubules and neurofilaments that are bounded by a plasma membrane known as the axolemma. Outside the plasma membrane of the axon is the myelin sheath, which is composed of the tightly wrapped plasma membrane of a Schwann cell. What aspects of the cells in this image react with the stain to make them a deep, dark, black color, such as the multiple layers that are the myelin sheath? Myelin sheaths can extend for one or two millimeters, depending on the diameter of the axon. Axon diameters can be as small as 1 to 20 micrometers. Because a micrometer is 1/1000 of a millimeter, this means that the length of a myelin sheath can be 100–1000 times the diameter of the axon. Figure 12.8, Figure 12.11, and Figure 12.12 show the myelin sheath surrounding an axon segment, but are not to scale. If the myelin sheath were drawn to scale, the neuron would have to be immense—possibly covering an entire wall of the room in which you are sitting. Figure 12.13 The Process of Myelination Myelinating glia wrap several layers of cell membrane around the cell membrane of an axon segment. A single Schwann cell insulates a segment of a peripheral nerve, whereas in the CNS, an oligodendrocyte may provide insulation for a few separate axon segments. EM × 1,460,000. (Micrograph provided by the Regents of University of Michigan Medical School © 2012) DISORDERS OF THE... Nervous Tissue Several diseases can result from the demyelination of axons. The causes of these diseases are not the same; some have genetic causes, some are caused by pathogens, and others are the result of autoimmune disorders. Though the causes are varied, the results are largely similar. The myelin insulation of axons is compromised, making electrical signaling slower. Multiple sclerosis (MS) is one such disease. It is an example of an autoimmune disease. The antibodies produced by lymphocytes (a type of white blood cell) mark myelin as something that should not be in the body. This causes inflammation and the destruction of the myelin in the central nervous system. As the insulation around the axons is destroyed by the disease, scarring becomes obvious. This is where the name of the disease comes from; sclerosis means hardening of tissue, which is what a scar is. Multiple scars are found in the white matter of the brain and spinal cord. The symptoms of MS include both somatic and autonomic deficits. Control of the musculature is compromised, as is control of organs such as the bladder. Guillain-Barré (pronounced gee-YAN bah-RAY) syndrome is an example of a demyelinating disease of the peripheral nervous system. It is also the result of an autoimmune reaction, but the inflammation is in peripheral nerves. Sensory symptoms or motor deficits are common, and autonomic failures can lead to changes in the heart rhythm or a drop in blood pressure, especially when standing, which causes dizziness. The Function of Nervous Tissue - Distinguish the major functions of the nervous system: sensation, integration, and response - List the sequence of events in a simple sensory receptor–motor response pathway Having looked at the components of nervous tissue, and the basic anatomy of the nervous system, next comes an understanding of how nervous tissue is capable of communicating within the nervous system. Before getting to the nuts and bolts of how this works, an illustration of how the components come together will be helpful. An example is summarized in Figure 12.14. Figure 12.14 Testing the Water (1) The sensory neuron has endings in the skin that sense a stimulus such as water temperature. The strength of the signal that starts here is dependent on the strength of the stimulus. (2) The graded potential from the sensory endings, if strong enough, will initiate an action potential at the initial segment of the axon (which is immediately adjacent to the sensory endings in the skin). (3) The axon of the peripheral sensory neuron enters the spinal cord and contacts another neuron in the gray matter. The contact is a synapse where another graded potential is caused by the release of a chemical signal from the axon terminals. (4) An action potential is initiated at the initial segment of this neuron and travels up the sensory pathway to a region of the brain called the thalamus. Another synapse passes the information along to the next neuron. (5) The sensory pathway ends when the signal reaches the cerebral cortex. (6) After integration with neurons in other parts of the cerebral cortex, a motor command is sent from the precentral gyrus of the frontal cortex. (7) The upper motor neuron sends an action potential down to the spinal cord. The target of the upper motor neuron is the dendrites of the lower motor neuron in the gray matter of the spinal cord. (8) The axon of the lower motor neuron emerges from the spinal cord in a nerve and connects to a muscle through a neuromuscular junction to cause contraction of the target muscle. Imagine you are about to take a shower in the morning before going to school. You have turned on the faucet to start the water as you prepare to get in the shower. After a few minutes, you expect the water to be a temperature that will be comfortable to enter. So you put your hand out into the spray of water. What happens next depends on how your nervous system interacts with the stimulus of the water temperature and what you do in response to that stimulus. Found in the skin of your fingers or toes is a type of sensory receptor that is sensitive to temperature, called a thermoreceptor. When you place your hand under the shower (Figure 12.15), the cell membrane of the thermoreceptors changes its electrical state (voltage). The amount of change is dependent on the strength of the stimulus (how hot the water is). This is called a graded potential. If the stimulus is strong, the voltage of the cell membrane will change enough to generate an electrical signal that will travel down the axon. You have learned about this type of signaling before, with respect to the interaction of nerves and muscles at the neuromuscular junction. The voltage at which such a signal is generated is called the threshold, and the resulting electrical signal is called an action potential. In this example, the action potential travels—a process known as propagation—along the axon from the axon hillock to the axon terminals and into the synaptic end bulbs. When this signal reaches the end bulbs, it causes the release of a signaling molecule called a neurotransmitter. Figure 12.15 The Sensory Input Receptors in the skin sense the temperature of the water. The neurotransmitter diffuses across the short distance of the synapse and binds to a receptor protein of the target neuron. When the molecular signal binds to the receptor, the cell membrane of the target neuron changes its electrical state and a new graded potential begins. If that graded potential is strong enough to reach threshold, the second neuron generates an action potential at its axon hillock. The target of this neuron is another neuron in the thalamus of the brain, the part of the CNS that acts as a relay for sensory information. At another synapse, neurotransmitter is released and binds to its receptor. The thalamus then sends the sensory information to the cerebral cortex, the outermost layer of gray matter in the brain, where conscious perception of that water temperature begins. Within the cerebral cortex, information is processed among many neurons, integrating the stimulus of the water temperature with other sensory stimuli, with your emotional state (you just aren't ready to wake up; the bed is calling to you), memories (perhaps of the lab notes you have to study before a quiz). Finally, a plan is developed about what to do, whether that is to turn the temperature up, turn the whole shower off and go back to bed, or step into the shower. To do any of these things, the cerebral cortex has to send a command out to your body to move muscles (Figure 12.16). Figure 12.16 The Motor Response On the basis of the sensory input and the integration in the CNS, a motor response is formulated and executed. A region of the cortex is specialized for sending signals down to the spinal cord for movement. The upper motor neuron is in this region, called the precentral gyrus of the frontal cortex, which has an axon that extends all the way down the spinal cord. At the level of the spinal cord at which this axon makes a synapse, a graded potential occurs in the cell membrane of a lower motor neuron. This second motor neuron is responsible for causing muscle fibers to contract. In the manner described in the chapter on muscle tissue, an action potential travels along the motor neuron axon into the periphery. The axon terminates on muscle fibers at the neuromuscular junction. Acetylcholine is released at this specialized synapse, which causes the muscle action potential to begin, following a large potential known as an end plate potential. When the lower motor neuron excites the muscle fiber, it contracts. All of this occurs in a fraction of a second, but this story is the basis of how the nervous system functions. CAREER CONNECTION Neurophysiologist Understanding how the nervous system works could be a driving force in your career. Studying neurophysiology is a very rewarding path to follow. It means that there is a lot of work to do, but the rewards are worth the effort. The career path of a research scientist can be straightforward: college, graduate school, postdoctoral research, academic research position at a university. A Bachelor’s degree in science will get you started, and for neurophysiology that might be in biology, psychology, computer science, engineering, or neuroscience. But the real specialization comes in graduate school. There are many different programs out there to study the nervous system, not just neuroscience itself. Most graduate programs are doctoral, meaning that a Master’s degree is not part of the work. These are usually considered five-year programs, with the first two years dedicated to course work and finding a research mentor, and the last three years dedicated to finding a research topic and pursuing that with a near single-mindedness. The research will usually result in a few publications in scientific journals, which will make up the bulk of a doctoral dissertation. After graduating with a Ph.D., researchers will go on to find specialized work called a postdoctoral fellowship within established labs. In this position, a researcher starts to establish their own research career with the hopes of finding an academic position at a research university. Other options are available if you are interested in how the nervous system works. Especially for neurophysiology, a medical degree might be more suitable so you can learn about the clinical applications of neurophysiology and possibly work with human subjects. An academic career is not a necessity. Biotechnology firms are eager to find motivated scientists ready to tackle the tough questions about how the nervous system works so that therapeutic chemicals can be tested on some of the most challenging disorders such as Alzheimer’s disease or Parkinson’s disease, or spinal cord injury. Others with a medical degree and a specialization in neuroscience go on to work directly with patients, diagnosing and treating mental disorders. You can do this as a psychiatrist, a neuropsychologist, a neuroscience nurse, or a neurodiagnostic technician, among other possible career paths. The Action Potential - Describe the components of the membrane that establish the resting membrane potential - Describe the changes that occur to the membrane that result in the action potential The functions of the nervous system—sensation, integration, and response—depend on the functions of the neurons underlying these pathways. To understand how neurons are able to communicate, it is necessary to describe the role of an excitable membrane in generating these signals. The basis of this communication is the action potential, which demonstrates how changes in the membrane can constitute a signal. Looking at the way these signals work in more variable circumstances involves a look at graded potentials, which will be covered in the next section. Electrically Active Cell Membranes Most cells in the body make use of charged particles, ions, to build up a charge across the cell membrane. Previously, this was shown to be a part of how muscle cells work. For skeletal muscles to contract, based on excitation–contraction coupling, requires input from a neuron. Both of the cells make use of the cell membrane to regulate ion movement between the extracellular fluid and cytosol. As you learned in the chapter on cells, the cell membrane is primarily responsible for regulating what can cross the membrane and what stays on only one side. The cell membrane is a phospholipid bilayer, so only substances that can pass directly through the hydrophobic core can diffuse through unaided. Charged particles, which are hydrophilic by definition, cannot pass through the cell membrane without assistance (Figure 12.17). Transmembrane proteins, specifically channel proteins, make this possible. Several passive transport channels, as well as active transport pumps, are necessary to generate a transmembrane potential and an action potential. Of special interest is the carrier protein referred to as the sodium/potassium pump that moves sodium ions (Na+) out of a cell and potassium ions (K+) into a cell, thus regulating ion concentration on both sides of the cell membrane. Figure 12.17 Cell Membrane and Transmembrane Proteins The cell membrane is composed of a phospholipid bilayer and has many transmembrane proteins, including different types of channel proteins that serve as ion channels. The sodium/potassium pump requires energy in the form of adenosine triphosphate (ATP), so it is also referred to as an ATPase. As was explained in the cell chapter, the concentration of Na+ is higher outside the cell than inside, and the concentration of K+is higher inside the cell than outside. That means that this pump is moving the ions against the concentration gradients for sodium and potassium, which is why it requires energy. In fact, the pump basically maintains those concentration gradients. Ion channels are pores that allow specific charged particles to cross the membrane in response to an existing concentration gradient. Proteins are capable of spanning the cell membrane, including its hydrophobic core, and can interact with the charge of ions because of the varied properties of amino acids found within specific domains or regions of the protein channel. Hydrophobic amino acids are found in the domains that are apposed to the hydrocarbon tails of the phospholipids. Hydrophilic amino acids are exposed to the fluid environments of the extracellular fluid and cytosol. Additionally, the ions will interact with the hydrophilic amino acids, which will be selective for the charge of the ion. Channels for cations (positive ions) will have negatively charged side chains in the pore. Channels for anions (negative ions) will have positively charged side chains in the pore. This is called electrochemical exclusion, meaning that the channel pore is charge-specific. Ion channels can also be specified by the diameter of the pore. The distance between the amino acids will be specific for the diameter of the ion when it dissociates from the water molecules surrounding it. Because of the surrounding water molecules, larger pores are not ideal for smaller ions because the water molecules will interact, by hydrogen bonds, more readily than the amino acid side chains. This is called size exclusion. Some ion channels are selective for charge but not necessarily for size, and thus are called a nonspecific channel. These nonspecific channels allow cations—particularly Na+, K+, and Ca2+—to cross the membrane, but exclude anions. Ion channels do not always freely allow ions to diffuse across the membrane. Some are opened by certain events, meaning the channels are gated. So another way that channels can be categorized is on the basis of how they are gated. Although these classes of ion channels are found primarily in the cells of nervous or muscular tissue, they also can be found in the cells of epithelial and connective tissues. A ligand-gated channel opens because a signaling molecule, a ligand, binds to the extracellular region of the channel. This type of channel is also known as an ionotropic receptor because when the ligand, known as a neurotransmitter in the nervous system, binds to the protein, ions cross the membrane changing its charge (Figure 12.18). Figure 12.18 Ligand-Gated Channels When the ligand, in this case the neurotransmitter acetylcholine, binds to a specific location on the extracellular surface of the channel protein, the pore opens to allow select ions through. The ions, in this case, are cations of sodium, calcium, and potassium. A mechanically gated channel opens because of a physical distortion of the cell membrane. Many channels associated with the sense of touch (somatosensation) are mechanically gated. For example, as pressure is applied to the skin, these channels open and allow ions to enter the cell. Similar to this type of channel would be the channel that opens on the basis of temperature changes, as in testing the water in the shower (Figure 12.19). Figure 12.19 Mechanically Gated Channels When a mechanical change occurs in the surrounding tissue, such as pressure or touch, the channel is physically opened. Thermoreceptors work on a similar principle. When the local tissue temperature changes, the protein reacts by physically opening the channel. A voltage-gated channel is a channel that responds to changes in the electrical properties of the membrane in which it is embedded. Normally, the inner portion of the membrane is at a negative voltage. When that voltage becomes less negative, the channel begins to allow ions to cross the membrane (Figure 12.20). Figure 12.20 Voltage-Gated Channels Voltage-gated channels open when the transmembrane voltage changes around them. Amino acids in the structure of the protein are sensitive to charge and cause the pore to open to the selected ion. A leakage channel is randomly gated, meaning that it opens and closes at random, hence the reference to leaking. There is no actual event that opens the channel; instead, it has an intrinsic rate of switching between the open and closed states. Leakage channels contribute to the resting transmembrane voltage of the excitable membrane (Figure 12.21). Figure 12.21 Leakage Channels In certain situations, ions need to move across the membrane randomly. The particular electrical properties of certain cells are modified by the presence of this type of channel. The Membrane Potential The electrical state of the cell membrane can have several variations. These are all variations in the membrane potential. A potential is a distribution of charge across the cell membrane, measured in millivolts (mV). The standard is to compare the inside of the cell relative to the outside, so the membrane potential is a value representing the charge on the intracellular side of the membrane based on the outside being zero, relatively speaking (Figure 12.22). Figure 12.22 Measuring Charge across a Membrane with a Voltmeter A recording electrode is inserted into the cell and a reference electrode is outside the cell. By comparing the charge measured by these two electrodes, the transmembrane voltage is determined. It is conventional to express that value for the cytosol relative to the outside. The concentration of ions in extracellular and intracellular fluids is largely balanced, with a net neutral charge. However, a slight difference in charge occurs right at the membrane surface, both internally and externally. It is the difference in this very limited region that has all the power in neurons (and muscle cells) to generate electrical signals, including action potentials. Before these electrical signals can be described, the resting state of the membrane must be explained. When the cell is at rest, and the ion channels are closed (except for leakage channels which randomly open), ions are distributed across the membrane in a very predictable way. The concentration of Na+ outside the cell is 10 times greater than the concentration inside. Also, the concentration of K+ inside the cell is greater than outside. The cytosol contains a high concentration of anions, in the form of phosphate ions and negatively charged proteins. Large anions are a component of the inner cell membrane, including specialized phospholipids and proteins associated with the inner leaflet of the membrane (leaflet is a term used for one side of the lipid bilayer membrane). The negative charge is localized in the large anions. With the ions distributed across the membrane at these concentrations, the difference in charge is measured at -70 mV, the value described as the resting membrane potential. The exact value measured for the resting membrane potential varies between cells, but -70 mV is most commonly used as this value. This voltage would actually be much lower except for the contributions of some important proteins in the membrane. Leakage channels allow Na+ to slowly move into the cell or K+ to slowly move out, and the Na+/K+ pump restores them. This may appear to be a waste of energy, but each has a role in maintaining the membrane potential. The Action Potential Resting membrane potential describes the steady state of the cell, which is a dynamic process that is balanced by ion leakage and ion pumping. Without any outside influence, it will not change. To get an electrical signal started, the membrane potential has to change. This starts with a channel opening for Na+ in the membrane. Because the concentration of Na+ is higher outside the cell than inside the cell by a factor of 10, ions will rush into the cell that are driven largely by the concentration gradient. Because sodium is a positively charged ion, it will change the relative voltage immediately inside the cell relative to immediately outside. The resting potential is the state of the membrane at a voltage of -70 mV, so the sodium cation entering the cell will cause it to become less negative. This is known as depolarization, meaning the membrane potential moves toward zero. The concentration gradient for Na+ is so strong that it will continue to enter the cell even after the membrane potential has become zero, so that the voltage immediately around the pore begins to become positive. The electrical gradient also plays a role, as negative proteins below the membrane attract the sodium ion. The membrane potential will reach +30 mV by the time sodium has entered the cell. As the membrane potential reaches +30 mV, other voltage-gated channels are opening in the membrane. These channels are specific for the potassium ion. A concentration gradient acts on K+, as well. As K+ starts to leave the cell, taking a positive charge with it, the membrane potential begins to move back toward its resting voltage. This is called repolarization, meaning that the membrane voltage moves back toward the -70 mV value of the resting membrane potential. Repolarization returns the membrane potential to the -70 mV value that indicates the resting potential, but it actually overshoots that value. Potassium ions reach equilibrium when the membrane voltage is below -70 mV, so a period of hyperpolarization occurs while the K+ channels are open. Those K+ channels are slightly delayed in closing, accounting for this short overshoot. What has been described here is the action potential, which is presented as a graph of voltage over time in Figure 12.23. It is the electrical signal that nervous tissue generates for communication. The change in the membrane voltage from -70 mV at rest to +30 mV at the end of depolarization is a 100-mV change. That can also be written as a 0.1-V change. To put that value in perspective, think about a battery. An AA battery that you might find in a television remote has a voltage of 1.5 V, or a 9-V battery (the rectangular battery with two posts on one end) is, obviously, 9 V. The change seen in the action potential is one or two orders of magnitude less than the charge in these batteries. In fact, the membrane potential can be described as a battery. A charge is stored across the membrane that can be released under the correct conditions. A battery in your remote has stored a charge that is “released” when you push a button. Figure 12.23 Graph of Action Potential Plotting voltage measured across the cell membrane against time, the action potential begins with depolarization, followed by repolarization, which goes past the resting potential into hyperpolarization, and finally the membrane returns to rest. INTERACTIVE LINK What happens across the membrane of an electrically active cell is a dynamic process that is hard to visualize with static images or through text descriptions. View this animation to learn more about this process. What is the difference between the driving force for Na+ and K+? And what is similar about the movement of these two ions? The question is, now, what initiates the action potential? The description above conveniently glosses over that point. But it is vital to understanding what is happening. The membrane potential will stay at the resting voltage until something changes. The description above just says that a Na+ channel opens. Now, to say “a channel opens” does not mean that one individual transmembrane protein changes. Instead, it means that one kind of channel opens. There are a few different types of channels that allow Na+ to cross the membrane. A ligand-gated Na+ channel will open when a neurotransmitter binds to it and a mechanically gated Na+ channel will open when a physical stimulus affects a sensory receptor (like pressure applied to the skin compresses a touch receptor). Whether it is a neurotransmitter binding to its receptor protein or a sensory stimulus activating a sensory receptor cell, some stimulus gets the process started. Sodium starts to enter the cell and the membrane becomes less negative. A third type of channel that is an important part of depolarization in the action potential is the voltage-gated Na+ channel. The channels that start depolarizing the membrane because of a stimulus help the cell to depolarize from -70 mV to -55 mV. Once the membrane reaches that voltage, the voltage-gated Na+ channels open. This is what is known as the threshold. Any depolarization that does not change the membrane potential to -55 mV or higher will not reach threshold and thus will not result in an action potential. Also, any stimulus that depolarizes the membrane to -55 mV or beyond will cause a large number of channels to open and an action potential will be initiated. Because of the threshold, the action potential can be likened to a digital event—it either happens or it does not. If the threshold is not reached, then no action potential occurs. If depolarization reaches -55 mV, then the action potential continues and runs all the way to +30 mV, at which K+ causes repolarization, including the hyperpolarizing overshoot. Also, those changes are the same for every action potential, which means that once the threshold is reached, the exact same thing happens. A stronger stimulus, which might depolarize the membrane well past threshold, will not make a “bigger” action potential. Action potentials are “all or none.” Either the membrane reaches the threshold and everything occurs as described above, or the membrane does not reach the threshold and nothing else happens. All action potentials peak at the same voltage (+30 mV), so one action potential is not bigger than another. Stronger stimuli will initiate multiple action potentials more quickly, but the individual signals are not bigger. Thus, for example, you will not feel a greater sensation of pain, or have a stronger muscle contraction, because of the size of the action potential because they are not different sizes. As we have seen, the depolarization and repolarization of an action potential are dependent on two types of channels (the voltage-gated Na+ channel and the voltage-gated K+ channel). The voltage-gated Na+ channel actually has two gates. One is the activation gate, which opens when the membrane potential crosses -55 mV. The other gate is the inactivation gate, which closes after a specific period of time—on the order of a fraction of a millisecond. When a cell is at rest, the activation gate is closed and the inactivation gate is open. However, when the threshold is reached, the activation gate opens, allowing Na+ to rush into the cell. Timed with the peak of depolarization, the inactivation gate closes. During repolarization, no more sodium can enter the cell. When the membrane potential passes -55 mV again, the activation gate closes. After that, the inactivation gate re-opens, making the channel ready to start the whole process over again. The voltage-gated K+ channel has only one gate, which is sensitive to a membrane voltage of -50 mV. However, it does not open as quickly as the voltage-gated Na+ channel does. It might take a fraction of a millisecond for the channel to open once that voltage has been reached. The timing of this coincides exactly with when the Na+ flow peaks, so voltage-gated K+ channels open just as the voltage-gated Na+ channels are being inactivated. As the membrane potential repolarizes and the voltage passes -50 mV again, the channel closes—again, with a little delay. Potassium continues to leave the cell for a short while and the membrane potential becomes more negative, resulting in the hyperpolarizing overshoot. Then the channel closes again and the membrane can return to the resting potential because of the ongoing activity of the non-gated channels and the Na+/K+pump. All of this takes place within approximately 2 milliseconds (Figure 12.24). While an action potential is in progress, another one cannot be initiated. That effect is referred to as the refractory period. There are two phases of the refractory period: the absolute refractory period and the relative refractory period. During the absolute phase, another action potential will not start. This is because of the inactivation gate of the voltage-gated Na+ channel. Once that channel is back to its resting conformation (less than -55 mV), a new action potential could be started, but only by a stronger stimulus than the one that initiated the current action potential. This is because of the flow of K+ out of the cell. Because that ion is rushing out, any Na+that tries to enter will not depolarize the cell, but will only keep the cell from hyperpolarizing. Figure 12.24 Stages of an Action Potential Plotting voltage measured across the cell membrane against time, the events of the action potential can be related to specific changes in the membrane voltage. (1) At rest, the membrane voltage is -70 mV. (2) The membrane begins to depolarize when an external stimulus is applied. (3) The membrane voltage begins a rapid rise toward +30 mV. (4) The membrane voltage starts to return to a negative value. (5) Repolarization continues past the resting membrane voltage, resulting in hyperpolarization. (6) The membrane voltage returns to the resting value shortly after hyperpolarization. Propagation of the Action Potential The action potential is initiated at the beginning of the axon, at what is called the initial segment. There is a high density of voltage-gated Na+ channels so that rapid depolarization can take place here. Going down the length of the axon, the action potential is propagated because more voltage-gated Na+ channels are opened as the depolarization spreads. This spreading occurs because Na+ enters through the channel and moves along the inside of the cell membrane. As the Na+ moves, or flows, a short distance along the cell membrane, its positive charge depolarizes a little more of the cell membrane. As that depolarization spreads, new voltage-gated Na+ channels open and more ions rush into the cell, spreading the depolarization a little farther. Because voltage-gated Na+ channels are inactivated at the peak of the depolarization, they cannot be opened again for a brief time—the absolute refractory period. Because of this, depolarization spreading back toward previously opened channels has no effect. The action potential must propagate toward the axon terminals; as a result, the polarity of the neuron is maintained, as mentioned above. Propagation, as described above, applies to unmyelinated axons. When myelination is present, the action potential propagates differently. Sodium ions that enter the cell at the initial segment start to spread along the length of the axon segment, but there are no voltage-gated Na+ channels until the first node of Ranvier. Because there is not constant opening of these channels along the axon segment, the depolarization spreads at an optimal speed. The distance between nodes is the optimal distance to keep the membrane still depolarized above threshold at the next node. As Na+ spreads along the inside of the membrane of the axon segment, the charge starts to dissipate. If the node were any farther down the axon, that depolarization would have fallen off too much for voltage-gated Na+ channels to be activated at the next node of Ranvier. If the nodes were any closer together, the speed of propagation would be slower. Propagation along an unmyelinated axon is referred to as continuous conduction; along the length of a myelinated axon, it is saltatory conduction. Continuous conduction is slow because there are always voltage-gated Na+ channels opening, and more and more Na+ is rushing into the cell. Saltatory conduction is faster because the action potential basically jumps from one node to the next (saltare = “to leap”), and the new influx of Na+ renews the depolarized membrane. Along with the myelination of the axon, the diameter of the axon can influence the speed of conduction. Much as water runs faster in a wide river than in a narrow creek, Na+-based depolarization spreads faster down a wide axon than down a narrow one. This concept is known as resistance and is generally true for electrical wires or plumbing, just as it is true for axons, although the specific conditions are different at the scales of electrons or ions versus water in a river. HOMEOSTATIC IMBALANCES Potassium Concentration Glial cells, especially astrocytes, are responsible for maintaining the chemical environment of the CNS tissue. The concentrations of ions in the extracellular fluid are the basis for how the membrane potential is established and changes in electrochemical signaling. If the balance of ions is upset, drastic outcomes are possible. Normally the concentration of K+ is higher inside the neuron than outside. After the repolarizing phase of the action potential, K+ leakage channels and the Na+/K+ pump ensure that the ions return to their original locations. Following a stroke or other ischemic event, extracellular K+ levels are elevated. The astrocytes in the area are equipped to clear excess K+ to aid the pump. But when the level is far out of balance, the effects can be irreversible. Astrocytes can become reactive in cases such as these, which impairs their ability to maintain the local chemical environment. The glial cells enlarge and their processes swell. They lose their K+ buffering ability and the function of the pump is affected, or even reversed. One of the early signs of cell disease is this "leaking" of sodium ions into the body cells. This sodium/potassium imbalance negatively affects the internal chemistry of cells, preventing them from functioning normally. INTERACTIVE LINK Visit this site to see a virtual neurophysiology lab, and to observe electrophysiological processes in the nervous system, where scientists directly measure the electrical signals produced by neurons. Often, the action potentials occur so rapidly that watching a screen to see them occur is not helpful. A speaker is powered by the signals recorded from a neuron and it “pops” each time the neuron fires an action potential. These action potentials are firing so fast that it sounds like static on the radio. Electrophysiologists can recognize the patterns within that static to understand what is happening. Why is the leech model used for measuring the electrical activity of neurons instead of using humans? Communication Between Neurons - Explain the differences between the types of graded potentials - Categorize the major neurotransmitters by chemical type and effect The electrical changes taking place within a neuron, as described in the previous section, are similar to a light switch being turned on. A stimulus starts the depolarization, but the action potential runs on its own once a threshold has been reached. The question is now, “What flips the light switch on?” Temporary changes to the cell membrane voltage can result from neurons receiving information from the environment, or from the action of one neuron on another. These special types of potentials influence a neuron and determine whether an action potential will occur or not. Many of these transient signals originate at the synapse. Graded Potentials Local changes in the membrane potential are called graded potentials and are usually associated with the dendrites of a neuron. The amount of change in the membrane potential is determined by the size of the stimulus that causes it. In the example of testing the temperature of the shower, slightly warm water would only initiate a small change in a thermoreceptor, whereas hot water would cause a large amount of change in the membrane potential. Graded potentials can be of two sorts, either they are depolarizing or hyperpolarizing (Figure 12.25). For a membrane at the resting potential, a graded potential represents a change in that voltage either above -70 mV or below -70 mV. Depolarizing graded potentials are often the result of Na+ or Ca2+ entering the cell. Both of these ions have higher concentrations outside the cell than inside; because they have a positive charge, they will move into the cell causing it to become less negative relative to the outside. Hyperpolarizing graded potentials can be caused by K+ leaving the cell or Cl- entering the cell. If a positive charge moves out of a cell, the cell becomes more negative; if a negative charge enters the cell, the same thing happens. Figure 12.25 Graded Potentials Graded potentials are temporary changes in the membrane voltage, the characteristics of which depend on the size of the stimulus. Some types of stimuli cause depolarization of the membrane, whereas others cause hyperpolarization. It depends on the specific ion channels that are activated in the cell membrane. Types of Graded Potentials For the unipolar cells of sensory neurons—both those with free nerve endings and those within encapsulations—graded potentials develop in the dendrites that influence the generation of an action potential in the axon of the same cell. This is called a generator potential. For other sensory receptor cells, such as taste cells or photoreceptors of the retina, graded potentials in their membranes result in the release of neurotransmitters at synapses with sensory neurons. This is called a receptor potential. A postsynaptic potential (PSP) is the graded potential in the dendrites of a neuron that is receiving synapses from other cells. Postsynaptic potentials can be depolarizing or hyperpolarizing. Depolarization in a postsynaptic potential is called an excitatory postsynaptic potential (EPSP) because it causes the membrane potential to move toward threshold. Hyperpolarization in a postsynaptic potential is an inhibitory postsynaptic potential (IPSP) because it causes the membrane potential to move away from threshold. Summation All types of graded potentials will result in small changes of either depolarization or hyperpolarization in the voltage of a membrane. These changes can lead to the neuron reaching threshold if the changes add together, or summate. The combined effects of different types of graded potentials are illustrated in Figure 12.26. If the total change in voltage in the membrane is a positive 15 mV, meaning that the membrane depolarizes from -70 mV to -55 mV, then the graded potentials will result in the membrane reaching threshold. For receptor potentials, threshold is not a factor because the change in membrane potential for receptor cells directly causes neurotransmitter release. However, generator potentials can initiate action potentials in the sensory neuron axon, and postsynaptic potentials can initiate an action potential in the axon of other neurons. Graded potentials summate at a specific location at the beginning of the axon to initiate the action potential, namely the initial segment. For sensory neurons, which do not have a cell body between the dendrites and the axon, the initial segment is directly adjacent to the dendritic endings. For all other neurons, the axon hillock is essentially the initial segment of the axon, and it is where summation takes place. These locations have a high density of voltage-gated Na+ channels that initiate the depolarizing phase of the action potential. Summation can be spatial or temporal, meaning it can be the result of multiple graded potentials at different locations on the neuron, or all at the same place but separated in time. Spatial summation is related to associating the activity of multiple inputs to a neuron with each other. Temporal summation is the relationship of multiple action potentials from a single cell resulting in a significant change in the membrane potential. Spatial and temporal summation can act together, as well. Figure 12.26 Postsynaptic Potential Summation The result of summation of postsynaptic potentials is the overall change in the membrane potential. At point A, several different excitatory postsynaptic potentials add up to a large depolarization. At point B, a mix of excitatory and inhibitory postsynaptic potentials result in a different end result for the membrane potential. INTERACTIVE LINK Watch this video to learn about summation. The process of converting electrical signals to chemical signals and back requires subtle changes that can result in transient increases or decreases in membrane voltage. To cause a lasting change in the target cell, multiple signals are usually added together, or summated. Does spatial summation have to happen all at once, or can the separate signals arrive on the postsynaptic neuron at slightly different times? Explain your answer. Synapses There are two types of connections between electrically active cells, chemical synapses and electrical synapses. In a chemical synapse, a chemical signal—namely, a neurotransmitter—is released from one cell and it affects the other cell. In an electrical synapse, there is a direct connection between the two cells so that ions can pass directly from one cell to the next. If one cell is depolarized in an electrical synapse, the joined cell also depolarizes because the ions pass between the cells. Chemical synapses involve the transmission of chemical information from one cell to the next. This section will concentrate on the chemical type of synapse. An example of a chemical synapse is the neuromuscular junction (NMJ) described in the chapter on muscle tissue. In the nervous system, there are many more synapses that are essentially the same as the NMJ. All synapses have common characteristics, which can be summarized in this list: - presynaptic element - neurotransmitter (packaged in vesicles) - synaptic cleft - receptor proteins - postsynaptic element - neurotransmitter elimination or re-uptake For the NMJ, these characteristics are as follows: the presynaptic element is the motor neuron's axon terminals, the neurotransmitter is acetylcholine, the synaptic cleft is the space between the cells where the neurotransmitter diffuses, the receptor protein is the nicotinic acetylcholine receptor, the postsynaptic element is the sarcolemma of the muscle cell, and the neurotransmitter is eliminated by acetylcholinesterase. Other synapses are similar to this, and the specifics are different, but they all contain the same characteristics. Neurotransmitter Release When an action potential reaches the axon terminals, voltage-gated Ca2+ channels in the membrane of the synaptic end bulb open. The concentration of Ca2+ increases inside the end bulb, and the Ca2+ ion associates with proteins in the outer surface of neurotransmitter vesicles. The Ca2+ facilitates the merging of the vesicle with the presynaptic membrane so that the neurotransmitter is released through exocytosis into the small gap between the cells, known as the synaptic cleft. Once in the synaptic cleft, the neurotransmitter diffuses the short distance to the postsynaptic membrane and can interact with neurotransmitter receptors. Receptors are specific for the neurotransmitter, and the two fit together like a key and lock. One neurotransmitter binds to its receptor and will not bind to receptors for other neurotransmitters, making the binding a specific chemical event (Figure 12.27). Figure 12.27 The Synapse The synapse is a connection between a neuron and its target cell (which is not necessarily a neuron). The presynaptic element is the synaptic end bulb of the axon where Ca2+ enters the bulb to cause vesicle fusion and neurotransmitter release. The neurotransmitter diffuses across the synaptic cleft to bind to its receptor. The neurotransmitter is cleared from the synapse either by enzymatic degradation, neuronal reuptake, or glial reuptake. Neurotransmitter Systems There are several systems of neurotransmitters that are found at various synapses in the nervous system. These groups refer to the chemicals that are the neurotransmitters, and within the groups are specific systems. The first group, which is a neurotransmitter system of its own, is the cholinergic system. It is the system based on acetylcholine. This includes the NMJ as an example of a cholinergic synapse, but cholinergic synapses are found in other parts of the nervous system. They are in the autonomic nervous system, as well as distributed throughout the brain. The cholinergic system has two types of receptors, the nicotinic receptor is found in the NMJ as well as other synapses. There is also an acetylcholine receptor known as the muscarinic receptor. Both of these receptors are named for drugs that interact with the receptor in addition to acetylcholine. Nicotine will bind to the nicotinic receptor and activate it similar to acetylcholine. Muscarine, a product of certain mushrooms, will bind to the muscarinic receptor. However, nicotine will not bind to the muscarinic receptor and muscarine will not bind to the nicotinic receptor. Another group of neurotransmitters are amino acids. This includes glutamate (Glu), GABA (gamma-aminobutyric acid, a derivative of glutamate), and glycine (Gly). These amino acids have an amino group and a carboxyl group in their chemical structures. Glutamate is one of the 20 amino acids that are used to make proteins. Each amino acid neurotransmitter would be part of its own system, namely the glutamatergic, GABAergic, and glycinergic systems. They each have their own receptors and do not interact with each other. Amino acid neurotransmitters are eliminated from the synapse by reuptake. A pump in the cell membrane of the presynaptic element, or sometimes a neighboring glial cell, will clear the amino acid from the synaptic cleft so that it can be recycled, repackaged in vesicles, and released again. Another class of neurotransmitter is the biogenic amine, a group of neurotransmitters that are enzymatically made from amino acids. They have amino groups in them, but no longer have carboxyl groups and are therefore no longer classified as amino acids. Serotonin is made from tryptophan. It is the basis of the serotonergic system, which has its own specific receptors. Serotonin is transported back into the presynaptic cell for repackaging. Other biogenic amines are made from tyrosine, and include dopamine, norepinephrine, and epinephrine. Dopamine is part of its own system, the dopaminergic system, which has dopamine receptors. Dopamine is removed from the synapse by transport proteins in the presynaptic cell membrane. Norepinephrine and epinephrine belong to the adrenergic neurotransmitter system. The two molecules are very similar and bind to the same receptors, which are referred to as alpha and beta receptors. Norepinephrine and epinephrine are also transported back into the presynaptic cell. The chemical epinephrine (epi- = “on”; “-nephrine” = kidney) is also known as adrenaline (renal = “kidney”), and norepinephrine is sometimes referred to as noradrenaline. The adrenal gland produces epinephrine and norepinephrine to be released into the blood stream as hormones. A neuropeptide is a neurotransmitter molecule made up of chains of amino acids connected by peptide bonds. This is what a protein is, but the term protein implies a certain length to the molecule. Some neuropeptides are quite short, such as met-enkephalin, which is five amino acids long. Others are long, such as beta-endorphin, which is 31 amino acids long. Neuropeptides are often released at synapses in combination with another neurotransmitter, and they often act as hormones in other systems of the body, such as vasoactive intestinal peptide (VIP) or substance P. The effect of a neurotransmitter on the postsynaptic element is entirely dependent on the receptor protein. First, if there is no receptor protein in the membrane of the postsynaptic element, then the neurotransmitter has no effect. The depolarizing or hyperpolarizing effect is also dependent on the receptor. When acetylcholine binds to the nicotinic receptor, the postsynaptic cell is depolarized. This is because the receptor is a cation channel and positively charged Na+ will rush into the cell. However, when acetylcholine binds to the muscarinic receptor, of which there are several variants, it might cause depolarization or hyperpolarization of the target cell. The amino acid neurotransmitters, glutamate, glycine, and GABA, are almost exclusively associated with just one effect. Glutamate is considered an excitatory amino acid, but only because Glu receptors in the adult cause depolarization of the postsynaptic cell. Glycine and GABA are considered inhibitory amino acids, again because their receptors cause hyperpolarization. The biogenic amines have mixed effects. For example, the dopamine receptors that are classified as D1 receptors are excitatory whereas D2-type receptors are inhibitory. Biogenic amine receptors and neuropeptide receptors can have even more complex effects because some may not directly affect the membrane potential, but rather have an effect on gene transcription or other metabolic processes in the neuron. The characteristics of the various neurotransmitter systems presented in this section are organized in Table 12.3. The important thing to remember about neurotransmitters, and signaling chemicals in general, is that the effect is entirely dependent on the receptor. Neurotransmitters bind to one of two classes of receptors at the cell surface, ionotropic or metabotropic (Figure 12.28). Ionotropic receptors are ligand-gated ion channels, such as the nicotinic receptor for acetylcholine or the glycine receptor. A metabotropic receptor involves a complex of proteins that result in metabolic changes within the cell. The receptor complex includes the transmembrane receptor protein, a G protein, and an effector protein. The neurotransmitter, referred to as the first messenger, binds to the receptor protein on the extracellular surface of the cell, and the intracellular side of the protein initiates activity of the G protein. The G protein is a guanosine triphosphate (GTP) hydrolase that physically moves from the receptor protein to the effector protein to activate the latter. An effector protein is an enzyme that catalyzes the generation of a new molecule, which acts as the intracellular mediator of the signal that binds to the receptor. This intracellular mediator is called the second messenger. Different receptors use different second messengers. Two common examples of second messengers are cyclic adenosine monophosphate (cAMP) and inositol triphosphate (IP3). The enzyme adenylate cyclase (an example of an effector protein) makes cAMP, and phospholipase C is the enzyme that makes IP3. Second messengers, after they are produced by the effector protein, cause metabolic changes within the cell. These changes are most likely the activation of other enzymes in the cell. In neurons, they often modify ion channels, either opening or closing them. These enzymes can also cause changes in the cell, such as the activation of genes in the nucleus, and therefore the increased synthesis of proteins. In neurons, these kinds of changes are often the basis of stronger connections between cells at the synapse and may be the basis of learning and memory. Figure 12.28 Receptor Types (a) An ionotropic receptor is a channel that opens when the neurotransmitter binds to it. (b) A metabotropic receptor is a complex that causes metabolic changes in the cell when the neurotransmitter binds to it (1). After binding, the G protein hydrolyzes GTP and moves to the effector protein (2). When the G protein contacts the effector protein, a second messenger is generated, such as cAMP (3). The second messenger can then go on to cause changes in the neuron, such as opening or closing ion channels, metabolic changes, and changes in gene transcription. INTERACTIVE LINK Watch this video to learn about the release of a neurotransmitter. The action potential reaches the end of the axon, called the axon terminal, and a chemical signal is released to tell the target cell to do something—either to initiate a new action potential, or to suppress that activity. In a very short space, the electrical signal of the action potential is changed into the chemical signal of a neurotransmitter and then back to electrical changes in the target cell membrane. What is the importance of voltage-gated calcium channels in the release of neurotransmitters? Characteristics of Neurotransmitter Systems \| System \| Cholinergic \| Amino acids \| Biogenic amines \| Neuropeptides \| \|---\|---\|---\|---\|---\| \| Neurotransmitters \| Acetylcholine \| Glutamate, glycine, GABA \| Serotonin (5-HT), dopamine, norepinephrine, (epinephrine) \| Met-enkephalin, beta-endorphin, VIP, Substance P, etc. \| \| Receptors \| Nicotinic and muscarinic receptors \| Glu receptors, gly receptors, GABA receptors \| 5-HT receptors, D1 and D2 receptors, α-adrenergic and β-adrenergic receptors \| Receptors are too numerous to list, but are specific to the peptides. \| \| Elimination \| Degradation by acetylcholinesterase \| Reuptake by neurons or glia \| Reuptake by neurons \| Degradation by enzymes called peptidases \| \| Postsynaptic effect \| Nicotinic receptor causes depolarization. Muscarinic receptors can cause both depolarization or hyperpolarization depending on the subtype. \| Glu receptors cause depolarization. Gly and GABA receptors cause hyperpolarization. \| Depolarization or hyperpolarization depends on the specific receptor. For example, D1 receptors cause depolarization and D2 receptors cause hyperpolarization. \| Depolarization or hyperpolarization depends on the specific receptor. \| Table 12.3 DISORDERS OF THE... Nervous System The underlying cause of some neurodegenerative diseases, such as Alzheimer’s and Parkinson’s, appears to be related to proteins—specifically, to proteins behaving badly. One of the strongest theories of what causes Alzheimer’s disease is based on the accumulation of beta-amyloid plaques, dense conglomerations of a protein that is not functioning correctly. Parkinson’s disease is linked to an increase in a protein known as alpha-synuclein that is toxic to the cells of the substantia nigra nucleus in the midbrain. For proteins to function correctly, they are dependent on their three-dimensional shape. The linear sequence of amino acids folds into a three-dimensional shape that is based on the interactions between and among those amino acids. When the folding is disturbed, and proteins take on a different shape, they stop functioning correctly. But the disease is not necessarily the result of functional loss of these proteins; rather, these altered proteins start to accumulate and may become toxic. For example, in Alzheimer’s, the hallmark of the disease is the accumulation of these amyloid plaques in the cerebral cortex. The term coined to describe this sort of disease is “proteopathy” and it includes other diseases. Creutzfeld-Jacob disease, the human variant of the prion disease known as mad cow disease in the bovine, also involves the accumulation of amyloid plaques, similar to Alzheimer’s. Diseases of other organ systems can fall into this group as well, such as cystic fibrosis or type 2 diabetes. Recognizing the relationship between these diseases has suggested new therapeutic possibilities. Interfering with the accumulation of the proteins, and possibly as early as their original production within the cell, may unlock new ways to alleviate these devastating diseases. Key Terms - absolute refractory period - time during an action period when another action potential cannot be generated because the voltage-gated Na+ channel is inactivated - action potential - change in voltage of a cell membrane in response to a stimulus that results in transmission of an electrical signal; unique to neurons and muscle fibers - activation gate - part of the voltage-gated Na+ channel that opens when the membrane voltage reaches threshold - astrocyte - glial cell type of the CNS that provides support for neurons and maintains the blood-brain barrier - autonomic nervous system (ANS) - functional division of the nervous system that is responsible for homeostatic reflexes that coordinate control of cardiac and smooth muscle, as well as glandular tissue - axon - single process of the neuron that carries an electrical signal (action potential) away from the cell body toward a target cell - axon hillock - tapering of the neuron cell body that gives rise to the axon - axon segment - single stretch of the axon insulated by myelin and bounded by nodes of Ranvier at either end (except for the first, which is after the initial segment, and the last, which is followed by the axon terminal) - axon terminal - end of the axon, where there are usually several branches extending toward the target cell - axoplasm - cytoplasm of an axon, which is different in composition than the cytoplasm of the neuronal cell body - biogenic amine - class of neurotransmitters that are enzymatically derived from amino acids but no longer contain a carboxyl group - bipolar - shape of a neuron with two processes extending from the neuron cell body—the axon and one dendrite - blood-brain barrier (BBB) - physiological barrier between the circulatory system and the central nervous system that establishes a privileged blood supply, restricting the flow of substances into the CNS - brain - the large organ of the central nervous system composed of white and gray matter, contained within the cranium and continuous with the spinal cord - central nervous system (CNS) - anatomical division of the nervous system located within the cranial and vertebral cavities, namely the brain and spinal cord - cerebral cortex - outermost layer of gray matter in the brain, where conscious perception takes place - cerebrospinal fluid (CSF) - circulatory medium within the CNS that is produced by ependymal cells in the choroid plexus filtering the blood - chemical synapse - connection between two neurons, or between a neuron and its target, where a neurotransmitter diffuses across a very short distance - cholinergic system - neurotransmitter system of acetylcholine, which includes its receptors and the enzyme acetylcholinesterase - choroid plexus - specialized structure containing ependymal cells that line blood capillaries and filter blood to produce CSF in the four ventricles of the brain - continuous conduction - slow propagation of an action potential along an unmyelinated axon owing to voltage-gated Na+ channels located along the entire length of the cell membrane - dendrite - one of many branchlike processes that extends from the neuron cell body and functions as a contact for incoming signals (synapses) from other neurons or sensory cells - depolarization - change in a cell membrane potential from rest toward zero - effector protein - enzyme that catalyzes the generation of a new molecule, which acts as the intracellular mediator of the signal that binds to the receptor - electrical synapse - connection between two neurons, or any two electrically active cells, where ions flow directly through channels spanning their adjacent cell membranes - electrochemical exclusion - principle of selectively allowing ions through a channel on the basis of their charge - enteric nervous system (ENS) - neural tissue associated with the digestive system that is responsible for nervous control through autonomic connections - ependymal cell - glial cell type in the CNS responsible for producing cerebrospinal fluid - excitable membrane - cell membrane that regulates the movement of ions so that an electrical signal can be generated - excitatory postsynaptic potential (EPSP) - graded potential in the postsynaptic membrane that is the result of depolarization and makes an action potential more likely to occur - G protein - guanosine triphosphate (GTP) hydrolase that physically moves from the receptor protein to the effector protein to activate the latter - ganglion - localized collection of neuron cell bodies in the peripheral nervous system - gated - property of a channel that determines how it opens under specific conditions, such as voltage change or physical deformation - generator potential - graded potential from dendrites of a unipolar cell which generates the action potential in the initial segment of that cell’s axon - glial cell - one of the various types of neural tissue cells responsible for maintenance of the tissue, and largely responsible for supporting neurons - graded potential - change in the membrane potential that varies in size, depending on the size of the stimulus that elicits it - gray matter - regions of the nervous system containing cell bodies of neurons with few or no myelinated axons; actually may be more pink or tan in color, but called gray in contrast to white matter - inactivation gate - part of a voltage-gated Na+ channel that closes when the membrane potential reaches +30 mV - inhibitory postsynaptic potential (IPSP) - graded potential in the postsynaptic membrane that is the result of hyperpolarization and makes an action potential less likely to occur - initial segment - first part of the axon as it emerges from the axon hillock, where the electrical signals known as action potentials are generated - integration - nervous system function that combines sensory perceptions and higher cognitive functions (memories, learning, emotion, etc.) to produce a response - ionotropic receptor - neurotransmitter receptor that acts as an ion channel gate, and opens by the binding of the neurotransmitter - leakage channel - ion channel that opens randomly and is not gated to a specific event, also known as a non-gated channel - ligand-gated channels - another name for an ionotropic receptor for which a neurotransmitter is the ligand - lower motor neuron - second neuron in the motor command pathway that is directly connected to the skeletal muscle - mechanically gated channel - ion channel that opens when a physical event directly affects the structure of the protein - membrane potential - distribution of charge across the cell membrane, based on the charges of ions - metabotropic receptor - neurotransmitter receptor that involves a complex of proteins that cause metabolic changes in a cell - microglia - glial cell type in the CNS that serves as the resident component of the immune system - multipolar - shape of a neuron that has multiple processes—the axon and two or more dendrites - muscarinic receptor - type of acetylcholine receptor protein that is characterized by also binding to muscarine and is a metabotropic receptor - myelin - lipid-rich insulating substance surrounding the axons of many neurons, allowing for faster transmission of electrical signals - myelin sheath - lipid-rich layer of insulation that surrounds an axon, formed by oligodendrocytes in the CNS and Schwann cells in the PNS; facilitates the transmission of electrical signals - nerve - cord-like bundle of axons located in the peripheral nervous system that transmits sensory input and response output to and from the central nervous system - neuron - neural tissue cell that is primarily responsible for generating and propagating electrical signals into, within, and out of the nervous system - neuropeptide - neurotransmitter type that includes protein molecules and shorter chains of amino acids - neurotransmitter - chemical signal that is released from the synaptic end bulb of a neuron to cause a change in the target cell - nicotinic receptor - type of acetylcholine receptor protein that is characterized by also binding to nicotine and is an ionotropic receptor - node of Ranvier - gap between two myelinated regions of an axon, allowing for strengthening of the electrical signal as it propagates down the axon - nonspecific channel - channel that is not specific to one ion over another, such as a nonspecific cation channel that allows any positively charged ion across the membrane - nucleus - in the nervous system, a localized collection of neuron cell bodies that are functionally related; a “center” of neural function - oligodendrocyte - glial cell type in the CNS that provides the myelin insulation for axons in tracts - peripheral nervous system (PNS) - anatomical division of the nervous system that is largely outside the cranial and vertebral cavities, namely all parts except the brain and spinal cord - postsynaptic potential (PSP) - graded potential in the postsynaptic membrane caused by the binding of neurotransmitter to protein receptors - precentral gyrus of the frontal cortex - region of the cerebral cortex responsible for generating motor commands, where the upper motor neuron cell body is located - process - in cells, an extension of a cell body; in the case of neurons, this includes the axon and dendrites - propagation - movement of an action potential along the length of an axon - receptor potential - graded potential in a specialized sensory cell that directly causes the release of neurotransmitter without an intervening action potential - refractory period - time after the initiation of an action potential when another action potential cannot be generated - relative refractory period - time during the refractory period when a new action potential can only be initiated by a stronger stimulus than the current action potential because voltage-gated K+ channels are not closed - repolarization - return of the membrane potential to its normally negative voltage at the end of the action potential - resistance - property of an axon that relates to the ability of particles to diffuse through the cytoplasm; this is inversely proportional to the fiber diameter - response - nervous system function that causes a target tissue (muscle or gland) to produce an event as a consequence to stimuli - resting membrane potential - the difference in voltage measured across a cell membrane under steady-state conditions, typically -70 mV - saltatory conduction - quick propagation of the action potential along a myelinated axon owing to voltage-gated Na+ channels being present only at the nodes of Ranvier - satellite cell - glial cell type in the PNS that provides support for neurons in the ganglia - Schwann cell - glial cell type in the PNS that provides the myelin insulation for axons in nerves - sensation - nervous system function that receives information from the environment and translates it into the electrical signals of nervous tissue - size exclusion - principle of selectively allowing ions through a channel on the basis of their relative size - soma - in neurons, that portion of the cell that contains the nucleus; the cell body, as opposed to the cell processes (axons and dendrites) - somatic nervous system (SNS) - functional division of the nervous system that is concerned with conscious perception, voluntary movement, and skeletal muscle reflexes - spatial summation - combination of graded potentials across the neuronal cell membrane caused by signals from separate presynaptic elements that add up to initiate an action potential - spinal cord - organ of the central nervous system found within the vertebral cavity and connected with the periphery through spinal nerves; mediates reflex behaviors - stimulus - an event in the external or internal environment that registers as activity in a sensory neuron - summate - to add together, as in the cumulative change in postsynaptic potentials toward reaching threshold in the membrane, either across a span of the membrane or over a certain amount of time - synapse - narrow junction across which a chemical signal passes from neuron to the next, initiating a new electrical signal in the target cell - synaptic cleft - small gap between cells in a chemical synapse where neurotransmitter diffuses from the presynaptic element to the postsynaptic element - synaptic end bulb - swelling at the end of an axon where neurotransmitter molecules are released onto a target cell across a synapse - temporal summation - combination of graded potentials at the same location on a neuron resulting in a strong signal from one input - thalamus - region of the central nervous system that acts as a relay for sensory pathways - thermoreceptor - type of sensory receptor capable of transducing temperature stimuli into neural action potentials - threshold - membrane voltage at which an action potential is initiated - tract - bundle of axons in the central nervous system having the same function and point of origin - unipolar - shape of a neuron which has only one process that includes both the axon and dendrite - upper motor neuron - first neuron in the motor command pathway with its cell body in the cerebral cortex that synapses on the lower motor neuron in the spinal cord - ventricle - central cavity within the brain where CSF is produced and circulates - voltage-gated channel - ion channel that opens because of a change in the charge distributed across the membrane where it is located - white matter - regions of the nervous system containing mostly myelinated axons, making the tissue appear white because of the high lipid content of myelin Chapter Review 12.1 Basic Structure and Function of the Nervous System The nervous system can be separated into divisions on the basis of anatomy and physiology. The anatomical divisions are the central and peripheral nervous systems. The CNS is the brain and spinal cord. The PNS is everything else. Functionally, the nervous system can be divided into those regions that are responsible for sensation, those that are responsible for integration, and those that are responsible for generating responses. All of these functional areas are found in both the central and peripheral anatomy. Considering the anatomical regions of the nervous system, there are specific names for the structures within each division. A localized collection of neuron cell bodies is referred to as a nucleus in the CNS and as a ganglion in the PNS. A bundle of axons is referred to as a tract in the CNS and as a nerve in the PNS. Whereas nuclei and ganglia are specifically in the central or peripheral divisions, axons can cross the boundary between the two. A single axon can be part of a nerve and a tract. The name for that specific structure depends on its location. Nervous tissue can also be described as gray matter and white matter on the basis of its appearance in unstained tissue. These descriptions are more often used in the CNS. Gray matter is where nuclei are found and white matter is where tracts are found. In the PNS, ganglia are basically gray matter and nerves are white matter. The nervous system can also be divided on the basis of how it controls the body. The somatic nervous system (SNS) is responsible for functions that result in moving skeletal muscles. Any sensory or integrative functions that result in the movement of skeletal muscle would be considered somatic. The autonomic nervous system (ANS) is responsible for functions that affect cardiac or smooth muscle tissue, or that cause glands to produce their secretions. Autonomic functions are distributed between central and peripheral regions of the nervous system. The sensations that lead to autonomic functions can be the same sensations that are part of initiating somatic responses. Somatic and autonomic integrative functions may overlap as well. A special division of the nervous system is the enteric nervous system, which is responsible for controlling the digestive organs. Parts of the autonomic nervous system overlap with the enteric nervous system. The enteric nervous system is exclusively found in the periphery because it is the nervous tissue in the organs of the digestive system. 12.2 Nervous Tissue Nervous tissue contains two major cell types, neurons and glial cells. Neurons are the cells responsible for communication through electrical signals. Glial cells are supporting cells, maintaining the environment around the neurons. Neurons are polarized cells, based on the flow of electrical signals along their membrane. Signals are received at the dendrites, are passed along the cell body, and propagate along the axon towards the target, which may be another neuron, muscle tissue, or a gland. Many axons are insulated by a lipid-rich substance called myelin. Specific types of glial cells provide this insulation. Several types of glial cells are found in the nervous system, and they can be categorized by the anatomical division in which they are found. In the CNS, astrocytes, oligodendrocytes, microglia, and ependymal cells are found. Astrocytes are important for maintaining the chemical environment around the neuron and are crucial for regulating the blood-brain barrier. Oligodendrocytes are the myelinating glia in the CNS. Microglia act as phagocytes and play a role in immune surveillance. Ependymal cells are responsible for filtering the blood to produce cerebrospinal fluid, which is a circulatory fluid that performs some of the functions of blood in the brain and spinal cord because of the BBB. In the PNS, satellite cells are supporting cells for the neurons, and Schwann cells insulate peripheral axons. 12.3 The Function of Nervous Tissue Sensation starts with the activation of a sensory ending, such as the thermoreceptor in the skin sensing the temperature of the water. The sensory endings in the skin initiate an electrical signal that travels along the sensory axon within a nerve into the spinal cord, where it synapses with a neuron in the gray matter of the spinal cord. The temperature information represented in that electrical signal is passed to the next neuron by a chemical signal that diffuses across the small gap of the synapse and initiates a new electrical signal in the target cell. That signal travels through the sensory pathway to the brain, passing through the thalamus, where conscious perception of the water temperature is made possible by the cerebral cortex. Following integration of that information with other cognitive processes and sensory information, the brain sends a command back down to the spinal cord to initiate a motor response by controlling a skeletal muscle. The motor pathway is composed of two cells, the upper motor neuron and the lower motor neuron. The upper motor neuron has its cell body in the cerebral cortex and synapses on a cell in the gray matter of the spinal cord. The lower motor neuron is that cell in the gray matter of the spinal cord and its axon extends into the periphery where it synapses with a skeletal muscle in a neuromuscular junction. 12.4 The Action Potential The nervous system is characterized by electrical signals that are sent from one area to another. Whether those areas are close or very far apart, the signal must travel along an axon. The basis of the electrical signal is the controlled distribution of ions across the membrane. Transmembrane ion channels regulate when ions can move in or out of the cell, so that a precise signal is generated. This signal is the action potential which has a very characteristic shape based on voltage changes across the membrane in a given time period. The membrane is normally at rest with established Na+ and K+ concentrations on either side. A stimulus will start the depolarization of the membrane, and voltage-gated channels will result in further depolarization followed by repolarization of the membrane. A slight overshoot of hyperpolarization marks the end of the action potential. While an action potential is in progress, another cannot be generated under the same conditions. While the voltage-gated Na+ channel is inactivated, absolutely no action potentials can be generated. Once that channel has returned to its resting state, a new action potential is possible, but it must be started by a relatively stronger stimulus to overcome the K+ leaving the cell. The action potential travels down the axon as voltage-gated ion channels are opened by the spreading depolarization. In unmyelinated axons, this happens in a continuous fashion because there are voltage-gated channels throughout the membrane. In myelinated axons, propagation is described as saltatory because voltage-gated channels are only found at the nodes of Ranvier and the electrical events seem to “jump” from one node to the next. Saltatory conduction is faster than continuous conduction, meaning that myelinated axons propagate their signals faster. The diameter of the axon also makes a difference as ions diffusing within the cell have less resistance in a wider space. 12.5 Communication Between Neurons The basis of the electrical signal within a neuron is the action potential that propagates down the axon. For a neuron to generate an action potential, it needs to receive input from another source, either another neuron or a sensory stimulus. That input will result in opening ion channels in the neuron, resulting in a graded potential based on the strength of the stimulus. Graded potentials can be depolarizing or hyperpolarizing and can summate to affect the probability of the neuron reaching threshold. Graded potentials can be the result of sensory stimuli. If the sensory stimulus is received by the dendrites of a unipolar sensory neuron, such as the sensory neuron ending in the skin, the graded potential is called a generator potential because it can directly generate the action potential in the initial segment of the axon. If the sensory stimulus is received by a specialized sensory receptor cell, the graded potential is called a receptor potential. Graded potentials produced by interactions between neurons at synapses are called postsynaptic potentials (PSPs). A depolarizing graded potential at a synapse is called an excitatory PSP, and a hyperpolarizing graded potential at a synapse is called an inhibitory PSP. Synapses are the contacts between neurons, which can either be chemical or electrical in nature. Chemical synapses are far more common. At a chemical synapse, neurotransmitter is released from the presynaptic element and diffuses across the synaptic cleft. The neurotransmitter binds to a receptor protein and causes a change in the postsynaptic membrane (the PSP). The neurotransmitter must be inactivated or removed from the synaptic cleft so that the stimulus is limited in time. The particular characteristics of a synapse vary based on the neurotransmitter system produced by that neuron. The cholinergic system is found at the neuromuscular junction and in certain places within the nervous system. Amino acids, such as glutamate, glycine, and gamma-aminobutyric acid (GABA) are used as neurotransmitters. Other neurotransmitters are the result of amino acids being enzymatically changed, as in the biogenic amines, or being covalently bonded together, as in the neuropeptides. Interactive Link Questions In 2003, the Nobel Prize in Physiology or Medicine was awarded to Paul C. Lauterbur and Sir Peter Mansfield for discoveries related to magnetic resonance imaging (MRI). This is a tool to see the structures of the body (not just the nervous system) that depends on magnetic fields associated with certain atomic nuclei. The utility of this technique in the nervous system is that fat tissue and water appear as different shades between black and white. Because white matter is fatty (from myelin) and gray matter is not, they can be easily distinguished in MRI images. Visit the Nobel Prize website to play an interactive game that demonstrates the use of this technology and compares it with other types of imaging technologies. Also, the results from an MRI session are compared with images obtained from x-ray or computed tomography. How do the imaging techniques shown in this game indicate the separation of white and gray matter compared with the freshly dissected tissue shown earlier? 2.Visit this site to read about a woman that notices that her daughter is having trouble walking up the stairs. This leads to the discovery of a hereditary condition that affects the brain and spinal cord. The electromyography and MRI tests indicated deficiencies in the spinal cord and cerebellum, both of which are responsible for controlling coordinated movements. To what functional division of the nervous system would these structures belong? 3.Visit this site to learn about how nervous tissue is composed of neurons and glial cells. The neurons are dynamic cells with the ability to make a vast number of connections and to respond incredibly quickly to stimuli and to initiate movements based on those stimuli. They are the focus of intense research as failures in physiology can lead to devastating illnesses. Why are neurons only found in animals? Based on what this article says about neuron function, why wouldn’t they be helpful for plants or microorganisms? 4.View the University of Michigan Webscope to see an electron micrograph of a cross-section of a myelinated nerve fiber. The axon contains microtubules and neurofilaments, bounded by a plasma membrane known as the axolemma. Outside the plasma membrane of the axon is the myelin sheath, which is composed of the tightly wrapped plasma membrane of a Schwann cell. What aspects of the cells in this image react with the stain that makes them the deep, dark, black color, such as the multiple layers that are the myelin sheath? 5.What happens across the membrane of an electrically active cell is a dynamic process that is hard to visualize with static images or through text descriptions. View this animation to really understand the process. What is the difference between the driving force for Na+ and K+? And what is similar about the movement of these two ions? 6.Visit this site to see a virtual neurophysiology lab, and to observe electrophysiological processes in the nervous system, where scientists directly measure the electrical signals produced by neurons. Often, the action potentials occur so rapidly that watching a screen to see them occur is not helpful. A speaker is powered by the signals recorded from a neuron and it “pops” each time the neuron fires an action potential. These action potentials are firing so fast that it sounds like static on the radio. Electrophysiologists can recognize the patterns within that static to understand what is happening. Why is the leech model used for measuring the electrical activity of neurons instead of using humans? 7.Watch this video to learn about summation. The process of converting electrical signals to chemical signals and back requires subtle changes that can result in transient increases or decreases in membrane voltage. To cause a lasting change in the target cell, multiple signals are usually added together, or summated. Does spatial summation have to happen all at once, or can the separate signals arrive on the postsynaptic neuron at slightly different times? Explain your answer. 8.Watch this video to learn about the release of a neurotransmitter. The action potential reaches the end of the axon, called the axon terminal, and a chemical signal is released to tell the target cell to do something, either initiate a new action potential, or to suppress that activity. In a very short space, the electrical signal of the action potential is changed into the chemical signal of a neurotransmitter, and then back to electrical changes in the target cell membrane. What is the importance of voltage-gated calcium channels in the release of neurotransmitters? Review Questions Which of the following cavities contains a component of the central nervous system? - abdominal - pelvic - cranial - thoracic Which structure predominates in the white matter of the brain? - myelinated axons - neuronal cell bodies - ganglia of the parasympathetic nerves - bundles of dendrites from the enteric nervous system Which part of a neuron transmits an electrical signal to a target cell? - dendrites - soma - cell body - axon Which term describes a bundle of axons in the peripheral nervous system? - nucleus - ganglion - tract - nerve Which functional division of the nervous system would be responsible for the physiological changes seen during exercise (e.g., increased heart rate and sweating)? - somatic - autonomic - enteric - central What type of glial cell provides myelin for the axons in a tract? - oligodendrocyte - astrocyte - Schwann cell - satellite cell Which part of a neuron contains the nucleus? - dendrite - soma - axon - synaptic end bulb Which of the following substances is least able to cross the blood-brain barrier? - water - sodium ions - glucose - white blood cells What type of glial cell is the resident macrophage behind the blood-brain barrier? - microglia - astrocyte - Schwann cell - satellite cell What two types of macromolecules are the main components of myelin? - carbohydrates and lipids - proteins and nucleic acids - lipids and proteins - carbohydrates and nucleic acids If a thermoreceptor is sensitive to temperature sensations, what would a chemoreceptor be sensitive to? - light - sound - molecules - vibration Which of these locations is where the greatest level of integration is taking place in the example of testing the temperature of the shower? - skeletal muscle - spinal cord - thalamus - cerebral cortex How long does all the signaling through the sensory pathway, within the central nervous system, and through the motor command pathway take? - 1 to 2 minutes - 1 to 2 seconds - fraction of a second - varies with graded potential What is the target of an upper motor neuron? - cerebral cortex - lower motor neuron - skeletal muscle - thalamus What ion enters a neuron causing depolarization of the cell membrane? - sodium - chloride - potassium - phosphate Voltage-gated Na+ channels open upon reaching what state? - resting potential - threshold - repolarization - overshoot What does a ligand-gated channel require in order to open? - increase in concentration of Na+ ions - binding of a neurotransmitter - increase in concentration of K+ ions - depolarization of the membrane What does a mechanically gated channel respond to? - physical stimulus - chemical stimulus - increase in resistance - decrease in resistance Which of the following voltages would most likely be measured during the relative refractory period? - +30 mV - 0 mV - -45 mV - -80 mv Which of the following is probably going to propagate an action potential fastest? - a thin, unmyelinated axon - a thin, myelinated axon - a thick, unmyelinated axon - a thick, myelinated axon How much of a change in the membrane potential is necessary for the summation of postsynaptic potentials to result in an action potential being generated? - +30 mV - +15 mV - +10 mV - -15 mV A channel opens on a postsynaptic membrane that causes a negative ion to enter the cell. What type of graded potential is this? - depolarizing - repolarizing - hyperpolarizing - non-polarizing What neurotransmitter is released at the neuromuscular junction? - norepinephrine - serotonin - dopamine - acetylcholine What type of receptor requires an effector protein to initiate a signal? - biogenic amine - ionotropic receptor - cholinergic system - metabotropic receptor Which of the following neurotransmitters is associated with inhibition exclusively? - GABA - acetylcholine - glutamate - norepinephrine Critical Thinking Questions What responses are generated by the nervous system when you run on a treadmill? Include an example of each type of tissue that is under nervous system control. 35.When eating food, what anatomical and functional divisions of the nervous system are involved in the perceptual experience? 36.Multiple sclerosis is a demyelinating disease affecting the central nervous system. What type of cell would be the most likely target of this disease? Why? 37.Which type of neuron, based on its shape, is best suited for relaying information directly from one neuron to another? Explain why. 38.Sensory fibers, or pathways, are referred to as “afferent.” Motor fibers, or pathways, are referred to as “efferent.” What can you infer about the meaning of these two terms (afferent and efferent) in a structural or anatomical context? 39.If a person has a motor disorder and cannot move their arm voluntarily, but their muscles have tone, which motor neuron—upper or lower—is probably affected? Explain why. 40.What does it mean for an action potential to be an “all or none” event? 41.The conscious perception of pain is often delayed because of the time it takes for the sensations to reach the cerebral cortex. Why would this be the case based on propagation of the axon potential? 42.If a postsynaptic cell has synapses from five different cells, and three cause EPSPs and two of them cause IPSPs, give an example of a series of depolarizations and hyperpolarizations that would result in the neuron reaching threshold. 43.Why is the receptor the important element determining the effect a neurotransmitter has on a target cell?	oercommons	2025-03-18T00:37:01.405722	null	{ "license": "Creative Commons - Attribution - https://creativecommons.org/licenses/by/4.0/", "url": "https://oercommons.org/courseware/lesson/56375/overview", "title": "Anatomy and Physiology, Regulation, Integration, and Control", "author": null }
https://oercommons.org/courseware/lesson/56376/overview	Anatomy of the Nervous System Introduction Figure 13.1 Human Nervous System The ability to balance like an acrobat combines functions throughout the nervous system. The central and peripheral divisions coordinate control of the body using the senses of balance, body position, and touch on the soles of the feet. (credit: Rhett Sutphin) CHAPTER OBJECTIVES After studying this chapter, you will be able to: - Relate the developmental processes of the embryonic nervous system to the adult structures - Name the major regions of the adult nervous system - Locate regions of the cerebral cortex on the basis of anatomical landmarks common to all human brains - Describe the regions of the spinal cord in cross-section - List the cranial nerves in order of anatomical location and provide the central and peripheral connections - List the spinal nerves by vertebral region and by which nerve plexus each supplies The nervous system is responsible for controlling much of the body, both through somatic (voluntary) and autonomic (involuntary) functions. The structures of the nervous system must be described in detail to understand how many of these functions are possible. There is a physiological concept known as localization of function that states that certain structures are specifically responsible for prescribed functions. It is an underlying concept in all of anatomy and physiology, but the nervous system illustrates the concept very well. Fresh, unstained nervous tissue can be described as gray or white matter, and within those two types of tissue it can be very hard to see any detail. However, as specific regions and structures have been described, they were related to specific functions. Understanding these structures and the functions they perform requires a detailed description of the anatomy of the nervous system, delving deep into what the central and peripheral structures are. The place to start this study of the nervous system is the beginning of the individual human life, within the womb. The embryonic development of the nervous system allows for a simple framework on which progressively more complicated structures can be built. With this framework in place, a thorough investigation of the nervous system is possible. The Embryologic Perspective - Describe the growth and differentiation of the neural tube - Relate the different stages of development to the adult structures of the central nervous system - Explain the expansion of the ventricular system of the adult brain from the central canal of the neural tube - Describe the connections of the diencephalon and cerebellum on the basis of patterns of embryonic development The brain is a complex organ composed of gray parts and white matter, which can be hard to distinguish. Starting from an embryologic perspective allows you to understand more easily how the parts relate to each other. The embryonic nervous system begins as a very simple structure—essentially just a straight line, which then gets increasingly complex. Looking at the development of the nervous system with a couple of early snapshots makes it easier to understand the whole complex system. Many structures that appear to be adjacent in the adult brain are not connected, and the connections that exist may seem arbitrary. But there is an underlying order to the system that comes from how different parts develop. By following the developmental pattern, it is possible to learn what the major regions of the nervous system are. The Neural Tube To begin, a sperm cell and an egg cell fuse to become a fertilized egg. The fertilized egg cell, or zygote, starts dividing to generate the cells that make up an entire organism. Sixteen days after fertilization, the developing embryo’s cells belong to one of three germ layers that give rise to the different tissues in the body. The endoderm, or inner tissue, is responsible for generating the lining tissues of various spaces within the body, such as the mucosae of the digestive and respiratory systems. The mesoderm, or middle tissue, gives rise to most of the muscle and connective tissues. Finally the ectoderm, or outer tissue, develops into the integumentary system (the skin) and the nervous system. It is probably not difficult to see that the outer tissue of the embryo becomes the outer covering of the body. But how is it responsible for the nervous system? As the embryo develops, a portion of the ectoderm differentiates into a specialized region of neuroectoderm, which is the precursor for the tissue of the nervous system. Molecular signals induce cells in this region to differentiate into the neuroepithelium, forming a neural plate. The cells then begin to change shape, causing the tissue to buckle and fold inward (Figure 13.2). A neural groove forms, visible as a line along the dorsal surface of the embryo. The ridge-like edge on either side of the neural groove is referred as the neural fold. As the neural folds come together and converge, the underlying structure forms into a tube just beneath the ectoderm called the neural tube. Cells from the neural folds then separate from the ectoderm to form a cluster of cells referred to as the neural crest, which runs lateral to the neural tube. The neural crest migrates away from the nascent, or embryonic, central nervous system (CNS) that will form along the neural groove and develops into several parts of the peripheral nervous system (PNS), including the enteric nervous tissue. Many tissues that are not part of the nervous system also arise from the neural crest, such as craniofacial cartilage and bone, and melanocytes. Figure 13.2 Early Embryonic Development of Nervous System The neuroectoderm begins to fold inward to form the neural groove. As the two sides of the neural groove converge, they form the neural tube, which lies beneath the ectoderm. The anterior end of the neural tube will develop into the brain, and the posterior portion will become the spinal cord. The neural crest develops into peripheral structures. At this point, the early nervous system is a simple, hollow tube. It runs from the anterior end of the embryo to the posterior end. Beginning at 25 days, the anterior end develops into the brain, and the posterior portion becomes the spinal cord. This is the most basic arrangement of tissue in the nervous system, and it gives rise to the more complex structures by the fourth week of development. Primary Vesicles As the anterior end of the neural tube starts to develop into the brain, it undergoes a couple of enlargements; the result is the production of sac-like vesicles. Similar to a child’s balloon animal, the long, straight neural tube begins to take on a new shape. Three vesicles form at the first stage, which are called primary vesicles. These vesicles are given names that are based on Greek words, the main root word being enkephalon, which means “brain” (en- = “inside”; kephalon = “head”). The prefix to each generally corresponds to its position along the length of the developing nervous system. The prosencephalon (pros- = “in front”) is the forward-most vesicle, and the term can be loosely translated to mean forebrain. The mesencephalon (mes- = “middle”) is the next vesicle, which can be called the midbrain. The third vesicle at this stage is the rhombencephalon. The first part of this word is also the root of the word rhombus, which is a geometrical figure with four sides of equal length (a square is a rhombus with 90° angles). Whereas prosencephalon and mesencephalon translate into the English words forebrain and midbrain, there is not a word for “four-sided-figure-brain.” However, the third vesicle can be called the hindbrain. One way of thinking about how the brain is arranged is to use these three regions—forebrain, midbrain, and hindbrain—which are based on the primary vesicle stage of development (Figure 13.3a). Secondary Vesicles The brain continues to develop, and the vesicles differentiate further (see Figure 13.3b). The three primary vesicles become five secondary vesicles. The prosencephalon enlarges into two new vesicles called the telencephalon and the diencephalon. The telecephalon will become the cerebrum. The diencephalon gives rise to several adult structures; two that will be important are the thalamus and the hypothalamus. In the embryonic diencephalon, a structure known as the eye cup develops, which will eventually become the retina, the nervous tissue of the eye called the retina. This is a rare example of nervous tissue developing as part of the CNS structures in the embryo, but becoming a peripheral structure in the fully formed nervous system. The mesencephalon does not differentiate into any finer divisions. The midbrain is an established region of the brain at the primary vesicle stage of development and remains that way. The rest of the brain develops around it and constitutes a large percentage of the mass of the brain. Dividing the brain into forebrain, midbrain, and hindbrain is useful in considering its developmental pattern, but the midbrain is a small proportion of the entire brain, relatively speaking. The rhombencephalon develops into the metencephalon and myelencephalon. The metencephalon corresponds to the adult structure known as the pons and also gives rise to the cerebellum. The cerebellum (from the Latin meaning “little brain”) accounts for about 10 percent of the mass of the brain and is an important structure in itself. The most significant connection between the cerebellum and the rest of the brain is at the pons, because the pons and cerebellum develop out of the same vesicle. The myelencephalon corresponds to the adult structure known as the medulla oblongata. The structures that come from the mesencephalon and rhombencephalon, except for the cerebellum, are collectively considered the brain stem, which specifically includes the midbrain, pons, and medulla. Figure 13.3 Primary and Secondary Vesicle Stages of Development The embryonic brain develops complexity through enlargements of the neural tube called vesicles; (a) The primary vesicle stage has three regions, and (b) the secondary vesicle stage has five regions. INTERACTIVE LINK Watch this animation to examine the development of the brain, starting with the neural tube. As the anterior end of the neural tube develops, it enlarges into the primary vesicles that establish the forebrain, midbrain, and hindbrain. Those structures continue to develop throughout the rest of embryonic development and into adolescence. They are the basis of the structure of the fully developed adult brain. How would you describe the difference in the relative sizes of the three regions of the brain when comparing the early (25th embryonic day) brain and the adult brain? Spinal Cord Development While the brain is developing from the anterior neural tube, the spinal cord is developing from the posterior neural tube. However, its structure does not differ from the basic layout of the neural tube. It is a long, straight cord with a small, hollow space down the center. The neural tube is defined in terms of its anterior versus posterior portions, but it also has a dorsal–ventral dimension. As the neural tube separates from the rest of the ectoderm, the side closest to the surface is dorsal, and the deeper side is ventral. As the spinal cord develops, the cells making up the wall of the neural tube proliferate and differentiate into the neurons and glia of the spinal cord. The dorsal tissues will be associated with sensory functions, and the ventral tissues will be associated with motor functions. Relating Embryonic Development to the Adult Brain Embryonic development can help in understanding the structure of the adult brain because it establishes a framework on which more complex structures can be built. First, the neural tube establishes the anterior–posterior dimension of the nervous system, which is called the neuraxis. The embryonic nervous system in mammals can be said to have a standard arrangement. Humans (and other primates, to some degree) make this complicated by standing up and walking on two legs. The anterior–posterior dimension of the neuraxis overlays the superior–inferior dimension of the body. However, there is a major curve between the brain stem and forebrain, which is called the cephalic flexure. Because of this, the neuraxis starts in an inferior position—the end of the spinal cord—and ends in an anterior position, the front of the cerebrum. If this is confusing, just imagine a four-legged animal standing up on two legs. Without the flexure in the brain stem, and at the top of the neck, that animal would be looking straight up instead of straight in front (Figure 13.4). Figure 13.4 Human Neuraxis The mammalian nervous system is arranged with the neural tube running along an anterior to posterior axis, from nose to tail for a four-legged animal like a dog. Humans, as two-legged animals, have a bend in the neuraxis between the brain stem and the diencephalon, along with a bend in the neck, so that the eyes and the face are oriented forward. In summary, the primary vesicles help to establish the basic regions of the nervous system: forebrain, midbrain, and hindbrain. These divisions are useful in certain situations, but they are not equivalent regions. The midbrain is small compared with the hindbrain and particularly the forebrain. The secondary vesicles go on to establish the major regions of the adult nervous system that will be followed in this text. The telencephalon is the cerebrum, which is the major portion of the human brain. The diencephalon continues to be referred to by this Greek name, because there is no better term for it (dia- = “through”). The diencephalon is between the cerebrum and the rest of the nervous system and can be described as the region through which all projections have to pass between the cerebrum and everything else. The brain stem includes the midbrain, pons, and medulla, which correspond to the mesencephalon, metencephalon, and myelencephalon. The cerebellum, being a large portion of the brain, is considered a separate region. Table 13.1 connects the different stages of development to the adult structures of the CNS. One other benefit of considering embryonic development is that certain connections are more obvious because of how these adult structures are related. The retina, which began as part of the diencephalon, is primarily connected to the diencephalon. The eyes are just inferior to the anterior-most part of the cerebrum, but the optic nerve extends back to the thalamus as the optic tract, with branches into a region of the hypothalamus. There is also a connection of the optic tract to the midbrain, but the mesencephalon is adjacent to the diencephalon, so that is not difficult to imagine. The cerebellum originates out of the metencephalon, and its largest white matter connection is to the pons, also from the metencephalon. There are connections between the cerebellum and both the medulla and midbrain, which are adjacent structures in the secondary vesicle stage of development. In the adult brain, the cerebellum seems close to the cerebrum, but there is no direct connection between them. Another aspect of the adult CNS structures that relates to embryonic development is the ventricles—open spaces within the CNS where cerebrospinal fluid circulates. They are the remnant of the hollow center of the neural tube. The four ventricles and the tubular spaces associated with them can be linked back to the hollow center of the embryonic brain (see Table 13.1). Stages of Embryonic Development \| Neural tube \| Primary vesicle stage \| Secondary vesicle stage \| Adult structures \| Ventricles \| \|---\|---\|---\|---\|---\| \| Anterior neural tube \| Prosencephalon \| Telencephalon \| Cerebrum \| Lateral ventricles \| \| Anterior neural tube \| Prosencephalon \| Diencephalon \| Diencephalon \| Third ventricle \| \| Anterior neural tube \| Mesencephalon \| Mesencephalon \| Midbrain \| Cerebral aqueduct \| \| Anterior neural tube \| Rhombencephalon \| Metencephalon \| Pons cerebellum \| Fourth ventricle \| \| Anterior neural tube \| Rhombencephalon \| Myelencephalon \| Medulla \| Fourth ventricle \| \| Posterior neural tube \| Spinal cord \| Central canal \| Table 13.1 DISORDERS OF THE... Nervous System Early formation of the nervous system depends on the formation of the neural tube. A groove forms along the dorsal surface of the embryo, which becomes deeper until its edges meet and close off to form the tube. If this fails to happen, especially in the posterior region where the spinal cord forms, a developmental defect called spina bifida occurs. The closing of the neural tube is important for more than just the proper formation of the nervous system. The surrounding tissues are dependent on the correct development of the tube. The connective tissues surrounding the CNS can be involved as well. There are three classes of this disorder: occulta, meningocele, and myelomeningocele (Figure 13.5). The first type, spina bifida occulta, is the mildest because the vertebral bones do not fully surround the spinal cord, but the spinal cord itself is not affected. No functional differences may be noticed, which is what the word occulta means; it is hidden spina bifida. The other two types both involve the formation of a cyst—a fluid-filled sac of the connective tissues that cover the spinal cord called the meninges. “Meningocele” means that the meninges protrude through the spinal column but nerves may not be involved and few symptoms are present, though complications may arise later in life. “Myelomeningocele” means that the meninges protrude and spinal nerves are involved, and therefore severe neurological symptoms can be present. Often surgery to close the opening or to remove the cyst is necessary. The earlier that surgery can be performed, the better the chances of controlling or limiting further damage or infection at the opening. For many children with meningocele, surgery will alleviate the pain, although they may experience some functional loss. Because the myelomeningocele form of spina bifida involves more extensive damage to the nervous tissue, neurological damage may persist, but symptoms can often be handled. Complications of the spinal cord may present later in life, but overall life expectancy is not reduced. Figure 13.5 Spinal Bifida (a) Spina bifida is a birth defect of the spinal cord caused when the neural tube does not completely close, but the rest of development continues. The result is the emergence of meninges and neural tissue through the vertebral column. (b) Fetal myelomeningocele is evident in this ultrasound taken at 21 weeks. INTERACTIVE LINK Watch this video to learn about the white matter in the cerebrum that develops during childhood and adolescence. This is a composite of MRI images taken of the brains of people from 5 years of age through 20 years of age, demonstrating how the cerebrum changes. As the color changes to blue, the ratio of gray matter to white matter changes. The caption for the video describes it as “less gray matter,” which is another way of saying “more white matter.” If the brain does not finish developing until approximately 20 years of age, can teenagers be held responsible for behaving badly? The Central Nervous System - Name the major regions of the adult brain - Describe the connections between the cerebrum and brain stem through the diencephalon, and from those regions into the spinal cord - Recognize the complex connections within the subcortical structures of the basal nuclei - Explain the arrangement of gray and white matter in the spinal cord The brain and the spinal cord are the central nervous system, and they represent the main organs of the nervous system. The spinal cord is a single structure, whereas the adult brain is described in terms of four major regions: the cerebrum, the diencephalon, the brain stem, and the cerebellum. A person’s conscious experiences are based on neural activity in the brain. The regulation of homeostasis is governed by a specialized region in the brain. The coordination of reflexes depends on the integration of sensory and motor pathways in the spinal cord. The Cerebrum The iconic gray mantle of the human brain, which appears to make up most of the mass of the brain, is the cerebrum (Figure 13.6). The wrinkled portion is the cerebral cortex, and the rest of the structure is beneath that outer covering. There is a large separation between the two sides of the cerebrum called the longitudinal fissure. It separates the cerebrum into two distinct halves, a right and left cerebral hemisphere. Deep within the cerebrum, the white matter of the corpus callosum provides the major pathway for communication between the two hemispheres of the cerebral cortex. Figure 13.6 The Cerebrum The cerebrum is a large component of the CNS in humans, and the most obvious aspect of it is the folded surface called the cerebral cortex. Many of the higher neurological functions, such as memory, emotion, and consciousness, are the result of cerebral function. The complexity of the cerebrum is different across vertebrate species. The cerebrum of the most primitive vertebrates is not much more than the connection for the sense of smell. In mammals, the cerebrum comprises the outer gray matter that is the cortex (from the Latin word meaning “bark of a tree”) and several deep nuclei that belong to three important functional groups. The basal nuclei are responsible for cognitive processing, the most important function being that associated with planning movements. The basal forebrain contains nuclei that are important in learning and memory. The limbic cortex is the region of the cerebral cortex that is part of the limbic system, a collection of structures involved in emotion, memory, and behavior. Cerebral Cortex The cerebrum is covered by a continuous layer of gray matter that wraps around either side of the forebrain—the cerebral cortex. This thin, extensive region of wrinkled gray matter is responsible for the higher functions of the nervous system. A gyrus(plural = gyri) is the ridge of one of those wrinkles, and a sulcus (plural = sulci) is the groove between two gyri. The pattern of these folds of tissue indicates specific regions of the cerebral cortex. The head is limited by the size of the birth canal, and the brain must fit inside the cranial cavity of the skull. Extensive folding in the cerebral cortex enables more gray matter to fit into this limited space. If the gray matter of the cortex were peeled off of the cerebrum and laid out flat, its surface area would be roughly equal to one square meter. The folding of the cortex maximizes the amount of gray matter in the cranial cavity. During embryonic development, as the telencephalon expands within the skull, the brain goes through a regular course of growth that results in everyone’s brain having a similar pattern of folds. The surface of the brain can be mapped on the basis of the locations of large gyri and sulci. Using these landmarks, the cortex can be separated into four major regions, or lobes (Figure 13.7). The lateral sulcus that separates the temporal lobe from the other regions is one such landmark. Superior to the lateral sulcus are the parietal lobe and frontal lobe, which are separated from each other by the central sulcus. The posterior region of the cortex is the occipital lobe, which has no obvious anatomical border between it and the parietal or temporal lobes on the lateral surface of the brain. From the medial surface, an obvious landmark separating the parietal and occipital lobes is called the parieto-occipital sulcus. The fact that there is no obvious anatomical border between these lobes is consistent with the functions of these regions being interrelated. Figure 13.7 Lobes of the Cerebral Cortex The cerebral cortex is divided into four lobes. Extensive folding increases the surface area available for cerebral functions. Different regions of the cerebral cortex can be associated with particular functions, a concept known as localization of function. In the early 1900s, a German neuroscientist named Korbinian Brodmann performed an extensive study of the microscopic anatomy—the cytoarchitecture—of the cerebral cortex and divided the cortex into 52 separate regions on the basis of the histology of the cortex. His work resulted in a system of classification known as Brodmann’s areas, which is still used today to describe the anatomical distinctions within the cortex (Figure 13.8). The results from Brodmann’s work on the anatomy align very well with the functional differences within the cortex. Areas 17 and 18 in the occipital lobe are responsible for primary visual perception. That visual information is complex, so it is processed in the temporal and parietal lobes as well. The temporal lobe is associated with primary auditory sensation, known as Brodmann’s areas 41 and 42 in the superior temporal lobe. Because regions of the temporal lobe are part of the limbic system, memory is an important function associated with that lobe. Memory is essentially a sensory function; memories are recalled sensations such as the smell of Mom’s baking or the sound of a barking dog. Even memories of movement are really the memory of sensory feedback from those movements, such as stretching muscles or the movement of the skin around a joint. Structures in the temporal lobe are responsible for establishing long-term memory, but the ultimate location of those memories is usually in the region in which the sensory perception was processed. The main sensation associated with the parietal lobe is somatosensation, meaning the general sensations associated with the body. Posterior to the central sulcus is the postcentral gyrus, the primary somatosensory cortex, which is identified as Brodmann’s areas 1, 2, and 3. All of the tactile senses are processed in this area, including touch, pressure, tickle, pain, itch, and vibration, as well as more general senses of the body such as proprioception and kinesthesia, which are the senses of body position and movement, respectively. Anterior to the central sulcus is the frontal lobe, which is primarily associated with motor functions. The precentral gyrus is the primary motor cortex. Cells from this region of the cerebral cortex are the upper motor neurons that instruct cells in the spinal cord to move skeletal muscles. Anterior to this region are a few areas that are associated with planned movements. The premotor area is responsible for thinking of a movement to be made. The frontal eye fields are important in eliciting eye movements and in attending to visual stimuli. Broca’s area is responsible for the production of language, or controlling movements responsible for speech; in the vast majority of people, it is located only on the left side. Anterior to these regions is the prefrontal lobe, which serves cognitive functions that can be the basis of personality, short-term memory, and consciousness. The prefrontal lobotomy is an outdated mode of treatment for personality disorders (psychiatric conditions) that profoundly affected the personality of the patient. Figure 13.8 Brodmann's Areas of the Cerebral Cortex Brodmann mapping of functionally distinct regions of the cortex was based on its cytoarchitecture at a microscopic level. Subcortical structures Beneath the cerebral cortex are sets of nuclei known as subcortical nuclei that augment cortical processes. The nuclei of the basal forebrain serve as the primary location for acetylcholine production, which modulates the overall activity of the cortex, possibly leading to greater attention to sensory stimuli. Alzheimer’s disease is associated with a loss of neurons in the basal forebrain. The hippocampus and amygdala are medial-lobe structures that, along with the adjacent cortex, are involved in long-term memory formation and emotional responses. The basal nuclei are a set of nuclei in the cerebrum responsible for comparing cortical processing with the general state of activity in the nervous system to influence the likelihood of movement taking place. For example, while a student is sitting in a classroom listening to a lecture, the basal nuclei will keep the urge to jump up and scream from actually happening. (The basal nuclei are also referred to as the basal ganglia, although that is potentially confusing because the term ganglia is typically used for peripheral structures.) The major structures of the basal nuclei that control movement are the caudate, putamen, and globus pallidus, which are located deep in the cerebrum. The caudate is a long nucleus that follows the basic C-shape of the cerebrum from the frontal lobe, through the parietal and occipital lobes, into the temporal lobe. The putamen is mostly deep in the anterior regions of the frontal and parietal lobes. Together, the caudate and putamen are called the striatum. The globus pallidus is a layered nucleus that lies just medial to the putamen; they are called the lenticular nuclei because they look like curved pieces fitting together like lenses. The globus pallidus has two subdivisions, the external and internal segments, which are lateral and medial, respectively. These nuclei are depicted in a frontal section of the brain in Figure 13.9. Figure 13.9 Frontal Section of Cerebral Cortex and Basal Nuclei The major components of the basal nuclei, shown in a frontal section of the brain, are the caudate (just lateral to the lateral ventricle), the putamen (inferior to the caudate and separated by the large white-matter structure called the internal capsule), and the globus pallidus (medial to the putamen). The basal nuclei in the cerebrum are connected with a few more nuclei in the brain stem that together act as a functional group that forms a motor pathway. Two streams of information processing take place in the basal nuclei. All input to the basal nuclei is from the cortex into the striatum (Figure 13.10). The direct pathway is the projection of axons from the striatum to the globus pallidus internal segment (GPi) and the substantia nigra pars reticulata (SNr). The GPi/SNr then projects to the thalamus, which projects back to the cortex. The indirect pathway is the projection of axons from the striatum to the globus pallidus external segment (GPe), then to the subthalamic nucleus (STN), and finally to GPi/SNr. The two streams both target the GPi/SNr, but one has a direct projection and the other goes through a few intervening nuclei. The direct pathway causes the disinhibitionof the thalamus (inhibition of one cell on a target cell that then inhibits the first cell), whereas the indirect pathway causes, or reinforces, the normal inhibition of the thalamus. The thalamus then can either excite the cortex (as a result of the direct pathway) or fail to excite the cortex (as a result of the indirect pathway). Figure 13.10 Connections of Basal Nuclei Input to the basal nuclei is from the cerebral cortex, which is an excitatory connection releasing glutamate as a neurotransmitter. This input is to the striatum, or the caudate and putamen. In the direct pathway, the striatum projects to the internal segment of the globus pallidus and the substantia nigra pars reticulata (GPi/SNr). This is an inhibitory pathway, in which GABA is released at the synapse, and the target cells are hyperpolarized and less likely to fire. The output from the basal nuclei is to the thalamus, which is an inhibitory projection using GABA. The switch between the two pathways is the substantia nigra pars compacta, which projects to the striatum and releases the neurotransmitter dopamine. Dopamine receptors are either excitatory (D1-type receptors) or inhibitory (D2-type receptors). The direct pathway is activated by dopamine, and the indirect pathway is inhibited by dopamine. When the substantia nigra pars compacta is firing, it signals to the basal nuclei that the body is in an active state, and movement will be more likely. When the substantia nigra pars compacta is silent, the body is in a passive state, and movement is inhibited. To illustrate this situation, while a student is sitting listening to a lecture, the substantia nigra pars compacta would be silent and the student less likely to get up and walk around. Likewise, while the professor is lecturing, and walking around at the front of the classroom, the professor’s substantia nigra pars compacta would be active, in keeping with his or her activity level. INTERACTIVE LINK Watch this video to learn about the basal nuclei (also known as the basal ganglia), which have two pathways that process information within the cerebrum. As shown in this video, the direct pathway is the shorter pathway through the system that results in increased activity in the cerebral cortex and increased motor activity. The direct pathway is described as resulting in “disinhibition” of the thalamus. What does disinhibition mean? What are the two neurons doing individually to cause this? INTERACTIVE LINK Watch this video to learn about the basal nuclei (also known as the basal ganglia), which have two pathways that process information within the cerebrum. As shown in this video, the indirect pathway is the longer pathway through the system that results in decreased activity in the cerebral cortex, and therefore less motor activity. The indirect pathway has an extra couple of connections in it, including disinhibition of the subthalamic nucleus. What is the end result on the thalamus, and therefore on movement initiated by the cerebral cortex? EVERYDAY CONNECTION The Myth of Left Brain/Right Brain There is a persistent myth that people are “right-brained” or “left-brained,” which is an oversimplification of an important concept about the cerebral hemispheres. There is some lateralization of function, in which the left side of the brain is devoted to language function and the right side is devoted to spatial and nonverbal reasoning. Whereas these functions are predominantly associated with those sides of the brain, there is no monopoly by either side on these functions. Many pervasive functions, such as language, are distributed globally around the cerebrum. Some of the support for this misconception has come from studies of split brains. A drastic way to deal with a rare and devastating neurological condition (intractable epilepsy) is to separate the two hemispheres of the brain. After sectioning the corpus callosum, a split-brained patient will have trouble producing verbal responses on the basis of sensory information processed on the right side of the cerebrum, leading to the idea that the left side is responsible for language function. However, there are well-documented cases of language functions lost from damage to the right side of the brain. The deficits seen in damage to the left side of the brain are classified as aphasia, a loss of speech function; damage on the right side can affect the use of language. Right-side damage can result in a loss of ability to understand figurative aspects of speech, such as jokes, irony, or metaphors. Nonverbal aspects of speech can be affected by damage to the right side, such as facial expression or body language, and right-side damage can lead to a “flat affect” in speech, or a loss of emotional expression in speech—sounding like a robot when talking. The Diencephalon The diencephalon is the one region of the adult brain that retains its name from embryologic development. The etymology of the word diencephalon translates to “through brain.” It is the connection between the cerebrum and the rest of the nervous system, with one exception. The rest of the brain, the spinal cord, and the PNS all send information to the cerebrum through the diencephalon. Output from the cerebrum passes through the diencephalon. The single exception is the system associated with olfaction, or the sense of smell, which connects directly with the cerebrum. In the earliest vertebrate species, the cerebrum was not much more than olfactory bulbs that received peripheral information about the chemical environment (to call it smell in these organisms is imprecise because they lived in the ocean). The diencephalon is deep beneath the cerebrum and constitutes the walls of the third ventricle. The diencephalon can be described as any region of the brain with “thalamus” in its name. The two major regions of the diencephalon are the thalamus itself and the hypothalamus (Figure 13.11). There are other structures, such as the epithalamus, which contains the pineal gland, or the subthalamus, which includes the subthalamic nucleus that is part of the basal nuclei. Thalamus The thalamus is a collection of nuclei that relay information between the cerebral cortex and the periphery, spinal cord, or brain stem. All sensory information, except for the sense of smell, passes through the thalamus before processing by the cortex. Axons from the peripheral sensory organs, or intermediate nuclei, synapse in the thalamus, and thalamic neurons project directly to the cerebrum. It is a requisite synapse in any sensory pathway, except for olfaction. The thalamus does not just pass the information on, it also processes that information. For example, the portion of the thalamus that receives visual information will influence what visual stimuli are important, or what receives attention. The cerebrum also sends information down to the thalamus, which usually communicates motor commands. This involves interactions with the cerebellum and other nuclei in the brain stem. The cerebrum interacts with the basal nuclei, which involves connections with the thalamus. The primary output of the basal nuclei is to the thalamus, which relays that output to the cerebral cortex. The cortex also sends information to the thalamus that will then influence the effects of the basal nuclei. Hypothalamus Inferior and slightly anterior to the thalamus is the hypothalamus, the other major region of the diencephalon. The hypothalamus is a collection of nuclei that are largely involved in regulating homeostasis. The hypothalamus is the executive region in charge of the autonomic nervous system and the endocrine system through its regulation of the anterior pituitary gland. Other parts of the hypothalamus are involved in memory and emotion as part of the limbic system. Figure 13.11 The Diencephalon The diencephalon is composed primarily of the thalamus and hypothalamus, which together define the walls of the third ventricle. The thalami are two elongated, ovoid structures on either side of the midline that make contact in the middle. The hypothalamus is inferior and anterior to the thalamus, culminating in a sharp angle to which the pituitary gland is attached. Brain Stem The midbrain and hindbrain (composed of the pons and the medulla) are collectively referred to as the brain stem (Figure 13.12). The structure emerges from the ventral surface of the forebrain as a tapering cone that connects the brain to the spinal cord. Attached to the brain stem, but considered a separate region of the adult brain, is the cerebellum. The midbrain coordinates sensory representations of the visual, auditory, and somatosensory perceptual spaces. The pons is the main connection with the cerebellum. The pons and the medulla regulate several crucial functions, including the cardiovascular and respiratory systems and rates. The cranial nerves connect through the brain stem and provide the brain with the sensory input and motor output associated with the head and neck, including most of the special senses. The major ascending and descending pathways between the spinal cord and brain, specifically the cerebrum, pass through the brain stem. Figure 13.12 The Brain Stem The brain stem comprises three regions: the midbrain, the pons, and the medulla. Midbrain One of the original regions of the embryonic brain, the midbrain is a small region between the thalamus and pons. It is separated into the tectum and tegmentum, from the Latin words for roof and floor, respectively. The cerebral aqueduct passes through the center of the midbrain, such that these regions are the roof and floor of that canal. The tectum is composed of four bumps known as the colliculi (singular = colliculus), which means “little hill” in Latin. The inferior colliculus is the inferior pair of these enlargements and is part of the auditory brain stem pathway. Neurons of the inferior colliculus project to the thalamus, which then sends auditory information to the cerebrum for the conscious perception of sound. The superior colliculus is the superior pair and combines sensory information about visual space, auditory space, and somatosensory space. Activity in the superior colliculus is related to orienting the eyes to a sound or touch stimulus. If you are walking along the sidewalk on campus and you hear chirping, the superior colliculus coordinates that information with your awareness of the visual location of the tree right above you. That is the correlation of auditory and visual maps. If you suddenly feel something wet fall on your head, your superior colliculus integrates that with the auditory and visual maps and you know that the chirping bird just relieved itself on you. You want to look up to see the culprit, but do not. The tegmentum is continuous with the gray matter of the rest of the brain stem. Throughout the midbrain, pons, and medulla, the tegmentum contains the nuclei that receive and send information through the cranial nerves, as well as regions that regulate important functions such as those of the cardiovascular and respiratory systems. Pons The word pons comes from the Latin word for bridge. It is visible on the anterior surface of the brain stem as the thick bundle of white matter attached to the cerebellum. The pons is the main connection between the cerebellum and the brain stem. The bridge-like white matter is only the anterior surface of the pons; the gray matter beneath that is a continuation of the tegmentum from the midbrain. Gray matter in the tegmentum region of the pons contains neurons receiving descending input from the forebrain that is sent to the cerebellum. Medulla The medulla is the region known as the myelencephalon in the embryonic brain. The initial portion of the name, “myel,” refers to the significant white matter found in this region—especially on its exterior, which is continuous with the white matter of the spinal cord. The tegmentum of the midbrain and pons continues into the medulla because this gray matter is responsible for processing cranial nerve information. A diffuse region of gray matter throughout the brain stem, known as the reticular formation, is related to sleep and wakefulness, such as general brain activity and attention. The Cerebellum The cerebellum, as the name suggests, is the “little brain.” It is covered in gyri and sulci like the cerebrum, and looks like a miniature version of that part of the brain (Figure 13.13). The cerebellum is largely responsible for comparing information from the cerebrum with sensory feedback from the periphery through the spinal cord. It accounts for approximately 10 percent of the mass of the brain. Figure 13.13 The Cerebellum The cerebellum is situated on the posterior surface of the brain stem. Descending input from the cerebellum enters through the large white matter structure of the pons. Ascending input from the periphery and spinal cord enters through the fibers of the inferior olive. Output goes to the midbrain, which sends a descending signal to the spinal cord. Descending fibers from the cerebrum have branches that connect to neurons in the pons. Those neurons project into the cerebellum, providing a copy of motor commands sent to the spinal cord. Sensory information from the periphery, which enters through spinal or cranial nerves, is copied to a nucleus in the medulla known as the inferior olive. Fibers from this nucleus enter the cerebellum and are compared with the descending commands from the cerebrum. If the primary motor cortex of the frontal lobe sends a command down to the spinal cord to initiate walking, a copy of that instruction is sent to the cerebellum. Sensory feedback from the muscles and joints, proprioceptive information about the movements of walking, and sensations of balance are sent to the cerebellum through the inferior olive and the cerebellum compares them. If walking is not coordinated, perhaps because the ground is uneven or a strong wind is blowing, then the cerebellum sends out a corrective command to compensate for the difference between the original cortical command and the sensory feedback. The output of the cerebellum is into the midbrain, which then sends a descending input to the spinal cord to correct the messages going to skeletal muscles. The Spinal Cord The description of the CNS is concentrated on the structures of the brain, but the spinal cord is another major organ of the system. Whereas the brain develops out of expansions of the neural tube into primary and then secondary vesicles, the spinal cord maintains the tube structure and is only specialized into certain regions. As the spinal cord continues to develop in the newborn, anatomical features mark its surface. The anterior midline is marked by the anterior median fissure, and the posterior midline is marked by the posterior median sulcus. Axons enter the posterior side through the dorsal (posterior) nerve root, which marks the posterolateral sulcus on either side. The axons emerging from the anterior side do so through the ventral (anterior) nerve root. Note that it is common to see the terms dorsal (dorsal = “back”) and ventral (ventral = “belly”) used interchangeably with posterior and anterior, particularly in reference to nerves and the structures of the spinal cord. You should learn to be comfortable with both. On the whole, the posterior regions are responsible for sensory functions and the anterior regions are associated with motor functions. This comes from the initial development of the spinal cord, which is divided into the basal plate and the alar plate. The basal plate is closest to the ventral midline of the neural tube, which will become the anterior face of the spinal cord and gives rise to motor neurons. The alar plate is on the dorsal side of the neural tube and gives rise to neurons that will receive sensory input from the periphery. The length of the spinal cord is divided into regions that correspond to the regions of the vertebral column. The name of a spinal cord region corresponds to the level at which spinal nerves pass through the intervertebral foramina. Immediately adjacent to the brain stem is the cervical region, followed by the thoracic, then the lumbar, and finally the sacral region. The spinal cord is not the full length of the vertebral column because the spinal cord does not grow significantly longer after the first or second year, but the skeleton continues to grow. The nerves that emerge from the spinal cord pass through the intervertebral formina at the respective levels. As the vertebral column grows, these nerves grow with it and result in a long bundle of nerves that resembles a horse’s tail and is named the cauda equina. The sacral spinal cord is at the level of the upper lumbar vertebral bones. The spinal nerves extend from their various levels to the proper level of the vertebral column. Gray Horns In cross-section, the gray matter of the spinal cord has the appearance of an ink-blot test, with the spread of the gray matter on one side replicated on the other—a shape reminiscent of a bulbous capital “H.” As shown in Figure 13.14, the gray matter is subdivided into regions that are referred to as horns. The posterior horn is responsible for sensory processing. The anterior horn sends out motor signals to the skeletal muscles. The lateral horn, which is only found in the thoracic, upper lumbar, and sacral regions, is the central component of the sympathetic division of the autonomic nervous system. Some of the largest neurons of the spinal cord are the multipolar motor neurons in the anterior horn. The fibers that cause contraction of skeletal muscles are the axons of these neurons. The motor neuron that causes contraction of the big toe, for example, is located in the sacral spinal cord. The axon that has to reach all the way to the belly of that muscle may be a meter in length. The neuronal cell body that maintains that long fiber must be quite large, possibly several hundred micrometers in diameter, making it one of the largest cells in the body. Figure 13.14 Cross-section of Spinal Cord The cross-section of a thoracic spinal cord segment shows the posterior, anterior, and lateral horns of gray matter, as well as the posterior, anterior, and lateral columns of white matter. LM × 40. (Micrograph provided by the Regents of University of Michigan Medical School © 2012) White Columns Just as the gray matter is separated into horns, the white matter of the spinal cord is separated into columns. Ascending tractsof nervous system fibers in these columns carry sensory information up to the brain, whereas descending tracts carry motor commands from the brain. Looking at the spinal cord longitudinally, the columns extend along its length as continuous bands of white matter. Between the two posterior horns of gray matter are the posterior columns. Between the two anterior horns, and bounded by the axons of motor neurons emerging from that gray matter area, are the anterior columns. The white matter on either side of the spinal cord, between the posterior horn and the axons of the anterior horn neurons, are the lateral columns. The posterior columns are composed of axons of ascending tracts. The anterior and lateral columns are composed of many different groups of axons of both ascending and descending tracts—the latter carrying motor commands down from the brain to the spinal cord to control output to the periphery. INTERACTIVE LINK Watch this video to learn about the gray matter of the spinal cord that receives input from fibers of the dorsal (posterior) root and sends information out through the fibers of the ventral (anterior) root. As discussed in this video, these connections represent the interactions of the CNS with peripheral structures for both sensory and motor functions. The cervical and lumbar spinal cords have enlargements as a result of larger populations of neurons. What are these enlargements responsible for? DISORDERS OF THE... Basal Nuclei Parkinson’s disease is a disorder of the basal nuclei, specifically of the substantia nigra, that demonstrates the effects of the direct and indirect pathways. Parkinson’s disease is the result of neurons in the substantia nigra pars compacta dying. These neurons release dopamine into the striatum. Without that modulatory influence, the basal nuclei are stuck in the indirect pathway, without the direct pathway being activated. The direct pathway is responsible for increasing cortical movement commands. The increased activity of the indirect pathway results in the hypokinetic disorder of Parkinson’s disease. Parkinson’s disease is neurodegenerative, meaning that neurons die that cannot be replaced, so there is no cure for the disorder. Treatments for Parkinson’s disease are aimed at increasing dopamine levels in the striatum. Currently, the most common way of doing that is by providing the amino acid L-DOPA, which is a precursor to the neurotransmitter dopamine and can cross the blood-brain barrier. With levels of the precursor elevated, the remaining cells of the substantia nigra pars compacta can make more neurotransmitter and have a greater effect. Unfortunately, the patient will become less responsive to L-DOPA treatment as time progresses, and it can cause increased dopamine levels elsewhere in the brain, which are associated with psychosis or schizophrenia. INTERACTIVE LINK Visit this site for a thorough explanation of Parkinson’s disease. INTERACTIVE LINK Compared with the nearest evolutionary relative, the chimpanzee, the human has a brain that is huge. At a point in the past, a common ancestor gave rise to the two species of humans and chimpanzees. That evolutionary history is long and is still an area of intense study. But something happened to increase the size of the human brain relative to the chimpanzee. Read this article in which the author explores the current understanding of why this happened. According to one hypothesis about the expansion of brain size, what tissue might have been sacrificed so energy was available to grow our larger brain? Based on what you know about that tissue and nervous tissue, why would there be a trade-off between them in terms of energy use? Circulation and the Central Nervous System - Describe the vessels that supply the CNS with blood - Name the components of the ventricular system and the regions of the brain in which each is located - Explain the production of cerebrospinal fluid and its flow through the ventricles - Explain how a disruption in circulation would result in a stroke The CNS is crucial to the operation of the body, and any compromise in the brain and spinal cord can lead to severe difficulties. The CNS has a privileged blood supply, as suggested by the blood-brain barrier. The function of the tissue in the CNS is crucial to the survival of the organism, so the contents of the blood cannot simply pass into the central nervous tissue. To protect this region from the toxins and pathogens that may be traveling through the blood stream, there is strict control over what can move out of the general systems and into the brain and spinal cord. Because of this privilege, the CNS needs specialized structures for the maintenance of circulation. This begins with a unique arrangement of blood vessels carrying fresh blood into the CNS. Beyond the supply of blood, the CNS filters that blood into cerebrospinal fluid (CSF), which is then circulated through the cavities of the brain and spinal cord called ventricles. Blood Supply to the Brain A lack of oxygen to the CNS can be devastating, and the cardiovascular system has specific regulatory reflexes to ensure that the blood supply is not interrupted. There are multiple routes for blood to get into the CNS, with specializations to protect that blood supply and to maximize the ability of the brain to get an uninterrupted perfusion. Arterial Supply The major artery carrying recently oxygenated blood away from the heart is the aorta. The very first branches off the aorta supply the heart with nutrients and oxygen. The next branches give rise to the common carotid arteries, which further branch into the internal carotid arteries. The external carotid arteries supply blood to the tissues on the surface of the cranium. The bases of the common carotids contain stretch receptors that immediately respond to the drop in blood pressure upon standing. The orthostatic reflex is a reaction to this change in body position, so that blood pressure is maintained against the increasing effect of gravity (orthostatic means “standing up”). Heart rate increases—a reflex of the sympathetic division of the autonomic nervous system—and this raises blood pressure. The internal carotid artery enters the cranium through the carotid canal in the temporal bone. A second set of vessels that supply the CNS are the vertebral arteries, which are protected as they pass through the neck region by the transverse foramina of the cervical vertebrae. The vertebral arteries enter the cranium through the foramen magnum of the occipital bone. Branches off the left and right vertebral arteries merge into the anterior spinal artery supplying the anterior aspect of the spinal cord, found along the anterior median fissure. The two vertebral arteries then merge into the basilar artery, which gives rise to branches to the brain stem and cerebellum. The left and right internal carotid arteries and branches of the basilar artery all become the circle of Willis, a confluence of arteries that can maintain perfusion of the brain even if narrowing or a blockage limits flow through one part (Figure 13.15). Figure 13.15 Circle of Willis The blood supply to the brain enters through the internal carotid arteries and the vertebral arteries, eventually giving rise to the circle of Willis. INTERACTIVE LINK Watch this animation to see how blood flows to the brain and passes through the circle of Willis before being distributed through the cerebrum. The circle of Willis is a specialized arrangement of arteries that ensure constant perfusion of the cerebrum even in the event of a blockage of one of the arteries in the circle. The animation shows the normal direction of flow through the circle of Willis to the middle cerebral artery. Where would the blood come from if there were a blockage just posterior to the middle cerebral artery on the left? Venous Return After passing through the CNS, blood returns to the circulation through a series of dural sinuses and veins (Figure 13.16). The superior sagittal sinus runs in the groove of the longitudinal fissure, where it absorbs CSF from the meninges. The superior sagittal sinus drains to the confluence of sinuses, along with the occipital sinuses and straight sinus, to then drain into the transverse sinuses. The transverse sinuses connect to the sigmoid sinuses, which then connect to the jugular veins. From there, the blood continues toward the heart to be pumped to the lungs for reoxygenation. Figure 13.16 Dural Sinuses and Veins Blood drains from the brain through a series of sinuses that connect to the jugular veins. Protective Coverings of the Brain and Spinal Cord The outer surface of the CNS is covered by a series of membranes composed of connective tissue called the meninges, which protect the brain. The dura mater is a thick fibrous layer and a strong protective sheath over the entire brain and spinal cord. It is anchored to the inner surface of the cranium and vertebral cavity. The arachnoid mater is a membrane of thin fibrous tissue that forms a loose sac around the CNS. Beneath the arachnoid is a thin, filamentous mesh called the arachnoid trabeculae, which looks like a spider web, giving this layer its name. Directly adjacent to the surface of the CNS is the pia mater, a thin fibrous membrane that follows the convolutions of gyri and sulci in the cerebral cortex and fits into other grooves and indentations (Figure 13.17). Figure 13.17 Meningeal Layers of Superior Sagittal Sinus The layers of the meninges in the longitudinal fissure of the superior sagittal sinus are shown, with the dura mater adjacent to the inner surface of the cranium, the pia mater adjacent to the surface of the brain, and the arachnoid and subarachnoid space between them. An arachnoid villus is shown emerging into the dural sinus to allow CSF to filter back into the blood for drainage. Dura Mater Like a thick cap covering the brain, the dura mater is a tough outer covering. The name comes from the Latin for “tough mother” to represent its physically protective role. It encloses the entire CNS and the major blood vessels that enter the cranium and vertebral cavity. It is directly attached to the inner surface of the bones of the cranium and to the very end of the vertebral cavity. There are infoldings of the dura that fit into large crevasses of the brain. Two infoldings go through the midline separations of the cerebrum and cerebellum; one forms a shelf-like tent between the occipital lobes of the cerebrum and the cerebellum, and the other surrounds the pituitary gland. The dura also surrounds and supports the venous sinuses. Arachnoid Mater The middle layer of the meninges is the arachnoid, named for the spider-web–like trabeculae between it and the pia mater. The arachnoid defines a sac-like enclosure around the CNS. The trabeculae are found in the subarachnoid space, which is filled with circulating CSF. The arachnoid emerges into the dural sinuses as the arachnoid granulations, where the CSF is filtered back into the blood for drainage from the nervous system. The subarachnoid space is filled with circulating CSF, which also provides a liquid cushion to the brain and spinal cord. Similar to clinical blood work, a sample of CSF can be withdrawn to find chemical evidence of neuropathology or metabolic traces of the biochemical functions of nervous tissue. Pia Mater The outer surface of the CNS is covered in the thin fibrous membrane of the pia mater. It is thought to have a continuous layer of cells providing a fluid-impermeable membrane. The name pia mater comes from the Latin for “tender mother,” suggesting the thin membrane is a gentle covering for the brain. The pia extends into every convolution of the CNS, lining the inside of the sulci in the cerebral and cerebellar cortices. At the end of the spinal cord, a thin filament extends from the inferior end of CNS at the upper lumbar region of the vertebral column to the sacral end of the vertebral column. Because the spinal cord does not extend through the lower lumbar region of the vertebral column, a needle can be inserted through the dura and arachnoid layers to withdraw CSF. This procedure is called a lumbar puncture and avoids the risk of damaging the central tissue of the spinal cord. Blood vessels that are nourishing the central nervous tissue are between the pia mater and the nervous tissue. DISORDERS OF THE... Meninges Meningitis is an inflammation of the meninges, the three layers of fibrous membrane that surround the CNS. Meningitis can be caused by infection by bacteria or viruses. The particular pathogens are not special to meningitis; it is just an inflammation of that specific set of tissues from what might be a broader infection. Bacterial meningitis can be caused by Streptococcus, Staphylococcus, or the tuberculosis pathogen, among many others. Viral meningitis is usually the result of common enteroviruses (such as those that cause intestinal disorders), but may be the result of the herpes virus or West Nile virus. Bacterial meningitis tends to be more severe. The symptoms associated with meningitis can be fever, chills, nausea, vomiting, light sensitivity, soreness of the neck, or severe headache. More important are the neurological symptoms, such as changes in mental state (confusion, memory deficits, and other dementia-type symptoms). A serious risk of meningitis can be damage to peripheral structures because of the nerves that pass through the meninges. Hearing loss is a common result of meningitis. The primary test for meningitis is a lumbar puncture. A needle inserted into the lumbar region of the spinal column through the dura mater and arachnoid membrane into the subarachnoid space can be used to withdraw the fluid for chemical testing. Fatality occurs in 5 to 40 percent of children and 20 to 50 percent of adults with bacterial meningitis. Treatment of bacterial meningitis is through antibiotics, but viral meningitis cannot be treated with antibiotics because viruses do not respond to that type of drug. Fortunately, the viral forms are milder. INTERACTIVE LINK Watch this video that describes the procedure known as the lumbar puncture, a medical procedure used to sample the CSF. Because of the anatomy of the CNS, it is a relative safe location to insert a needle. Why is the lumbar puncture performed in the lower lumbar area of the vertebral column? The Ventricular System Cerebrospinal fluid (CSF) circulates throughout and around the CNS. In other tissues, water and small molecules are filtered through capillaries as the major contributor to the interstitial fluid. In the brain, CSF is produced in special structures to perfuse through the nervous tissue of the CNS and is continuous with the interstitial fluid. Specifically, CSF circulates to remove metabolic wastes from the interstitial fluids of nervous tissues and return them to the blood stream. The ventricles are the open spaces within the brain where CSF circulates. In some of these spaces, CSF is produced by filtering of the blood that is performed by a specialized membrane known as a choroid plexus. The CSF circulates through all of the ventricles to eventually emerge into the subarachnoid space where it will be reabsorbed into the blood. The Ventricles There are four ventricles within the brain, all of which developed from the original hollow space within the neural tube, the central canal. The first two are named the lateral ventricles and are deep within the cerebrum. These ventricles are connected to the third ventricle by two openings called the interventricular foramina. The third ventricle is the space between the left and right sides of the diencephalon, which opens into the cerebral aqueduct that passes through the midbrain. The aqueduct opens into the fourth ventricle, which is the space between the cerebellum and the pons and upper medulla (Figure 13.18). Figure 13.18 Cerebrospinal Fluid Circulation The choroid plexus in the four ventricles produce CSF, which is circulated through the ventricular system and then enters the subarachnoid space through the median and lateral apertures. The CSF is then reabsorbed into the blood at the arachnoid granulations, where the arachnoid membrane emerges into the dural sinuses. As the telencephalon enlarges and grows into the cranial cavity, it is limited by the space within the skull. The telencephalon is the most anterior region of what was the neural tube, but cannot grow past the limit of the frontal bone of the skull. Because the cerebrum fits into this space, it takes on a C-shaped formation, through the frontal, parietal, occipital, and finally temporal regions. The space within the telencephalon is stretched into this same C-shape. The two ventricles are in the left and right sides, and were at one time referred to as the first and second ventricles. The interventricular foramina connect the frontal region of the lateral ventricles with the third ventricle. The third ventricle is the space bounded by the medial walls of the hypothalamus and thalamus. The two thalami touch in the center in most brains as the massa intermedia, which is surrounded by the third ventricle. The cerebral aqueduct opens just inferior to the epithalamus and passes through the midbrain. The tectum and tegmentum of the midbrain are the roof and floor of the cerebral aqueduct, respectively. The aqueduct opens up into the fourth ventricle. The floor of the fourth ventricle is the dorsal surface of the pons and upper medulla (that gray matter making a continuation of the tegmentum of the midbrain). The fourth ventricle then narrows into the central canal of the spinal cord. The ventricular system opens up to the subarachnoid space from the fourth ventricle. The single median aperture and the pair of lateral apertures connect to the subarachnoid space so that CSF can flow through the ventricles and around the outside of the CNS. Cerebrospinal fluid is produced within the ventricles by a type of specialized membrane called a choroid plexus. Ependymal cells (one of the types of glial cells described in the introduction to the nervous system) surround blood capillaries and filter the blood to make CSF. The fluid is a clear solution with a limited amount of the constituents of blood. It is essentially water, small molecules, and electrolytes. Oxygen and carbon dioxide are dissolved into the CSF, as they are in blood, and can diffuse between the fluid and the nervous tissue. Cerebrospinal Fluid Circulation The choroid plexuses are found in all four ventricles. Observed in dissection, they appear as soft, fuzzy structures that may still be pink, depending on how well the circulatory system is cleared in preparation of the tissue. The CSF is produced from components extracted from the blood, so its flow out of the ventricles is tied to the pulse of cardiovascular circulation. From the lateral ventricles, the CSF flows into the third ventricle, where more CSF is produced, and then through the cerebral aqueduct into the fourth ventricle where even more CSF is produced. A very small amount of CSF is filtered at any one of the plexuses, for a total of about 500 milliliters daily, but it is continuously made and pulses through the ventricular system, keeping the fluid moving. From the fourth ventricle, CSF can continue down the central canal of the spinal cord, but this is essentially a cul-de-sac, so more of the fluid leaves the ventricular system and moves into the subarachnoid space through the median and lateral apertures. Within the subarachnoid space, the CSF flows around all of the CNS, providing two important functions. As with elsewhere in its circulation, the CSF picks up metabolic wastes from the nervous tissue and moves it out of the CNS. It also acts as a liquid cushion for the brain and spinal cord. By surrounding the entire system in the subarachnoid space, it provides a thin buffer around the organs within the strong, protective dura mater. The arachnoid granulations are outpocketings of the arachnoid membrane into the dural sinuses so that CSF can be reabsorbed into the blood, along with the metabolic wastes. From the dural sinuses, blood drains out of the head and neck through the jugular veins, along with the rest of the circulation for blood, to be reoxygenated by the lungs and wastes to be filtered out by the kidneys (Table 13.2). INTERACTIVE LINK Watch this animation that shows the flow of CSF through the brain and spinal cord, and how it originates from the ventricles and then spreads into the space within the meninges, where the fluids then move into the venous sinuses to return to the cardiovascular circulation. What are the structures that produce CSF and where are they found? How are the structures indicated in this animation? Components of CSF Circulation \| Lateral ventricles \| Third ventricle \| Cerebral aqueduct \| Fourth ventricle \| Central canal \| Subarachnoid space \| \| \|---\|---\|---\|---\|---\|---\|---\| \| Location in CNS \| Cerebrum \| Diencephalon \| Midbrain \| Between pons/upper medulla and cerebellum \| Spinal cord \| External to entire CNS \| \| Blood vessel structure \| Choroid plexus \| Choroid plexus \| None \| Choroid plexus \| None \| Arachnoid granulations \| Table 13.2 DISORDERS OF THE... Central Nervous System The supply of blood to the brain is crucial to its ability to perform many functions. Without a steady supply of oxygen, and to a lesser extent glucose, the nervous tissue in the brain cannot keep up its extensive electrical activity. These nutrients get into the brain through the blood, and if blood flow is interrupted, neurological function is compromised. The common name for a disruption of blood supply to the brain is a stroke. It is caused by a blockage to an artery in the brain. The blockage is from some type of embolus: a blood clot, a fat embolus, or an air bubble. When the blood cannot travel through the artery, the surrounding tissue that is deprived starves and dies. Strokes will often result in the loss of very specific functions. A stroke in the lateral medulla, for example, can cause a loss in the ability to swallow. Sometimes, seemingly unrelated functions will be lost because they are dependent on structures in the same region. Along with the swallowing in the previous example, a stroke in that region could affect sensory functions from the face or extremities because important white matter pathways also pass through the lateral medulla. Loss of blood flow to specific regions of the cortex can lead to the loss of specific higher functions, from the ability to recognize faces to the ability to move a particular region of the body. Severe or limited memory loss can be the result of a temporal lobe stroke. Related to strokes are transient ischemic attacks (TIAs), which can also be called “mini-strokes.” These are events in which a physical blockage may be temporary, cutting off the blood supply and oxygen to a region, but not to the extent that it causes cell death in that region. While the neurons in that area are recovering from the event, neurological function may be lost. Function can return if the area is able to recover from the event. Recovery from a stroke (or TIA) is strongly dependent on the speed of treatment. Often, the person who is present and notices something is wrong must then make a decision. The mnemonic FAST helps people remember what to look for when someone is dealing with sudden losses of neurological function. If someone complains of feeling “funny,” check these things quickly: Look at the person’s face. Does he or she have problems moving Face muscles and making regular facial expressions? Ask the person to raise his or her Arms above the head. Can the person lift one arm but not the other? Has the person’s Speech changed? Is he or she slurring words or having trouble saying things? If any of these things have happened, then it is Time to call for help. Sometimes, treatment with blood-thinning drugs can alleviate the problem, and recovery is possible. If the tissue is damaged, the amazing thing about the nervous system is that it is adaptable. With physical, occupational, and speech therapy, victims of strokes can recover, or more accurately relearn, functions. The Peripheral Nervous System - Describe the structures found in the PNS - Distinguish between somatic and autonomic structures, including the special peripheral structures of the enteric nervous system - Name the twelve cranial nerves and explain the functions associated with each - Describe the sensory and motor components of spinal nerves and the plexuses that they pass through The PNS is not as contained as the CNS because it is defined as everything that is not the CNS. Some peripheral structures are incorporated into the other organs of the body. In describing the anatomy of the PNS, it is necessary to describe the common structures, the nerves and the ganglia, as they are found in various parts of the body. Many of the neural structures that are incorporated into other organs are features of the digestive system; these structures are known as the enteric nervous systemand are a special subset of the PNS. Ganglia A ganglion is a group of neuron cell bodies in the periphery. Ganglia can be categorized, for the most part, as either sensory ganglia or autonomic ganglia, referring to their primary functions. The most common type of sensory ganglion is a dorsal (posterior) root ganglion. These ganglia are the cell bodies of neurons with axons that are sensory endings in the periphery, such as in the skin, and that extend into the CNS through the dorsal nerve root. The ganglion is an enlargement of the nerve root. Under microscopic inspection, it can be seen to include the cell bodies of the neurons, as well as bundles of fibers that are the posterior nerve root (Figure 13.19). The cells of the dorsal root ganglion are unipolar cells, classifying them by shape. Also, the small round nuclei of satellite cells can be seen surrounding—as if they were orbiting—the neuron cell bodies. Figure 13.19 Dorsal Root Ganglion The cell bodies of sensory neurons, which are unipolar neurons by shape, are seen in this photomicrograph. Also, the fibrous region is composed of the axons of these neurons that are passing through the ganglion to be part of the dorsal nerve root (tissue source: canine). LM × 40. (Micrograph provided by the Regents of University of Michigan Medical School © 2012) Figure 13.20 Spinal Cord and Root Ganglion The slide includes both a cross-section of the lumbar spinal cord and a section of the dorsal root ganglion (see also Figure 13.19) (tissue source: canine). LM × 1600. (Micrograph provided by the Regents of University of Michigan Medical School © 2012) INTERACTIVE LINK View the University of Michigan WebScope to explore the tissue sample in greater detail. If you zoom in on the dorsal root ganglion, you can see smaller satellite glial cells surrounding the large cell bodies of the sensory neurons. From what structure do satellite cells derive during embryologic development? Another type of sensory ganglion is a cranial nerve ganglion. This is analogous to the dorsal root ganglion, except that it is associated with a cranial nerve instead of a spinal nerve. The roots of cranial nerves are within the cranium, whereas the ganglia are outside the skull. For example, the trigeminal ganglion is superficial to the temporal bone whereas its associated nerve is attached to the mid-pons region of the brain stem. The neurons of cranial nerve ganglia are also unipolar in shape with associated satellite cells. The other major category of ganglia are those of the autonomic nervous system, which is divided into the sympathetic and parasympathetic nervous systems. The sympathetic chain ganglia constitute a row of ganglia along the vertebral column that receive central input from the lateral horn of the thoracic and upper lumbar spinal cord. Superior to the chain ganglia are three paravertebral ganglia in the cervical region. Three other autonomic ganglia that are related to the sympathetic chain are the prevertebral ganglia, which are located outside of the chain but have similar functions. They are referred to as prevertebral because they are anterior to the vertebral column. The neurons of these autonomic ganglia are multipolar in shape, with dendrites radiating out around the cell body where synapses from the spinal cord neurons are made. The neurons of the chain, paravertebral, and prevertebral ganglia then project to organs in the head and neck, thoracic, abdominal, and pelvic cavities to regulate the sympathetic aspect of homeostatic mechanisms. Another group of autonomic ganglia are the terminal ganglia that receive input from cranial nerves or sacral spinal nerves and are responsible for regulating the parasympathetic aspect of homeostatic mechanisms. These two sets of ganglia, sympathetic and parasympathetic, often project to the same organs—one input from the chain ganglia and one input from a terminal ganglion—to regulate the overall function of an organ. For example, the heart receives two inputs such as these; one increases heart rate, and the other decreases it. The terminal ganglia that receive input from cranial nerves are found in the head and neck, as well as the thoracic and upper abdominal cavities, whereas the terminal ganglia that receive sacral input are in the lower abdominal and pelvic cavities. Terminal ganglia below the head and neck are often incorporated into the wall of the target organ as a plexus. A plexus, in a general sense, is a network of fibers or vessels. This can apply to nervous tissue (as in this instance) or structures containing blood vessels (such as a choroid plexus). For example, the enteric plexus is the extensive network of axons and neurons in the wall of the small and large intestines. The enteric plexus is actually part of the enteric nervous system, along with the gastric plexuses and the esophageal plexus. Though the enteric nervous system receives input originating from central neurons of the autonomic nervous system, it does not require CNS input to function. In fact, it operates independently to regulate the digestive system. Nerves Bundles of axons in the PNS are referred to as nerves. These structures in the periphery are different than the central counterpart, called a tract. Nerves are composed of more than just nervous tissue. They have connective tissues invested in their structure, as well as blood vessels supplying the tissues with nourishment. The outer surface of a nerve is a surrounding layer of fibrous connective tissue called the epineurium. Within the nerve, axons are further bundled into fascicles, which are each surrounded by their own layer of fibrous connective tissue called perineurium. Finally, individual axons are surrounded by loose connective tissue called the endoneurium (Figure 13.21). These three layers are similar to the connective tissue sheaths for muscles. Nerves are associated with the region of the CNS to which they are connected, either as cranial nerves connected to the brain or spinal nerves connected to the spinal cord. Figure 13.21 Nerve Structure The structure of a nerve is organized by the layers of connective tissue on the outside, around each fascicle, and surrounding the individual nerve fibers (tissue source: simian). LM × 40. (Micrograph provided by the Regents of University of Michigan Medical School © 2012) Figure 13.22 Close-Up of Nerve Trunk Zoom in on this slide of a nerve trunk to examine the endoneurium, perineurium, and epineurium in greater detail (tissue source: simian). LM × 1600. (Micrograph provided by the Regents of University of Michigan Medical School © 2012) INTERACTIVE LINK View the University of Michigan WebScope to explore the tissue sample in greater detail. With what structures in a skeletal muscle are the endoneurium, perineurium, and epineurium comparable? Cranial Nerves The nerves attached to the brain are the cranial nerves, which are primarily responsible for the sensory and motor functions of the head and neck (one of these nerves targets organs in the thoracic and abdominal cavities as part of the parasympathetic nervous system). There are twelve cranial nerves, which are designated CNI through CNXII for “Cranial Nerve,” using Roman numerals for 1 through 12. They can be classified as sensory nerves, motor nerves, or a combination of both, meaning that the axons in these nerves originate out of sensory ganglia external to the cranium or motor nuclei within the brain stem. Sensory axons enter the brain to synapse in a nucleus. Motor axons connect to skeletal muscles of the head or neck. Three of the nerves are solely composed of sensory fibers; five are strictly motor; and the remaining four are mixed nerves. Learning the cranial nerves is a tradition in anatomy courses, and students have always used mnemonic devices to remember the nerve names. A traditional mnemonic is the rhyming couplet, “On Old Olympus’ Towering Tops/A Finn And German Viewed Some Hops,” in which the initial letter of each word corresponds to the initial letter in the name of each nerve. The names of the nerves have changed over the years to reflect current usage and more accurate naming. An exercise to help learn this sort of information is to generate a mnemonic using words that have personal significance. The names of the cranial nerves are listed in Table 13.3 along with a brief description of their function, their source (sensory ganglion or motor nucleus), and their target (sensory nucleus or skeletal muscle). They are listed here with a brief explanation of each nerve (Figure 13.23). The olfactory nerve and optic nerve are responsible for the sense of smell and vision, respectively. The oculomotor nerve is responsible for eye movements by controlling four of the extraocular muscles. It is also responsible for lifting the upper eyelid when the eyes point up, and for pupillary constriction. The trochlear nerve and the abducens nerve are both responsible for eye movement, but do so by controlling different extraocular muscles. The trigeminal nerve is responsible for cutaneous sensations of the face and controlling the muscles of mastication. The facial nerve is responsible for the muscles involved in facial expressions, as well as part of the sense of taste and the production of saliva. The vestibulocochlear nerve is responsible for the senses of hearing and balance. The glossopharyngeal nerve is responsible for controlling muscles in the oral cavity and upper throat, as well as part of the sense of taste and the production of saliva. The vagus nerve is responsible for contributing to homeostatic control of the organs of the thoracic and upper abdominal cavities. The spinal accessory nerveis responsible for controlling the muscles of the neck, along with cervical spinal nerves. The hypoglossal nerve is responsible for controlling the muscles of the lower throat and tongue. Figure 13.23 The Cranial Nerves The anatomical arrangement of the roots of the cranial nerves observed from an inferior view of the brain. Three of the cranial nerves also contain autonomic fibers, and a fourth is almost purely a component of the autonomic system. The oculomotor, facial, and glossopharyngeal nerves contain fibers that contact autonomic ganglia. The oculomotor fibers initiate pupillary constriction, whereas the facial and glossopharyngeal fibers both initiate salivation. The vagus nerve primarily targets autonomic ganglia in the thoracic and upper abdominal cavities. INTERACTIVE LINK Visit this site to read about a man who wakes with a headache and a loss of vision. His regular doctor sent him to an ophthalmologist to address the vision loss. The ophthalmologist recognizes a greater problem and immediately sends him to the emergency room. Once there, the patient undergoes a large battery of tests, but a definite cause cannot be found. A specialist recognizes the problem as meningitis, but the question is what caused it originally. How can that be cured? The loss of vision comes from swelling around the optic nerve, which probably presented as a bulge on the inside of the eye. Why is swelling related to meningitis going to push on the optic nerve? Another important aspect of the cranial nerves that lends itself to a mnemonic is the functional role each nerve plays. The nerves fall into one of three basic groups. They are sensory, motor, or both (see Table 13.3). The sentence, “Some Say Marry Money But My Brother Says Brains Beauty Matter More,” corresponds to the basic function of each nerve. The first, second, and eighth nerves are purely sensory: the olfactory (CNI), optic (CNII), and vestibulocochlear (CNVIII) nerves. The three eye-movement nerves are all motor: the oculomotor (CNIII), trochlear (CNIV), and abducens (CNVI). The spinal accessory (CNXI) and hypoglossal (CNXII) nerves are also strictly motor. The remainder of the nerves contain both sensory and motor fibers. They are the trigeminal (CNV), facial (CNVII), glossopharyngeal (CNIX), and vagus (CNX) nerves. The nerves that convey both are often related to each other. The trigeminal and facial nerves both concern the face; one concerns the sensations and the other concerns the muscle movements. The facial and glossopharyngeal nerves are both responsible for conveying gustatory, or taste, sensations as well as controlling salivary glands. The vagus nerve is involved in visceral responses to taste, namely the gag reflex. This is not an exhaustive list of what these combination nerves do, but there is a thread of relation between them. Cranial Nerves \| Mnemonic \| # \| Name \| Function (S/M/B) \| Central connection (nuclei) \| Peripheral connection (ganglion or muscle) \| \|---\|---\|---\|---\|---\|---\| \| On \| I \| Olfactory \| Smell (S) \| Olfactory bulb \| Olfactory epithelium \| \| Old \| II \| Optic \| Vision (S) \| Hypothalamus/thalamus/midbrain \| Retina (retinal ganglion cells) \| \| Olympus’ \| III \| Oculomotor \| Eye movements (M) \| Oculomotor nucleus \| Extraocular muscles (other 4), levator palpebrae superioris, ciliary ganglion (autonomic) \| \| Towering \| IV \| Trochlear \| Eye movements (M) \| Trochlear nucleus \| Superior oblique muscle \| \| Tops \| V \| Trigeminal \| Sensory/motor – face (B) \| Trigeminal nuclei in the midbrain, pons, and medulla \| Trigeminal \| \| A \| VI \| Abducens \| Eye movements (M) \| Abducens nucleus \| Lateral rectus muscle \| \| Finn \| VII \| Facial \| Motor – face, Taste (B) \| Facial nucleus, solitary nucleus, superior salivatory nucleus \| Facial muscles, Geniculate ganglion, Pterygopalatine ganglion (autonomic) \| \| And \| VIII \| Auditory (Vestibulocochlear) \| Hearing/balance (S) \| Cochlear nucleus, Vestibular nucleus/cerebellum \| Spiral ganglion (hearing), Vestibular ganglion (balance) \| \| German \| IX \| Glossopharyngeal \| Motor – throat Taste (B) \| Solitary nucleus, inferior salivatory nucleus, nucleus ambiguus \| Pharyngeal muscles, Geniculate ganglion, Otic ganglion (autonomic) \| \| Viewed \| X \| Vagus \| Motor/sensory – viscera (autonomic) (B) \| Medulla \| Terminal ganglia serving thoracic and upper abdominal organs (heart and small intestines) \| \| Some \| XI \| Spinal Accessory \| Motor – head and neck (M) \| Spinal accessory nucleus \| Neck muscles \| \| Hops \| XII \| Hypoglossal \| Motor – lower throat (M) \| Hypoglossal nucleus \| Muscles of the larynx and lower pharynx \| Table 13.3 Spinal Nerves The nerves connected to the spinal cord are the spinal nerves. The arrangement of these nerves is much more regular than that of the cranial nerves. All of the spinal nerves are combined sensory and motor axons that separate into two nerve roots. The sensory axons enter the spinal cord as the dorsal nerve root. The motor fibers, both somatic and autonomic, emerge as the ventral nerve root. The dorsal root ganglion for each nerve is an enlargement of the spinal nerve. There are 31 spinal nerves, named for the level of the spinal cord at which each one emerges. There are eight pairs of cervical nerves designated C1 to C8, twelve thoracic nerves designated T1 to T12, five pairs of lumbar nerves designated L1 to L5, five pairs of sacral nerves designated S1 to S5, and one pair of coccygeal nerves. The nerves are numbered from the superior to inferior positions, and each emerges from the vertebral column through the intervertebral foramen at its level. The first nerve, C1, emerges between the first cervical vertebra and the occipital bone. The second nerve, C2, emerges between the first and second cervical vertebrae. The same occurs for C3 to C7, but C8 emerges between the seventh cervical vertebra and the first thoracic vertebra. For the thoracic and lumbar nerves, each one emerges between the vertebra that has the same designation and the next vertebra in the column. The sacral nerves emerge from the sacral foramina along the length of that unique vertebra. Spinal nerves extend outward from the vertebral column to enervate the periphery. The nerves in the periphery are not straight continuations of the spinal nerves, but rather the reorganization of the axons in those nerves to follow different courses. Axons from different spinal nerves will come together into a systemic nerve. This occurs at four places along the length of the vertebral column, each identified as a nerve plexus, whereas the other spinal nerves directly correspond to nerves at their respective levels. In this instance, the word plexus is used to describe networks of nerve fibers with no associated cell bodies. Of the four nerve plexuses, two are found at the cervical level, one at the lumbar level, and one at the sacral level (Figure 13.24). The cervical plexus is composed of axons from spinal nerves C1 through C5 and branches into nerves in the posterior neck and head, as well as the phrenic nerve, which connects to the diaphragm at the base of the thoracic cavity. The other plexus from the cervical level is the brachial plexus. Spinal nerves C4 through T1 reorganize through this plexus to give rise to the nerves of the arms, as the name brachial suggests. A large nerve from this plexus is the radial nerve from which the axillary nerve branches to go to the armpit region. The radial nerve continues through the arm and is paralleled by the ulnar nerve and the median nerve. The lumbar plexus arises from all the lumbar spinal nerves and gives rise to nerves enervating the pelvic region and the anterior leg. The femoral nerve is one of the major nerves from this plexus, which gives rise to the saphenous nerve as a branch that extends through the anterior lower leg. The sacral plexus comes from the lower lumbar nerves L4 and L5 and the sacral nerves S1 to S4. The most significant systemic nerve to come from this plexus is the sciatic nerve, which is a combination of the tibial nerve and the fibular nerve. The sciatic nerve extends across the hip joint and is most commonly associated with the condition sciatica, which is the result of compression or irritation of the nerve or any of the spinal nerves giving rise to it. These plexuses are described as arising from spinal nerves and giving rise to certain systemic nerves, but they contain fibers that serve sensory functions or fibers that serve motor functions. This means that some fibers extend from cutaneous or other peripheral sensory surfaces and send action potentials into the CNS. Those are axons of sensory neurons in the dorsal root ganglia that enter the spinal cord through the dorsal nerve root. Other fibers are the axons of motor neurons of the anterior horn of the spinal cord, which emerge in the ventral nerve root and send action potentials to cause skeletal muscles to contract in their target regions. For example, the radial nerve contains fibers of cutaneous sensation in the arm, as well as motor fibers that move muscles in the arm. Spinal nerves of the thoracic region, T2 through T11, are not part of the plexuses but rather emerge and give rise to the intercostal nerves found between the ribs, which articulate with the vertebrae surrounding the spinal nerve. Figure 13.24 Nerve Plexuses of the Body There are four main nerve plexuses in the human body. The cervical plexus supplies nerves to the posterior head and neck, as well as to the diaphragm. The brachial plexus supplies nerves to the arm. The lumbar plexus supplies nerves to the anterior leg. The sacral plexus supplies nerves to the posterior leg. AGING AND THE... Nervous System Anosmia is the loss of the sense of smell. It is often the result of the olfactory nerve being severed, usually because of blunt force trauma to the head. The sensory neurons of the olfactory epithelium have a limited lifespan of approximately one to four months, and new ones are made on a regular basis. The new neurons extend their axons into the CNS by growing along the existing fibers of the olfactory nerve. The ability of these neurons to be replaced is lost with age. Age-related anosmia is not the result of impact trauma to the head, but rather a slow loss of the sensory neurons with no new neurons born to replace them. Smell is an important sense, especially for the enjoyment of food. There are only five tastes sensed by the tongue, and two of them are generally thought of as unpleasant tastes (sour and bitter). The rich sensory experience of food is the result of odor molecules associated with the food, both as food is moved into the mouth, and therefore passes under the nose, and when it is chewed and molecules are released to move up the pharynx into the posterior nasal cavity. Anosmia results in a loss of the enjoyment of food. As the replacement of olfactory neurons declines with age, anosmia can set in. Without the sense of smell, many sufferers complain of food tasting bland. Often, the only way to enjoy food is to add seasoning that can be sensed on the tongue, which usually means adding table salt. The problem with this solution, however, is that this increases sodium intake, which can lead to cardiovascular problems through water retention and the associated increase in blood pressure. Key Terms - abducens nerve - sixth cranial nerve; responsible for contraction of one of the extraocular muscles - alar plate - developmental region of the spinal cord that gives rise to the posterior horn of the gray matter - amygdala - nucleus deep in the temporal lobe of the cerebrum that is related to memory and emotional behavior - anterior column - white matter between the anterior horns of the spinal cord composed of many different groups of axons of both ascending and descending tracts - anterior horn - gray matter of the spinal cord containing multipolar motor neurons, sometimes referred to as the ventral horn - anterior median fissure - deep midline feature of the anterior spinal cord, marking the separation between the right and left sides of the cord - anterior spinal artery - blood vessel from the merged branches of the vertebral arteries that runs along the anterior surface of the spinal cord - arachnoid granulation - outpocket of the arachnoid membrane into the dural sinuses that allows for reabsorption of CSF into the blood - arachnoid mater - middle layer of the meninges named for the spider-web–like trabeculae that extend between it and the pia mater - arachnoid trabeculae - filaments between the arachnoid and pia mater within the subarachnoid space - ascending tract - central nervous system fibers carrying sensory information from the spinal cord or periphery to the brain - axillary nerve - systemic nerve of the arm that arises from the brachial plexus - basal forebrain - nuclei of the cerebrum related to modulation of sensory stimuli and attention through broad projections to the cerebral cortex, loss of which is related to Alzheimer’s disease - basal nuclei - nuclei of the cerebrum (with a few components in the upper brain stem and diencephalon) that are responsible for assessing cortical movement commands and comparing them with the general state of the individual through broad modulatory activity of dopamine neurons; largely related to motor functions, as evidenced through the symptoms of Parkinson’s and Huntington’s diseases - basal plate - developmental region of the spinal cord that gives rise to the lateral and anterior horns of gray matter - basilar artery - blood vessel from the merged vertebral arteries that runs along the dorsal surface of the brain stem - brachial plexus - nerve plexus associated with the lower cervical spinal nerves and first thoracic spinal nerve - brain stem - region of the adult brain that includes the midbrain, pons, and medulla oblongata and develops from the mesencephalon, metencephalon, and myelencephalon of the embryonic brain - Broca’s area - region of the frontal lobe associated with the motor commands necessary for speech production and located only in the cerebral hemisphere responsible for language production, which is the left side in approximately 95 percent of the population - Brodmann’s areas - mapping of regions of the cerebral cortex based on microscopic anatomy that relates specific areas to functional differences, as described by Brodmann in the early 1900s - carotid canal - opening in the temporal bone through which the internal carotid artery enters the cranium - cauda equina - bundle of spinal nerve roots that descend from the lower spinal cord below the first lumbar vertebra and lie within the vertebral cavity; has the appearance of a horse's tail - caudate - nucleus deep in the cerebrum that is part of the basal nuclei; along with the putamen, it is part of the striatum - central canal - hollow space within the spinal cord that is the remnant of the center of the neural tube - central sulcus - surface landmark of the cerebral cortex that marks the boundary between the frontal and parietal lobes - cephalic flexure - curve in midbrain of the embryo that positions the forebrain ventrally - cerebellum - region of the adult brain connected primarily to the pons that developed from the metencephalon (along with the pons) and is largely responsible for comparing information from the cerebrum with sensory feedback from the periphery through the spinal cord - cerebral aqueduct - connection of the ventricular system between the third and fourth ventricles located in the midbrain - cerebral cortex - outer gray matter covering the forebrain, marked by wrinkles and folds known as gyri and sulci - cerebral hemisphere - one half of the bilaterally symmetrical cerebrum - cerebrum - region of the adult brain that develops from the telencephalon and is responsible for higher neurological functions such as memory, emotion, and consciousness - cervical plexus - nerve plexus associated with the upper cervical spinal nerves - choroid plexus - specialized structures containing ependymal cells lining blood capillaries that filter blood to produce CSF in the four ventricles of the brain - circle of Willis - unique anatomical arrangement of blood vessels around the base of the brain that maintains perfusion of blood into the brain even if one component of the structure is blocked or narrowed - common carotid artery - blood vessel that branches off the aorta (or the brachiocephalic artery on the right) and supplies blood to the head and neck - corpus callosum - large white matter structure that connects the right and left cerebral hemispheres - cranial nerve - one of twelve nerves connected to the brain that are responsible for sensory or motor functions of the head and neck - cranial nerve ganglion - sensory ganglion of cranial nerves - descending tract - central nervous system fibers carrying motor commands from the brain to the spinal cord or periphery - diencephalon - region of the adult brain that retains its name from embryonic development and includes the thalamus and hypothalamus - direct pathway - connections within the basal nuclei from the striatum to the globus pallidus internal segment and substantia nigra pars reticulata that disinhibit the thalamus to increase cortical control of movement - disinhibition - disynaptic connection in which the first synapse inhibits the second cell, which then stops inhibiting the final target - dorsal (posterior) nerve root - axons entering the posterior horn of the spinal cord - dorsal (posterior) root ganglion - sensory ganglion attached to the posterior nerve root of a spinal nerve - dura mater - tough, fibrous, outer layer of the meninges that is attached to the inner surface of the cranium and vertebral column and surrounds the entire CNS - dural sinus - any of the venous structures surrounding the brain, enclosed within the dura mater, which drain blood from the CNS to the common venous return of the jugular veins - endoneurium - innermost layer of connective tissue that surrounds individual axons within a nerve - enteric nervous system - peripheral structures, namely ganglia and nerves, that are incorporated into the digestive system organs - enteric plexus - neuronal plexus in the wall of the intestines, which is part of the enteric nervous system - epineurium - outermost layer of connective tissue that surrounds an entire nerve - epithalamus - region of the diecephalon containing the pineal gland - esophageal plexus - neuronal plexus in the wall of the esophagus that is part of the enteric nervous system - extraocular muscles - six skeletal muscles that control eye movement within the orbit - facial nerve - seventh cranial nerve; responsible for contraction of the facial muscles and for part of the sense of taste, as well as causing saliva production - fascicle - small bundles of nerve or muscle fibers enclosed by connective tissue - femoral nerve - systemic nerve of the anterior leg that arises from the lumbar plexus - fibular nerve - systemic nerve of the posterior leg that begins as part of the sciatic nerve - foramen magnum - large opening in the occipital bone of the skull through which the spinal cord emerges and the vertebral arteries enter the cranium - forebrain - anterior region of the adult brain that develops from the prosencephalon and includes the cerebrum and diencephalon - fourth ventricle - the portion of the ventricular system that is in the region of the brain stem and opens into the subarachnoid space through the median and lateral apertures - frontal eye field - region of the frontal lobe associated with motor commands to orient the eyes toward an object of visual attention - frontal lobe - region of the cerebral cortex directly beneath the frontal bone of the cranium - gastric plexuses - neuronal networks in the wall of the stomach that are part of the enteric nervous system - globus pallidus - nuclei deep in the cerebrum that are part of the basal nuclei and can be divided into the internal and external segments - glossopharyngeal nerve - ninth cranial nerve; responsible for contraction of muscles in the tongue and throat and for part of the sense of taste, as well as causing saliva production - gyrus - ridge formed by convolutions on the surface of the cerebrum or cerebellum - hindbrain - posterior region of the adult brain that develops from the rhombencephalon and includes the pons, medulla oblongata, and cerebellum - hippocampus - gray matter deep in the temporal lobe that is very important for long-term memory formation - hypoglossal nerve - twelfth cranial nerve; responsible for contraction of muscles of the tongue - hypothalamus - major region of the diencephalon that is responsible for coordinating autonomic and endocrine control of homeostasis - indirect pathway - connections within the basal nuclei from the striatum through the globus pallidus external segment and subthalamic nucleus to the globus pallidus internal segment/substantia nigra pars compacta that result in inhibition of the thalamus to decrease cortical control of movement - inferior colliculus - half of the midbrain tectum that is part of the brain stem auditory pathway - inferior olive - nucleus in the medulla that is involved in processing information related to motor control - intercostal nerve - systemic nerve in the thoracic cavity that is found between two ribs - internal carotid artery - branch from the common carotid artery that enters the cranium and supplies blood to the brain - interventricular foramina - openings between the lateral ventricles and third ventricle allowing for the passage of CSF - jugular veins - blood vessels that return “used” blood from the head and neck - kinesthesia - general sensory perception of movement of the body - lateral apertures - pair of openings from the fourth ventricle to the subarachnoid space on either side and between the medulla and cerebellum - lateral column - white matter of the spinal cord between the posterior horn on one side and the axons from the anterior horn on the same side; composed of many different groups of axons, of both ascending and descending tracts, carrying motor commands to and from the brain - lateral horn - region of the spinal cord gray matter in the thoracic, upper lumbar, and sacral regions that is the central component of the sympathetic division of the autonomic nervous system - lateral sulcus - surface landmark of the cerebral cortex that marks the boundary between the temporal lobe and the frontal and parietal lobes - lateral ventricles - portions of the ventricular system that are in the region of the cerebrum - limbic cortex - collection of structures of the cerebral cortex that are involved in emotion, memory, and behavior and are part of the larger limbic system - limbic system - structures at the edge (limit) of the boundary between the forebrain and hindbrain that are most associated with emotional behavior and memory formation - longitudinal fissure - large separation along the midline between the two cerebral hemispheres - lumbar plexus - nerve plexus associated with the lumbar spinal nerves - lumbar puncture - procedure used to withdraw CSF from the lower lumbar region of the vertebral column that avoids the risk of damaging CNS tissue because the spinal cord ends at the upper lumbar vertebrae - median aperture - singular opening from the fourth ventricle into the subarachnoid space at the midline between the medulla and cerebellum - median nerve - systemic nerve of the arm, located between the ulnar and radial nerves - meninges - protective outer coverings of the CNS composed of connective tissue - mesencephalon - primary vesicle of the embryonic brain that does not significantly change through the rest of embryonic development and becomes the midbrain - metencephalon - secondary vesicle of the embryonic brain that develops into the pons and the cerebellum - midbrain - middle region of the adult brain that develops from the mesencephalon - myelencephalon - secondary vesicle of the embryonic brain that develops into the medulla - nerve plexus - network of nerves without neuronal cell bodies included - neural crest - tissue that detaches from the edges of the neural groove and migrates through the embryo to develop into peripheral structures of both nervous and non-nervous tissues - neural fold - elevated edge of the neural groove - neural groove - region of the neural plate that folds into the dorsal surface of the embryo and closes off to become the neural tube - neural plate - thickened layer of neuroepithelium that runs longitudinally along the dorsal surface of an embryo and gives rise to nervous system tissue - neural tube - precursor to structures of the central nervous system, formed by the invagination and separation of neuroepithelium - neuraxis - central axis to the nervous system, from the posterior to anterior ends of the neural tube; the inferior tip of the spinal cord to the anterior surface of the cerebrum - occipital lobe - region of the cerebral cortex directly beneath the occipital bone of the cranium - occipital sinuses - dural sinuses along the edge of the occipital lobes of the cerebrum - oculomotor nerve - third cranial nerve; responsible for contraction of four of the extraocular muscles, the muscle in the upper eyelid, and pupillary constriction - olfaction - special sense responsible for smell, which has a unique, direct connection to the cerebrum - olfactory nerve - first cranial nerve; responsible for the sense of smell - optic nerve - second cranial nerve; responsible for visual sensation - orthostatic reflex - sympathetic function that maintains blood pressure when standing to offset the increased effect of gravity - paravertebral ganglia - autonomic ganglia superior to the sympathetic chain ganglia - parietal lobe - region of the cerebral cortex directly beneath the parietal bone of the cranium - parieto-occipital sulcus - groove in the cerebral cortex representing the border between the parietal and occipital cortices - perineurium - layer of connective tissue surrounding fascicles within a nerve - phrenic nerve - systemic nerve from the cervical plexus that enervates the diaphragm - pia mater - thin, innermost membrane of the meninges that directly covers the surface of the CNS - plexus - network of nerves or nervous tissue - postcentral gyrus - primary motor cortex located in the frontal lobe of the cerebral cortex - posterior columns - white matter of the spinal cord that lies between the posterior horns of the gray matter, sometimes referred to as the dorsal column; composed of axons of ascending tracts that carry sensory information up to the brain - posterior horn - gray matter region of the spinal cord in which sensory input arrives, sometimes referred to as the dorsal horn - posterior median sulcus - midline feature of the posterior spinal cord, marking the separation between right and left sides of the cord - posterolateral sulcus - feature of the posterior spinal cord marking the entry of posterior nerve roots and the separation between the posterior and lateral columns of the white matter - precentral gyrus - ridge just posterior to the central sulcus, in the parietal lobe, where somatosensory processing initially takes place in the cerebrum - prefrontal lobe - specific region of the frontal lobe anterior to the more specific motor function areas, which can be related to the early planning of movements and intentions to the point of being personality-type functions - premotor area - region of the frontal lobe responsible for planning movements that will be executed through the primary motor cortex - prevertebral ganglia - autonomic ganglia that are anterior to the vertebral column and functionally related to the sympathetic chain ganglia - primary vesicle - initial enlargements of the anterior neural tube during embryonic development that develop into the forebrain, midbrain, and hindbrain - proprioception - general sensory perceptions providing information about location and movement of body parts; the “sense of the self” - prosencephalon - primary vesicle of the embryonic brain that develops into the forebrain, which includes the cerebrum and diencephalon - putamen - nucleus deep in the cerebrum that is part of the basal nuclei; along with the caudate, it is part of the striatum - radial nerve - systemic nerve of the arm, the distal component of which is located near the radial bone - reticular formation - diffuse region of gray matter throughout the brain stem that regulates sleep, wakefulness, and states of consciousness - rhombencephalon - primary vesicle of the embryonic brain that develops into the hindbrain, which includes the pons, cerebellum, and medulla - sacral plexus - nerve plexus associated with the lower lumbar and sacral spinal nerves - saphenous nerve - systemic nerve of the lower anterior leg that is a branch from the femoral nerve - sciatic nerve - systemic nerve from the sacral plexus that is a combination of the tibial and fibular nerves and extends across the hip joint and gluteal region into the upper posterior leg - sciatica - painful condition resulting from inflammation or compression of the sciatic nerve or any of the spinal nerves that contribute to it - secondary vesicle - five vesicles that develop from primary vesicles, continuing the process of differentiation of the embryonic brain - sigmoid sinuses - dural sinuses that drain directly into the jugular veins - somatosensation - general senses related to the body, usually thought of as the senses of touch, which would include pain, temperature, and proprioception - spinal accessory nerve - eleventh cranial nerve; responsible for contraction of neck muscles - spinal nerve - one of 31 nerves connected to the spinal cord - straight sinus - dural sinus that drains blood from the deep center of the brain to collect with the other sinuses - striatum - the caudate and putamen collectively, as part of the basal nuclei, which receive input from the cerebral cortex - subarachnoid space - space between the arachnoid mater and pia mater that contains CSF and the fibrous connections of the arachnoid trabeculae - subcortical nucleus - all the nuclei beneath the cerebral cortex, including the basal nuclei and the basal forebrain - substantia nigra pars compacta - nuclei within the basal nuclei that release dopamine to modulate the function of the striatum; part of the motor pathway - substantia nigra pars reticulata - nuclei within the basal nuclei that serve as an output center of the nuclei; part of the motor pathway - subthalamus - nucleus within the basal nuclei that is part of the indirect pathway - sulcus - groove formed by convolutions in the surface of the cerebral cortex - superior colliculus - half of the midbrain tectum that is responsible for aligning visual, auditory, and somatosensory spatial perceptions - superior sagittal sinus - dural sinus that runs along the top of the longitudinal fissure and drains blood from the majority of the outer cerebrum - sympathetic chain ganglia - autonomic ganglia in a chain along the anterolateral aspect of the vertebral column that are responsible for contributing to homeostatic mechanisms of the autonomic nervous system - systemic nerve - nerve in the periphery distal to a nerve plexus or spinal nerve - tectum - region of the midbrain, thought of as the roof of the cerebral aqueduct, which is subdivided into the inferior and superior colliculi - tegmentum - region of the midbrain, thought of as the floor of the cerebral aqueduct, which continues into the pons and medulla as the floor of the fourth ventricle - telencephalon - secondary vesicle of the embryonic brain that develops into the cerebrum - temporal lobe - region of the cerebral cortex directly beneath the temporal bone of the cranium - terminal ganglion - autonomic ganglia that are near or within the walls of organs that are responsible for contributing to homeostatic mechanisms of the autonomic nervous system - thalamus - major region of the diencephalon that is responsible for relaying information between the cerebrum and the hindbrain, spinal cord, and periphery - third ventricle - portion of the ventricular system that is in the region of the diencephalon - tibial nerve - systemic nerve of the posterior leg that begins as part of the sciatic nerve - transverse sinuses - dural sinuses that drain along either side of the occipital–cerebellar space - trigeminal ganglion - sensory ganglion that contributes sensory fibers to the trigeminal nerve - trigeminal nerve - fifth cranial nerve; responsible for cutaneous sensation of the face and contraction of the muscles of mastication - trochlear nerve - fourth cranial nerve; responsible for contraction of one of the extraocular muscles - ulnar nerve - systemic nerve of the arm located close to the ulna, a bone of the forearm - vagus nerve - tenth cranial nerve; responsible for the autonomic control of organs in the thoracic and upper abdominal cavities - ventral (anterior) nerve root - axons emerging from the anterior or lateral horns of the spinal cord - ventricles - remnants of the hollow center of the neural tube that are spaces for cerebrospinal fluid to circulate through the brain - vertebral arteries - arteries that ascend along either side of the vertebral column through the transverse foramina of the cervical vertebrae and enter the cranium through the foramen magnum - vestibulocochlear nerve - eighth cranial nerve; responsible for the sensations of hearing and balance Chapter Review 13.1 The Embryologic Perspective The development of the nervous system starts early in embryonic development. The outer layer of the embryo, the ectoderm, gives rise to the skin and the nervous system. A specialized region of this layer, the neuroectoderm, becomes a groove that folds in and becomes the neural tube beneath the dorsal surface of the embryo. The anterior end of the neural tube develops into the brain, and the posterior region becomes the spinal cord. Tissues at the edges of the neural groove, when it closes off, are called the neural crest and migrate through the embryo to give rise to PNS structures as well as some non-nervous tissues. The brain develops from this early tube structure and gives rise to specific regions of the adult brain. As the neural tube grows and differentiates, it enlarges into three vesicles that correspond to the forebrain, midbrain, and hindbrain regions of the adult brain. Later in development, two of these three vesicles differentiate further, resulting in five vesicles. Those five vesicles can be aligned with the four major regions of the adult brain. The cerebrum is formed directly from the telencephalon. The diencephalon is the only region that keeps its embryonic name. The mesencephalon, metencephalon, and myelencephalon become the brain stem. The cerebellum also develops from the metencephalon and is a separate region of the adult brain. The spinal cord develops out of the rest of the neural tube and retains the tube structure, with the nervous tissue thickening and the hollow center becoming a very small central canal through the cord. The rest of the hollow center of the neural tube corresponds to open spaces within the brain called the ventricles, where cerebrospinal fluid is found. 13.2 The Central Nervous System The adult brain is separated into four major regions: the cerebrum, the diencephalon, the brain stem, and the cerebellum. The cerebrum is the largest portion and contains the cerebral cortex and subcortical nuclei. It is divided into two halves by the longitudinal fissure. The cortex is separated into the frontal, parietal, temporal, and occipital lobes. The frontal lobe is responsible for motor functions, from planning movements through executing commands to be sent to the spinal cord and periphery. The most anterior portion of the frontal lobe is the prefrontal cortex, which is associated with aspects of personality through its influence on motor responses in decision-making. The other lobes are responsible for sensory functions. The parietal lobe is where somatosensation is processed. The occipital lobe is where visual processing begins, although the other parts of the brain can contribute to visual function. The temporal lobe contains the cortical area for auditory processing, but also has regions crucial for memory formation. Nuclei beneath the cerebral cortex, known as the subcortical nuclei, are responsible for augmenting cortical functions. The basal nuclei receive input from cortical areas and compare it with the general state of the individual through the activity of a dopamine-releasing nucleus. The output influences the activity of part of the thalamus that can then increase or decrease cortical activity that often results in changes to motor commands. The basal forebrain is responsible for modulating cortical activity in attention and memory. The limbic system includes deep cerebral nuclei that are responsible for emotion and memory. The diencephalon includes the thalamus and the hypothalamus, along with some other structures. The thalamus is a relay between the cerebrum and the rest of the nervous system. The hypothalamus coordinates homeostatic functions through the autonomic and endocrine systems. The brain stem is composed of the midbrain, pons, and medulla. It controls the head and neck region of the body through the cranial nerves. There are control centers in the brain stem that regulate the cardiovascular and respiratory systems. The cerebellum is connected to the brain stem, primarily at the pons, where it receives a copy of the descending input from the cerebrum to the spinal cord. It can compare this with sensory feedback input through the medulla and send output through the midbrain that can correct motor commands for coordination. 13.3 Circulation and the Central Nervous System The CNS has a privileged blood supply established by the blood-brain barrier. Establishing this barrier are anatomical structures that help to protect and isolate the CNS. The arterial blood to the brain comes from the internal carotid and vertebral arteries, which both contribute to the unique circle of Willis that provides constant perfusion of the brain even if one of the blood vessels is blocked or narrowed. That blood is eventually filtered to make a separate medium, the CSF, that circulates within the spaces of the brain and then into the surrounding space defined by the meninges, the protective covering of the brain and spinal cord. The blood that nourishes the brain and spinal cord is behind the glial-cell–enforced blood-brain barrier, which limits the exchange of material from blood vessels with the interstitial fluid of the nervous tissue. Thus, metabolic wastes are collected in cerebrospinal fluid that circulates through the CNS. This fluid is produced by filtering blood at the choroid plexuses in the four ventricles of the brain. It then circulates through the ventricles and into the subarachnoid space, between the pia mater and the arachnoid mater. From the arachnoid granulations, CSF is reabsorbed into the blood, removing the waste from the privileged central nervous tissue. The blood, now with the reabsorbed CSF, drains out of the cranium through the dural sinuses. The dura mater is the tough outer covering of the CNS, which is anchored to the inner surface of the cranial and vertebral cavities. It surrounds the venous space known as the dural sinuses, which connect to the jugular veins, where blood drains from the head and neck. 13.4 The Peripheral Nervous System The PNS is composed of the groups of neurons (ganglia) and bundles of axons (nerves) that are outside of the brain and spinal cord. Ganglia are of two types, sensory or autonomic. Sensory ganglia contain unipolar sensory neurons and are found on the dorsal root of all spinal nerves as well as associated with many of the cranial nerves. Autonomic ganglia are in the sympathetic chain, the associated paravertebral or prevertebral ganglia, or in terminal ganglia near or within the organs controlled by the autonomic nervous system. Nerves are classified as cranial nerves or spinal nerves on the basis of their connection to the brain or spinal cord, respectively. The twelve cranial nerves can be strictly sensory in function, strictly motor in function, or a combination of the two functions. Sensory fibers are axons of sensory ganglia that carry sensory information into the brain and target sensory nuclei. Motor fibers are axons of motor neurons in motor nuclei of the brain stem and target skeletal muscles of the head and neck. Spinal nerves are all mixed nerves with both sensory and motor fibers. Spinal nerves emerge from the spinal cord and reorganize through plexuses, which then give rise to systemic nerves. Thoracic spinal nerves are not part of any plexus, but give rise to the intercostal nerves directly. Interactive Link Questions Watch this animation to examine the development of the brain, starting with the neural tube. As the anterior end of the neural tube develops, it enlarges into the primary vesicles that establish the forebrain, midbrain, and hindbrain. Those structures continue to develop throughout the rest of embryonic development and into adolescence. They are the basis of the structure of the fully developed adult brain. How would you describe the difference in the relative sizes of the three regions of the brain when comparing the early (25th embryonic day) brain and the adult brain? 2.Watch this video to learn about the white matter in the cerebrum that develops during childhood and adolescence. This is a composite of MRI images taken of the brains of people from 5 years of age through 20 years of age, demonstrating how the cerebrum changes. As the color changes to blue, the ratio of gray matter to white matter changes. The caption for the video describes it as “less gray matter,” which is another way of saying “more white matter.” If the brain does not finish developing until approximately 20 years of age, can teenagers be held responsible for behaving badly? 3.Watch this video to learn about the basal nuclei (also known as the basal ganglia), which have two pathways that process information within the cerebrum. As shown in this video, the direct pathway is the shorter pathway through the system that results in increased activity in the cerebral cortex and increased motor activity. The direct pathway is described as resulting in “disinhibition” of the thalamus. What does disinhibition mean? What are the two neurons doing individually to cause this? 4.Watch this video to learn about the basal nuclei (also known as the basal ganglia), which have two pathways that process information within the cerebrum. As shown in this video, the indirect pathway is the longer pathway through the system that results in decreased activity in the cerebral cortex, and therefore less motor activity. The indirect pathway has an extra couple of connections in it, including disinhibition of the subthalamic nucleus. What is the end result on the thalamus, and therefore on movement initiated by the cerebral cortex? 5.Watch this video to learn about the gray matter of the spinal cord that receives input from fibers of the dorsal (posterior) root and sends information out through the fibers of the ventral (anterior) root. As discussed in this video, these connections represent the interactions of the CNS with peripheral structures for both sensory and motor functions. The cervical and lumbar spinal cords have enlargements as a result of larger populations of neurons. What are these enlargements responsible for? 6.Compared with the nearest evolutionary relative, the chimpanzee, the human has a brain that is huge. At a point in the past, a common ancestor gave rise to the two species of humans and chimpanzees. That evolutionary history is long and is still an area of intense study. But something happened to increase the size of the human brain relative to the chimpanzee. Read this article in which the author explores the current understanding of why this happened. According to one hypothesis about the expansion of brain size, what tissue might have been sacrificed so energy was available to grow our larger brain? Based on what you know about that tissue and nervous tissue, why would there be a trade-off between them in terms of energy use? 7.Watch this animation to see how blood flows to the brain and passes through the circle of Willis before being distributed through the cerebrum. The circle of Willis is a specialized arrangement of arteries that ensure constant perfusion of the cerebrum even in the event of a blockage of one of the arteries in the circle. The animation shows the normal direction of flow through the circle of Willis to the middle cerebral artery. Where would the blood come from if there were a blockage just posterior to the middle cerebral artery on the left? 8.Watch this video that describes the procedure known as the lumbar puncture, a medical procedure used to sample the CSF. Because of the anatomy of the CNS, it is a relative safe location to insert a needle. Why is the lumbar puncture performed in the lower lumbar area of the vertebral column? 9.Watch this animation that shows the flow of CSF through the brain and spinal cord, and how it originates from the ventricles and then spreads into the space within the meninges, where the fluids then move into the venous sinuses to return to the cardiovascular circulation. What are the structures that produce CSF and where are they found? How are the structures indicated in this animation? 10.Figure 13.20 If you zoom in on the DRG, you can see smaller satellite glial cells surrounding the large cell bodies of the sensory neurons. From what structure do satellite cells derive during embryologic development? 11.Figure 13.22 To what structures in a skeletal muscle are the endoneurium, perineurium, and epineurium comparable? 12.Visit this site to read about a man who wakes with a headache and a loss of vision. His regular doctor sent him to an ophthalmologist to address the vision loss. The ophthalmologist recognizes a greater problem and immediately sends him to the emergency room. Once there, the patient undergoes a large battery of tests, but a definite cause cannot be found. A specialist recognizes the problem as meningitis, but the question is what caused it originally. How can that be cured? The loss of vision comes from swelling around the optic nerve, which probably presented as a bulge on the inside of the eye. Why is swelling related to meningitis going to push on the optic nerve? Review Questions Aside from the nervous system, which other organ system develops out of the ectoderm? - digestive - respiratory - integumentary - urinary Which primary vesicle of the embryonic nervous system does not differentiate into more vesicles at the secondary stage? - prosencephalon - mesencephalon - diencephalon - rhombencephalon Which adult structure(s) arises from the diencephalon? - thalamus, hypothalamus, retina - midbrain, pons, medulla - pons and cerebellum - cerebrum Which non-nervous tissue develops from the neuroectoderm? - respiratory mucosa - vertebral bone - digestive lining - craniofacial bone Which structure is associated with the embryologic development of the peripheral nervous system? - neural crest - neuraxis - rhombencephalon - neural tube Which lobe of the cerebral cortex is responsible for generating motor commands? - temporal - parietal - occipital - frontal What region of the diencephalon coordinates homeostasis? - thalamus - epithalamus - hypothalamus - subthalamus What level of the brain stem is the major input to the cerebellum? - midbrain - pons - medulla - spinal cord What region of the spinal cord contains motor neurons that direct the movement of skeletal muscles? - anterior horn - posterior horn - lateral horn - alar plate Brodmann’s areas map different regions of the ________ to particular functions. - cerebellum - cerebral cortex - basal forebrain - corpus callosum What blood vessel enters the cranium to supply the brain with fresh, oxygenated blood? - common carotid artery - jugular vein - internal carotid artery - aorta Which layer of the meninges surrounds and supports the sinuses that form the route through which blood drains from the CNS? - dura mater - arachnoid mater - subarachnoid - pia mater What type of glial cell is responsible for filtering blood to produce CSF at the choroid plexus? - ependymal cell - astrocyte - oligodendrocyte - Schwann cell Which portion of the ventricular system is found within the diencephalon? - lateral ventricles - third ventricle - cerebral aqueduct - fourth ventricle What condition causes a stroke? - inflammation of meninges - lumbar puncture - infection of cerebral spinal fluid - disruption of blood to the brain What type of ganglion contains neurons that control homeostatic mechanisms of the body? - sensory ganglion - dorsal root ganglion - autonomic ganglion - cranial nerve ganglion Which ganglion is responsible for cutaneous sensations of the face? - otic ganglion - vestibular ganglion - geniculate ganglion - trigeminal ganglion What is the name for a bundle of axons within a nerve? - fascicle - tract - nerve root - epineurium Which cranial nerve does not control functions in the head and neck? - olfactory - trochlear - glossopharyngeal - vagus Which of these structures is not under direct control of the peripheral nervous system? - trigeminal ganglion - gastric plexus - sympathetic chain ganglia - cervical plexus Critical Thinking Questions Studying the embryonic development of the nervous system makes it easier to understand the complexity of the adult nervous system. Give one example of how development in the embryonic nervous system explains a more complex structure in the adult nervous system. 34.What happens in development that suggests that there is a special relationship between the skeletal structure of the head and the nervous system? 35.Damage to specific regions of the cerebral cortex, such as through a stroke, can result in specific losses of function. What functions would likely be lost by a stroke in the temporal lobe? 36.Why do the anatomical inputs to the cerebellum suggest that it can compare motor commands and sensory feedback? 37.Why can the circle of Willis maintain perfusion of the brain even if there is a blockage in one part of the structure? 38.Meningitis is an inflammation of the meninges that can have severe effects on neurological function. Why is infection of this structure potentially so dangerous? 39.Why are ganglia and nerves not surrounded by protective structures like the meninges of the CNS? 40.Testing for neurological function involves a series of tests of functions associated with the cranial nerves. What functions, and therefore which nerves, are being tested by asking a patient to follow the tip of a pen with their eyes?	oercommons	2025-03-18T00:37:01.545446	null	{ "license": "Creative Commons - Attribution - https://creativecommons.org/licenses/by/4.0/", "url": "https://oercommons.org/courseware/lesson/56376/overview", "title": "Anatomy and Physiology, Regulation, Integration, and Control", "author": null }
https://oercommons.org/courseware/lesson/56377/overview	The Somatic Nervous System Introduction Figure 14.1 Too Hot to Touch When high temperature is sensed in the skin, a reflexive withdrawal is initiated by the muscles of the arm. Sensory neurons are activated by a stimulus, which is sent to the central nervous system, and a motor response is sent out to the skeletal muscles that control this movement. CHAPTER OBJECTIVES After studying this chapter, you will be able to: - Describe the components of the somatic nervous system - Name the modalities and submodalities of the sensory systems - Distinguish between general and special senses - Describe regions of the central nervous system that contribute to somatic functions - Explain the stimulus-response motor pathway The somatic nervous system is traditionally considered a division within the peripheral nervous system. However, this misses an important point: somatic refers to a functional division, whereas peripheral refers to an anatomic division. The somatic nervous system is responsible for our conscious perception of the environment and for our voluntary responses to that perception by means of skeletal muscles. Peripheral sensory neurons receive input from environmental stimuli, but the neurons that produce motor responses originate in the central nervous system. The distinction between the structures (i.e., anatomy) of the peripheral and central nervous systems and functions (i.e., physiology) of the somatic and autonomic systems can most easily be demonstrated through a simple reflex action. When you touch a hot stove, you pull your hand away. Sensory receptors in the skin sense extreme temperature and the early signs of tissue damage. This triggers an action potential, which travels along the sensory fiber from the skin, through the dorsal spinal root to the spinal cord, and directly activates a ventral horn motor neuron. That neuron sends a signal along its axon to excite the biceps brachii, causing contraction of the muscle and flexion of the forearm at the elbow to withdraw the hand from the hot stove. The withdrawal reflex has more components, such as inhibiting the opposing muscle and balancing posture while the arm is forcefully withdrawn, which will be further explored at the end of this chapter. The basic withdrawal reflex explained above includes sensory input (the painful stimulus), central processing (the synapse in the spinal cord), and motor output (activation of a ventral motor neuron that causes contraction of the biceps brachii). Expanding the explanation of the withdrawal reflex can include inhibition of the opposing muscle, or cross extension, either of which increase the complexity of the example by involving more central neurons. A collateral branch of the sensory axon would inhibit another ventral horn motor neuron so that the triceps brachii do not contract and slow the withdrawal down. The cross extensor reflex provides a counterbalancing movement on the other side of the body, which requires another collateral of the sensory axon to activate contraction of the extensor muscles in the contralateral limb. A more complex example of somatic function is conscious muscle movement. For example, reading of this text starts with visual sensory input to the retina, which then projects to the thalamus, and on to the cerebral cortex. A sequence of regions of the cerebral cortex process the visual information, starting in the primary visual cortex of the occipital lobe, and resulting in the conscious perception of these letters. Subsequent cognitive processing results in understanding of the content. As you continue reading, regions of the cerebral cortex in the frontal lobe plan how to move the eyes to follow the lines of text. The output from the cortex causes activity in motor neurons in the brain stem that cause movement of the extraocular muscles through the third, fourth, and sixth cranial nerves. This example also includes sensory input (the retinal projection to the thalamus), central processing (the thalamus and subsequent cortical activity), and motor output (activation of neurons in the brain stem that lead to coordinated contraction of extraocular muscles). Sensory Perception - Describe different types of sensory receptors - Describe the structures responsible for the special senses of taste, smell, hearing, balance, and vision - Distinguish how different tastes are transduced - Describe the means of mechanoreception for hearing and balance - List the supporting structures around the eye and describe the structure of the eyeball - Describe the processes of phototransduction A major role of sensory receptors is to help us learn about the environment around us, or about the state of our internal environment. Stimuli from varying sources, and of different types, are received and changed into the electrochemical signals of the nervous system. This occurs when a stimulus changes the cell membrane potential of a sensory neuron. The stimulus causes the sensory cell to produce an action potential that is relayed into the central nervous system (CNS), where it is integrated with other sensory information—or sometimes higher cognitive functions—to become a conscious perception of that stimulus. The central integration may then lead to a motor response. Describing sensory function with the term sensation or perception is a deliberate distinction. Sensation is the activation of sensory receptor cells at the level of the stimulus. Perception is the central processing of sensory stimuli into a meaningful pattern. Perception is dependent on sensation, but not all sensations are perceived. Receptors are the cells or structures that detect sensations. A receptor cell is changed directly by a stimulus. A transmembrane protein receptor is a protein in the cell membrane that mediates a physiological change in a neuron, most often through the opening of ion channels or changes in the cell signaling processes. Transmembrane receptors are activated by chemicals called ligands. For example, a molecule in food can serve as a ligand for taste receptors. Other transmembrane proteins, which are not accurately called receptors, are sensitive to mechanical or thermal changes. Physical changes in these proteins increase ion flow across the membrane, and can generate an action potential or a graded potential in the sensory neurons. Sensory Receptors Stimuli in the environment activate specialized receptor cells in the peripheral nervous system. Different types of stimuli are sensed by different types of receptor cells. Receptor cells can be classified into types on the basis of three different criteria: cell type, position, and function. Receptors can be classified structurally on the basis of cell type and their position in relation to stimuli they sense. They can also be classified functionally on the basis of the transduction of stimuli, or how the mechanical stimulus, light, or chemical changed the cell membrane potential. Structural Receptor Types The cells that interpret information about the environment can be either (1) a neuron that has a free nerve ending, with dendrites embedded in tissue that would receive a sensation; (2) a neuron that has an encapsulated ending in which the sensory nerve endings are encapsulated in connective tissue that enhances their sensitivity; or (3) a specialized receptor cell, which has distinct structural components that interpret a specific type of stimulus (Figure 14.2). The pain and temperature receptors in the dermis of the skin are examples of neurons that have free nerve endings. Also located in the dermis of the skin are lamellated corpuscles, neurons with encapsulated nerve endings that respond to pressure and touch. The cells in the retina that respond to light stimuli are an example of a specialized receptor, a photoreceptor. Figure 14.2 Receptor Classification by Cell Type Receptor cell types can be classified on the basis of their structure. Sensory neurons can have either (a) free nerve endings or (b) encapsulated endings. Photoreceptors in the eyes, such as rod cells, are examples of (c) specialized receptor cells. These cells release neurotransmitters onto a bipolar cell, which then synapses with the optic nerve neurons. Another way that receptors can be classified is based on their location relative to the stimuli. An exteroceptor is a receptor that is located near a stimulus in the external environment, such as the somatosensory receptors that are located in the skin. An interoceptor is one that interprets stimuli from internal organs and tissues, such as the receptors that sense the increase in blood pressure in the aorta or carotid sinus. Finally, a proprioceptor is a receptor located near a moving part of the body, such as a muscle, that interprets the positions of the tissues as they move. Functional Receptor Types A third classification of receptors is by how the receptor transduces stimuli into membrane potential changes. Stimuli are of three general types. Some stimuli are ions and macromolecules that affect transmembrane receptor proteins when these chemicals diffuse across the cell membrane. Some stimuli are physical variations in the environment that affect receptor cell membrane potentials. Other stimuli include the electromagnetic radiation from visible light. For humans, the only electromagnetic energy that is perceived by our eyes is visible light. Some other organisms have receptors that humans lack, such as the heat sensors of snakes, the ultraviolet light sensors of bees, or magnetic receptors in migratory birds. Receptor cells can be further categorized on the basis of the type of stimuli they transduce. Chemical stimuli can be interpreted by a chemoreceptor that interprets chemical stimuli, such as an object’s taste or smell. Osmoreceptors respond to solute concentrations of body fluids. Additionally, pain is primarily a chemical sense that interprets the presence of chemicals from tissue damage, or similar intense stimuli, through a nociceptor. Physical stimuli, such as pressure and vibration, as well as the sensation of sound and body position (balance), are interpreted through a mechanoreceptor. Another physical stimulus that has its own type of receptor is temperature, which is sensed through a thermoreceptor that is either sensitive to temperatures above (heat) or below (cold) normal body temperature. Sensory Modalities Ask anyone what the senses are, and they are likely to list the five major senses—taste, smell, touch, hearing, and sight. However, these are not all of the senses. The most obvious omission from this list is balance. Also, what is referred to simply as touch can be further subdivided into pressure, vibration, stretch, and hair-follicle position, on the basis of the type of mechanoreceptors that perceive these touch sensations. Other overlooked senses include temperature perception by thermoreceptors and pain perception by nociceptors. Within the realm of physiology, senses can be classified as either general or specific. A general sense is one that is distributed throughout the body and has receptor cells within the structures of other organs. Mechanoreceptors in the skin, muscles, or the walls of blood vessels are examples of this type. General senses often contribute to the sense of touch, as described above, or to proprioception (body movement) and kinesthesia (body movement), or to a visceral sense, which is most important to autonomic functions. A special sense is one that has a specific organ devoted to it, namely the eye, inner ear, tongue, or nose. Each of the senses is referred to as a sensory modality. Modality refers to the way that information is encoded, which is similar to the idea of transduction. The main sensory modalities can be described on the basis of how each is transduced. The chemical senses are taste and smell. The general sense that is usually referred to as touch includes chemical sensation in the form of nociception, or pain. Pressure, vibration, muscle stretch, and the movement of hair by an external stimulus, are all sensed by mechanoreceptors. Hearing and balance are also sensed by mechanoreceptors. Finally, vision involves the activation of photoreceptors. Listing all the different sensory modalities, which can number as many as 17, involves separating the five major senses into more specific categories, or submodalities, of the larger sense. An individual sensory modality represents the sensation of a specific type of stimulus. For example, the general sense of touch, which is known as somatosensation, can be separated into light pressure, deep pressure, vibration, itch, pain, temperature, or hair movement. Gustation (Taste) Only a few recognized submodalities exist within the sense of taste, or gustation. Until recently, only four tastes were recognized: sweet, salty, sour, and bitter. Research at the turn of the 20th century led to recognition of the fifth taste, umami, during the mid-1980s. Umami is a Japanese word that means “delicious taste,” and is often translated to mean savory. Very recent research has suggested that there may also be a sixth taste for fats, or lipids. Gustation is the special sense associated with the tongue. The surface of the tongue, along with the rest of the oral cavity, is lined by a stratified squamous epithelium. Raised bumps called papillae (singular = papilla) contain the structures for gustatory transduction. There are four types of papillae, based on their appearance (Figure 14.3): circumvallate, foliate, filiform, and fungiform. Within the structure of the papillae are taste buds that contain specialized gustatory receptor cells for the transduction of taste stimuli. These receptor cells are sensitive to the chemicals contained within foods that are ingested, and they release neurotransmitters based on the amount of the chemical in the food. Neurotransmitters from the gustatory cells can activate sensory neurons in the facial, glossopharyngeal, and vagus cranial nerves. Figure 14.3 The Tongue The tongue is covered with small bumps, called papillae, which contain taste buds that are sensitive to chemicals in ingested food or drink. Different types of papillae are found in different regions of the tongue. The taste buds contain specialized gustatory receptor cells that respond to chemical stimuli dissolved in the saliva. These receptor cells activate sensory neurons that are part of the facial and glossopharyngeal nerves. LM × 1600. (Micrograph provided by the Regents of University of Michigan Medical School © 2012) Salty taste is simply the perception of sodium ions (Na+) in the saliva. When you eat something salty, the salt crystals dissociate into the component ions Na+ and Cl–, which dissolve into the saliva in your mouth. The Na+ concentration becomes high outside the gustatory cells, creating a strong concentration gradient that drives the diffusion of the ion into the cells. The entry of Na+into these cells results in the depolarization of the cell membrane and the generation of a receptor potential. Sour taste is the perception of H+ concentration. Just as with sodium ions in salty flavors, these hydrogen ions enter the cell and trigger depolarization. Sour flavors are, essentially, the perception of acids in our food. Increasing hydrogen ion concentrations in the saliva (lowering saliva pH) triggers progressively stronger graded potentials in the gustatory cells. For example, orange juice—which contains citric acid—will taste sour because it has a pH value of approximately 3. Of course, it is often sweetened so that the sour taste is masked. The first two tastes (salty and sour) are triggered by the cations Na+ and H+. The other tastes result from food molecules binding to a G protein–coupled receptor. A G protein signal transduction system ultimately leads to depolarization of the gustatory cell. The sweet taste is the sensitivity of gustatory cells to the presence of glucose dissolved in the saliva. Other monosaccharides such as fructose, or artificial sweeteners such as aspartame (NutraSweet™), saccharine, or sucralose (Splenda™) also activate the sweet receptors. The affinity for each of these molecules varies, and some will taste sweeter than glucose because they bind to the G protein–coupled receptor differently. Bitter taste is similar to sweet in that food molecules bind to G protein–coupled receptors. However, there are a number of different ways in which this can happen because there are a large diversity of bitter-tasting molecules. Some bitter molecules depolarize gustatory cells, whereas others hyperpolarize gustatory cells. Likewise, some bitter molecules increase G protein activation within the gustatory cells, whereas other bitter molecules decrease G protein activation. The specific response depends on which molecule is binding to the receptor. One major group of bitter-tasting molecules are alkaloids. Alkaloids are nitrogen containing molecules that are commonly found in bitter-tasting plant products, such as coffee, hops (in beer), tannins (in wine), tea, and aspirin. By containing toxic alkaloids, the plant is less susceptible to microbe infection and less attractive to herbivores. Therefore, the function of bitter taste may primarily be related to stimulating the gag reflex to avoid ingesting poisons. Because of this, many bitter foods that are normally ingested are often combined with a sweet component to make them more palatable (cream and sugar in coffee, for example). The highest concentration of bitter receptors appear to be in the posterior tongue, where a gag reflex could still spit out poisonous food. The taste known as umami is often referred to as the savory taste. Like sweet and bitter, it is based on the activation of G protein–coupled receptors by a specific molecule. The molecule that activates this receptor is the amino acid L-glutamate. Therefore, the umami flavor is often perceived while eating protein-rich foods. Not surprisingly, dishes that contain meat are often described as savory. Once the gustatory cells are activated by the taste molecules, they release neurotransmitters onto the dendrites of sensory neurons. These neurons are part of the facial and glossopharyngeal cranial nerves, as well as a component within the vagus nerve dedicated to the gag reflex. The facial nerve connects to taste buds in the anterior third of the tongue. The glossopharyngeal nerve connects to taste buds in the posterior two thirds of the tongue. The vagus nerve connects to taste buds in the extreme posterior of the tongue, verging on the pharynx, which are more sensitive to noxious stimuli such as bitterness. INTERACTIVE LINK Watch this video to learn about Dr. Danielle Reed of the Monell Chemical Senses Center in Philadelphia, Pennsylvania, who became interested in science at an early age because of her sensory experiences. She recognized that her sense of taste was unique compared with other people she knew. Now, she studies the genetic differences between people and their sensitivities to taste stimuli. In the video, there is a brief image of a person sticking out their tongue, which has been covered with a colored dye. This is how Dr. Reed is able to visualize and count papillae on the surface of the tongue. People fall into two groups known as “tasters” and “non-tasters” based on the density of papillae on their tongue, which also indicates the number of taste buds. Non-tasters can taste food, but they are not as sensitive to certain tastes, such as bitterness. Dr. Reed discovered that she is a non-taster, which explains why she perceived bitterness differently than other people she knew. Are you very sensitive to tastes? Can you see any similarities among the members of your family? Olfaction (Smell) Like taste, the sense of smell, or olfaction, is also responsive to chemical stimuli. The olfactory receptor neurons are located in a small region within the superior nasal cavity (Figure 14.4). This region is referred to as the olfactory epithelium and contains bipolar sensory neurons. Each olfactory sensory neuron has dendrites that extend from the apical surface of the epithelium into the mucus lining the cavity. As airborne molecules are inhaled through the nose, they pass over the olfactory epithelial region and dissolve into the mucus. These odorant molecules bind to proteins that keep them dissolved in the mucus and help transport them to the olfactory dendrites. The odorant–protein complex binds to a receptor protein within the cell membrane of an olfactory dendrite. These receptors are G protein–coupled, and will produce a graded membrane potential in the olfactory neurons. The axon of an olfactory neuron extends from the basal surface of the epithelium, through an olfactory foramen in the cribriform plate of the ethmoid bone, and into the brain. The group of axons called the olfactory tract connect to the olfactory bulb on the ventral surface of the frontal lobe. From there, the axons split to travel to several brain regions. Some travel to the cerebrum, specifically to the primary olfactory cortex that is located in the inferior and medial areas of the temporal lobe. Others project to structures within the limbic system and hypothalamus, where smells become associated with long-term memory and emotional responses. This is how certain smells trigger emotional memories, such as the smell of food associated with one’s birthplace. Smell is the one sensory modality that does not synapse in the thalamus before connecting to the cerebral cortex. This intimate connection between the olfactory system and the cerebral cortex is one reason why smell can be a potent trigger of memories and emotion. The nasal epithelium, including the olfactory cells, can be harmed by airborne toxic chemicals. Therefore, the olfactory neurons are regularly replaced within the nasal epithelium, after which the axons of the new neurons must find their appropriate connections in the olfactory bulb. These new axons grow along the axons that are already in place in the cranial nerve. Figure 14.4 The Olfactory System (a) The olfactory system begins in the peripheral structures of the nasal cavity. (b) The olfactory receptor neurons are within the olfactory epithelium. (c) Axons of the olfactory receptor neurons project through the cribriform plate of the ethmoid bone and synapse with the neurons of the olfactory bulb (tissue source: simian). LM × 812. (Micrograph provided by the Regents of University of Michigan Medical School © 2012) DISORDERS OF THE... Olfactory System: Anosmia Blunt force trauma to the face, such as that common in many car accidents, can lead to the loss of the olfactory nerve, and subsequently, loss of the sense of smell. This condition is known as anosmia. When the frontal lobe of the brain moves relative to the ethmoid bone, the olfactory tract axons may be sheared apart. Professional fighters often experience anosmia because of repeated trauma to face and head. In addition, certain pharmaceuticals, such as antibiotics, can cause anosmia by killing all the olfactory neurons at once. If no axons are in place within the olfactory nerve, then the axons from newly formed olfactory neurons have no guide to lead them to their connections within the olfactory bulb. There are temporary causes of anosmia, as well, such as those caused by inflammatory responses related to respiratory infections or allergies. Loss of the sense of smell can result in food tasting bland. A person with an impaired sense of smell may require additional spice and seasoning levels for food to be tasted. Anosmia may also be related to some presentations of mild depression, because the loss of enjoyment of food may lead to a general sense of despair. The ability of olfactory neurons to replace themselves decreases with age, leading to age-related anosmia. This explains why some elderly people salt their food more than younger people do. However, this increased sodium intake can increase blood volume and blood pressure, increasing the risk of cardiovascular diseases in the elderly. Audition (Hearing) Hearing, or audition, is the transduction of sound waves into a neural signal that is made possible by the structures of the ear (Figure 14.5). The large, fleshy structure on the lateral aspect of the head is known as the auricle. Some sources will also refer to this structure as the pinna, though that term is more appropriate for a structure that can be moved, such as the external ear of a cat. The C-shaped curves of the auricle direct sound waves toward the auditory canal. The canal enters the skull through the external auditory meatus of the temporal bone. At the end of the auditory canal is the tympanic membrane, or ear drum, which vibrates after it is struck by sound waves. The auricle, ear canal, and tympanic membrane are often referred to as the external ear. The middle ear consists of a space spanned by three small bones called the ossicles. The three ossicles are the malleus, incus, and stapes, which are Latin names that roughly translate to hammer, anvil, and stirrup. The malleus is attached to the tympanic membrane and articulates with the incus. The incus, in turn, articulates with the stapes. The stapes is then attached to the inner ear, where the sound waves will be transduced into a neural signal. The middle ear is connected to the pharynx through the Eustachian tube, which helps equilibrate air pressure across the tympanic membrane. The tube is normally closed but will pop open when the muscles of the pharynx contract during swallowing or yawning. Figure 14.5 Structures of the Ear The external ear contains the auricle, ear canal, and tympanic membrane. The middle ear contains the ossicles and is connected to the pharynx by the Eustachian tube. The inner ear contains the cochlea and vestibule, which are responsible for audition and equilibrium, respectively. The inner ear is often described as a bony labyrinth, as it is composed of a series of canals embedded within the temporal bone. It has two separate regions, the cochlea and the vestibule, which are responsible for hearing and balance, respectively. The neural signals from these two regions are relayed to the brain stem through separate fiber bundles. However, these two distinct bundles travel together from the inner ear to the brain stem as the vestibulocochlear nerve. Sound is transduced into neural signals within the cochlear region of the inner ear, which contains the sensory neurons of the spiral ganglia. These ganglia are located within the spiral-shaped cochlea of the inner ear. The cochlea is attached to the stapes through the oval window. The oval window is located at the beginning of a fluid-filled tube within the cochlea called the scala vestibuli. The scala vestibuli extends from the oval window, travelling above the cochlear duct, which is the central cavity of the cochlea that contains the sound-transducing neurons. At the uppermost tip of the cochlea, the scala vestibuli curves over the top of the cochlear duct. The fluid-filled tube, now called the scala tympani, returns to the base of the cochlea, this time travelling under the cochlear duct. The scala tympani ends at the round window, which is covered by a membrane that contains the fluid within the scala. As vibrations of the ossicles travel through the oval window, the fluid of the scala vestibuli and scala tympani moves in a wave-like motion. The frequency of the fluid waves match the frequencies of the sound waves (Figure 14.6). The membrane covering the round window will bulge out or pucker in with the movement of the fluid within the scala tympani. Figure 14.6 Transmission of Sound Waves to Cochlea A sound wave causes the tympanic membrane to vibrate. This vibration is amplified as it moves across the malleus, incus, and stapes. The amplified vibration is picked up by the oval window causing pressure waves in the fluid of the scala vestibuli and scala tympani. The complexity of the pressure waves is determined by the changes in amplitude and frequency of the sound waves entering the ear. A cross-sectional view of the cochlea shows that the scala vestibuli and scala tympani run along both sides of the cochlear duct (Figure 14.7). The cochlear duct contains several organs of Corti, which tranduce the wave motion of the two scala into neural signals. The organs of Corti lie on top of the basilar membrane, which is the side of the cochlear duct located between the organs of Corti and the scala tympani. As the fluid waves move through the scala vestibuli and scala tympani, the basilar membrane moves at a specific spot, depending on the frequency of the waves. Higher frequency waves move the region of the basilar membrane that is close to the base of the cochlea. Lower frequency waves move the region of the basilar membrane that is near the tip of the cochlea. Figure 14.7 Cross Section of the Cochlea The three major spaces within the cochlea are highlighted. The scala tympani and scala vestibuli lie on either side of the cochlear duct. The organ of Corti, containing the mechanoreceptor hair cells, is adjacent to the scala tympani, where it sits atop the basilar membrane. The organs of Corti contain hair cells, which are named for the hair-like stereocilia extending from the cell’s apical surfaces (Figure 14.8). The stereocilia are an array of microvilli-like structures arranged from tallest to shortest. Protein fibers tether adjacent hairs together within each array, such that the array will bend in response to movements of the basilar membrane. The stereocilia extend up from the hair cells to the overlying tectorial membrane, which is attached medially to the organ of Corti. When the pressure waves from the scala move the basilar membrane, the tectorial membrane slides across the stereocilia. This bends the stereocilia either toward or away from the tallest member of each array. When the stereocilia bend toward the tallest member of their array, tension in the protein tethers opens ion channels in the hair cell membrane. This will depolarize the hair cell membrane, triggering nerve impulses that travel down the afferent nerve fibers attached to the hair cells. When the stereocilia bend toward the shortest member of their array, the tension on the tethers slackens and the ion channels close. When no sound is present, and the stereocilia are standing straight, a small amount of tension still exists on the tethers, keeping the membrane potential of the hair cell slightly depolarized. Figure 14.8 Hair Cell The hair cell is a mechanoreceptor with an array of stereocilia emerging from its apical surface. The stereocilia are tethered together by proteins that open ion channels when the array is bent toward the tallest member of their array, and closed when the array is bent toward the shortest member of their array. Figure 14.9 Cochlea and Organ of Corti LM × 412. (Micrograph provided by the Regents of University of Michigan Medical School © 2012) INTERACTIVE LINK View the University of Michigan WebScope to explore the tissue sample in greater detail. The basilar membrane is the thin membrane that extends from the central core of the cochlea to the edge. What is anchored to this membrane so that they can be activated by movement of the fluids within the cochlea? As stated above, a given region of the basilar membrane will only move if the incoming sound is at a specific frequency. Because the tectorial membrane only moves where the basilar membrane moves, the hair cells in this region will also only respond to sounds of this specific frequency. Therefore, as the frequency of a sound changes, different hair cells are activated all along the basilar membrane. The cochlea encodes auditory stimuli for frequencies between 20 and 20,000 Hz, which is the range of sound that human ears can detect. The unit of Hertz measures the frequency of sound waves in terms of cycles produced per second. Frequencies as low as 20 Hz are detected by hair cells at the apex, or tip, of the cochlea. Frequencies in the higher ranges of 20 KHz are encoded by hair cells at the base of the cochlea, close to the round and oval windows (Figure 14.10). Most auditory stimuli contain a mixture of sounds at a variety of frequencies and intensities (represented by the amplitude of the sound wave). The hair cells along the length of the cochlear duct, which are each sensitive to a particular frequency, allow the cochlea to separate auditory stimuli by frequency, just as a prism separates visible light into its component colors. Figure 14.10 Frequency Coding in the Cochlea The standing sound wave generated in the cochlea by the movement of the oval window deflects the basilar membrane on the basis of the frequency of sound. Therefore, hair cells at the base of the cochlea are activated only by high frequencies, whereas those at the apex of the cochlea are activated only by low frequencies. INTERACTIVE LINK Watch this video to learn more about how the structures of the ear convert sound waves into a neural signal by moving the “hairs,” or stereocilia, of the cochlear duct. Specific locations along the length of the duct encode specific frequencies, or pitches. The brain interprets the meaning of the sounds we hear as music, speech, noise, etc. Which ear structures are responsible for the amplification and transfer of sound from the external ear to the inner ear? INTERACTIVE LINK Watch this animation to learn more about the inner ear and to see the cochlea unroll, with the base at the back of the image and the apex at the front. Specific wavelengths of sound cause specific regions of the basilar membrane to vibrate, much like the keys of a piano produce sound at different frequencies. Based on the animation, where do frequencies—from high to low pitches—cause activity in the hair cells within the cochlear duct? Equilibrium (Balance) Along with audition, the inner ear is responsible for encoding information about equilibrium, the sense of balance. A similar mechanoreceptor—a hair cell with stereocilia—senses head position, head movement, and whether our bodies are in motion. These cells are located within the vestibule of the inner ear. Head position is sensed by the utricle and saccule, whereas head movement is sensed by the semicircular canals. The neural signals generated in the vestibular ganglion are transmitted through the vestibulocochlear nerve to the brain stem and cerebellum. The utricle and saccule are both largely composed of macula tissue (plural = maculae). The macula is composed of hair cells surrounded by support cells. The stereocilia of the hair cells extend into a viscous gel called the otolithic membrane (Figure 14.11). On top of the otolithic membrane is a layer of calcium carbonate crystals, called otoliths. The otoliths essentially make the otolithic membrane top-heavy. The otolithic membrane moves separately from the macula in response to head movements. Tilting the head causes the otolithic membrane to slide over the macula in the direction of gravity. The moving otolithic membrane, in turn, bends the sterocilia, causing some hair cells to depolarize as others hyperpolarize. The exact position of the head is interpreted by the brain based on the pattern of hair-cell depolarization. Figure 14.11 Linear Acceleration Coding by Maculae The maculae are specialized for sensing linear acceleration, such as when gravity acts on the tilting head, or if the head starts moving in a straight line. The difference in inertia between the hair cell stereocilia and the otolithic membrane in which they are embedded leads to a shearing force that causes the stereocilia to bend in the direction of that linear acceleration. The semicircular canals are three ring-like extensions of the vestibule. One is oriented in the horizontal plane, whereas the other two are oriented in the vertical plane. The anterior and posterior vertical canals are oriented at approximately 45 degrees relative to the sagittal plane (Figure 14.12). The base of each semicircular canal, where it meets with the vestibule, connects to an enlarged region known as the ampulla. The ampulla contains the hair cells that respond to rotational movement, such as turning the head while saying “no.” The stereocilia of these hair cells extend into the cupula, a membrane that attaches to the top of the ampulla. As the head rotates in a plane parallel to the semicircular canal, the fluid lags, deflecting the cupula in the direction opposite to the head movement. The semicircular canals contain several ampullae, with some oriented horizontally and others oriented vertically. By comparing the relative movements of both the horizontal and vertical ampullae, the vestibular system can detect the direction of most head movements within three-dimensional (3-D) space. Figure 14.12 Rotational Coding by Semicircular Canals Rotational movement of the head is encoded by the hair cells in the base of the semicircular canals. As one of the canals moves in an arc with the head, the internal fluid moves in the opposite direction, causing the cupula and stereocilia to bend. The movement of two canals within a plane results in information about the direction in which the head is moving, and activation of all six canals can give a very precise indication of head movement in three dimensions. Somatosensation (Touch) Somatosensation is considered a general sense, as opposed to the special senses discussed in this section. Somatosensation is the group of sensory modalities that are associated with touch, proprioception, and interoception. These modalities include pressure, vibration, light touch, tickle, itch, temperature, pain, proprioception, and kinesthesia. This means that its receptors are not associated with a specialized organ, but are instead spread throughout the body in a variety of organs. Many of the somatosensory receptors are located in the skin, but receptors are also found in muscles, tendons, joint capsules, ligaments, and in the walls of visceral organs. Two types of somatosensory signals that are transduced by free nerve endings are pain and temperature. These two modalities use thermoreceptors and nociceptors to transduce temperature and pain stimuli, respectively. Temperature receptors are stimulated when local temperatures differ from body temperature. Some thermoreceptors are sensitive to just cold and others to just heat. Nociception is the sensation of potentially damaging stimuli. Mechanical, chemical, or thermal stimuli beyond a set threshold will elicit painful sensations. Stressed or damaged tissues release chemicals that activate receptor proteins in the nociceptors. For example, the sensation of heat associated with spicy foods involves capsaicin, the active molecule in hot peppers. Capsaicin molecules bind to a transmembrane ion channel in nociceptors that is sensitive to temperatures above 37°C. The dynamics of capsaicin binding with this transmembrane ion channel is unusual in that the molecule remains bound for a long time. Because of this, it will decrease the ability of other stimuli to elicit pain sensations through the activated nociceptor. For this reason, capsaicin can be used as a topical analgesic, such as in products such as Icy Hot™. If you drag your finger across a textured surface, the skin of your finger will vibrate. Such low frequency vibrations are sensed by mechanoreceptors called Merkel cells, also known as type I cutaneous mechanoreceptors. Merkel cells are located in the stratum basale of the epidermis. Deep pressure and vibration is transduced by lamellated (Pacinian) corpuscles, which are receptors with encapsulated endings found deep in the dermis, or subcutaneous tissue. Light touch is transduced by the encapsulated endings known as tactile (Meissner) corpuscles. Follicles are also wrapped in a plexus of nerve endings known as the hair follicle plexus. These nerve endings detect the movement of hair at the surface of the skin, such as when an insect may be walking along the skin. Stretching of the skin is transduced by stretch receptors known as bulbous corpuscles. Bulbous corpuscles are also known as Ruffini corpuscles, or type II cutaneous mechanoreceptors. Other somatosensory receptors are found in the joints and muscles. Stretch receptors monitor the stretching of tendons, muscles, and the components of joints. For example, have you ever stretched your muscles before or after exercise and noticed that you can only stretch so far before your muscles spasm back to a less stretched state? This spasm is a reflex that is initiated by stretch receptors to avoid muscle tearing. Such stretch receptors can also prevent over-contraction of a muscle. In skeletal muscle tissue, these stretch receptors are called muscle spindles. Golgi tendon organs similarly transduce the stretch levels of tendons. Bulbous corpuscles are also present in joint capsules, where they measure stretch in the components of the skeletal system within the joint. The types of nerve endings, their locations, and the stimuli they transduce are presented in Table 14.1. Mechanoreceptors of Somatosensation \| Name \| Historical (eponymous) name \| Location(s) \| Stimuli \| \|---\|---\|---\|---\| \| Free nerve endings \| * \| Dermis, cornea, tongue, joint capsules, visceral organs \| Pain, temperature, mechanical deformation \| \| Mechanoreceptors \| Merkel’s discs \| Epidermal–dermal junction, mucosal membranes \| Low frequency vibration (5–15 Hz) \| \| Bulbous corpuscle \| Ruffini’s corpuscle \| Dermis, joint capsules \| Stretch \| \| Tactile corpuscle \| Meissner’s corpuscle \| Papillary dermis, especially in the fingertips and lips \| Light touch, vibrations below 50 Hz \| \| Lamellated corpuscle \| Pacinian corpuscle \| Deep dermis, subcutaneous tissue \| Deep pressure, high-frequency vibration (around 250 Hz) \| \| Hair follicle plexus \| * \| Wrapped around hair follicles in the dermis \| Movement of hair \| \| Muscle spindle \| * \| In line with skeletal muscle fibers \| Muscle contraction and stretch \| \| Tendon stretch organ \| Golgi tendon organ \| In line with tendons \| Stretch of tendons \| Table 14.1 *No corresponding eponymous name. Vision Vision is the special sense of sight that is based on the transduction of light stimuli received through the eyes. The eyes are located within either orbit in the skull. The bony orbits surround the eyeballs, protecting them and anchoring the soft tissues of the eye (Figure 14.13). The eyelids, with lashes at their leading edges, help to protect the eye from abrasions by blocking particles that may land on the surface of the eye. The inner surface of each lid is a thin membrane known as the palpebral conjunctiva. The conjunctiva extends over the white areas of the eye (the sclera), connecting the eyelids to the eyeball. Tears are produced by the lacrimal gland, located beneath the lateral edges of the nose. Tears produced by this gland flow through the lacrimal duct to the medial corner of the eye, where the tears flow over the conjunctiva, washing away foreign particles. Figure 14.13 The Eye in the Orbit The eye is located within the orbit and surrounded by soft tissues that protect and support its function. The orbit is surrounded by cranial bones of the skull. Movement of the eye within the orbit is accomplished by the contraction of six extraocular muscles that originate from the bones of the orbit and insert into the surface of the eyeball (Figure 14.14). Four of the muscles are arranged at the cardinal points around the eye and are named for those locations. They are the superior rectus, medial rectus, inferior rectus, and lateral rectus. When each of these muscles contract, the eye moves toward the contracting muscle. For example, when the superior rectus contracts, the eye rotates to look up. The superior oblique originates at the posterior orbit, near the origin of the four rectus muscles. However, the tendon of the oblique muscles threads through a pulley-like piece of cartilage known as the trochlea. The tendon inserts obliquely into the superior surface of the eye. The angle of the tendon through the trochlea means that contraction of the superior oblique rotates the eye medially. The inferior oblique muscle originates from the floor of the orbit and inserts into the inferolateral surface of the eye. When it contracts, it laterally rotates the eye, in opposition to the superior oblique. Rotation of the eye by the two oblique muscles is necessary because the eye is not perfectly aligned on the sagittal plane. When the eye looks up or down, the eye must also rotate slightly to compensate for the superior rectus pulling at approximately a 20-degree angle, rather than straight up. The same is true for the inferior rectus, which is compensated by contraction of the inferior oblique. A seventh muscle in the orbit is the levator palpebrae superioris, which is responsible for elevating and retracting the upper eyelid, a movement that usually occurs in concert with elevation of the eye by the superior rectus (see Figure 14.13). The extraocular muscles are innervated by three cranial nerves. The lateral rectus, which causes abduction of the eye, is innervated by the abducens nerve. The superior oblique is innervated by the trochlear nerve. All of the other muscles are innervated by the oculomotor nerve, as is the levator palpebrae superioris. The motor nuclei of these cranial nerves connect to the brain stem, which coordinates eye movements. Figure 14.14 Extraocular Muscles The extraocular muscles move the eye within the orbit. The eye itself is a hollow sphere composed of three layers of tissue. The outermost layer is the fibrous tunic, which includes the white sclera and clear cornea. The sclera accounts for five sixths of the surface of the eye, most of which is not visible, though humans are unique compared with many other species in having so much of the “white of the eye” visible (Figure 14.15). The transparent cornea covers the anterior tip of the eye and allows light to enter the eye. The middle layer of the eye is the vascular tunic, which is mostly composed of the choroid, ciliary body, and iris. The choroid is a layer of highly vascularized connective tissue that provides a blood supply to the eyeball. The choroid is posterior to the ciliary body, a muscular structure that is attached to the lens by suspensory ligaments, or zonule fibers. These two structures bend the lens, allowing it to focus light on the back of the eye. Overlaying the ciliary body, and visible in the anterior eye, is the iris—the colored part of the eye. The iris is a smooth muscle that opens or closes the pupil, which is the hole at the center of the eye that allows light to enter. The iris constricts the pupil in response to bright light and dilates the pupil in response to dim light. The innermost layer of the eye is the neural tunic, or retina, which contains the nervous tissue responsible for photoreception. The eye is also divided into two cavities: the anterior cavity and the posterior cavity. The anterior cavity is the space between the cornea and lens, including the iris and ciliary body. It is filled with a watery fluid called the aqueous humor. The posterior cavity is the space behind the lens that extends to the posterior side of the interior eyeball, where the retina is located. The posterior cavity is filled with a more viscous fluid called the vitreous humor. The retina is composed of several layers and contains specialized cells for the initial processing of visual stimuli. The photoreceptors (rods and cones) change their membrane potential when stimulated by light energy. The change in membrane potential alters the amount of neurotransmitter that the photoreceptor cells release onto bipolar cells in the outer synaptic layer. It is the bipolar cell in the retina that connects a photoreceptor to a retinal ganglion cell (RGC) in the inner synaptic layer. There, amacrine cells additionally contribute to retinal processing before an action potential is produced by the RGC. The axons of RGCs, which lie at the innermost layer of the retina, collect at the optic disc and leave the eye as the optic nerve(see Figure 14.15). Because these axons pass through the retina, there are no photoreceptors at the very back of the eye, where the optic nerve begins. This creates a “blind spot” in the retina, and a corresponding blind spot in our visual field. Figure 14.15 Structure of the Eye The sphere of the eye can be divided into anterior and posterior chambers. The wall of the eye is composed of three layers: the fibrous tunic, vascular tunic, and neural tunic. Within the neural tunic is the retina, with three layers of cells and two synaptic layers in between. The center of the retina has a small indentation known as the fovea. Note that the photoreceptors in the retina (rods and cones) are located behind the axons, RGCs, bipolar cells, and retinal blood vessels. A significant amount of light is absorbed by these structures before the light reaches the photoreceptor cells. However, at the exact center of the retina is a small area known as the fovea. At the fovea, the retina lacks the supporting cells and blood vessels, and only contains photoreceptors. Therefore, visual acuity, or the sharpness of vision, is greatest at the fovea. This is because the fovea is where the least amount of incoming light is absorbed by other retinal structures (see Figure 14.15). As one moves in either direction from this central point of the retina, visual acuity drops significantly. In addition, each photoreceptor cell of the fovea is connected to a single RGC. Therefore, this RGC does not have to integrate inputs from multiple photoreceptors, which reduces the accuracy of visual transduction. Toward the edges of the retina, several photoreceptors converge on RGCs (through the bipolar cells) up to a ratio of 50 to 1. The difference in visual acuity between the fovea and peripheral retina is easily evidenced by looking directly at a word in the middle of this paragraph. The visual stimulus in the middle of the field of view falls on the fovea and is in the sharpest focus. Without moving your eyes off that word, notice that words at the beginning or end of the paragraph are not in focus. The images in your peripheral vision are focused by the peripheral retina, and have vague, blurry edges and words that are not as clearly identified. As a result, a large part of the neural function of the eyes is concerned with moving the eyes and head so that important visual stimuli are centered on the fovea. Light falling on the retina causes chemical changes to pigment molecules in the photoreceptors, ultimately leading to a change in the activity of the RGCs. Photoreceptor cells have two parts, the inner segment and the outer segment (Figure 14.16). The inner segment contains the nucleus and other common organelles of a cell, whereas the outer segment is a specialized region in which photoreception takes place. There are two types of photoreceptors—rods and cones—which differ in the shape of their outer segment. The rod-shaped outer segments of the rod photoreceptor contain a stack of membrane-bound discs that contain the photosensitive pigment rhodopsin. The cone-shaped outer segments of the cone photoreceptor contain their photosensitive pigments in infoldings of the cell membrane. There are three cone photopigments, called opsins, which are each sensitive to a particular wavelength of light. The wavelength of visible light determines its color. The pigments in human eyes are specialized in perceiving three different primary colors: red, green, and blue. Figure 14.16 Photoreceptor (a) All photoreceptors have inner segments containing the nucleus and other important organelles and outer segments with membrane arrays containing the photosensitive opsin molecules. Rod outer segments are long columnar shapes with stacks of membrane-bound discs that contain the rhodopsin pigment. Cone outer segments are short, tapered shapes with folds of membrane in place of the discs in the rods. (b) Tissue of the retina shows a dense layer of nuclei of the rods and cones. LM × 800. (Micrograph provided by the Regents of University of Michigan Medical School © 2012) At the molecular level, visual stimuli cause changes in the photopigment molecule that lead to changes in membrane potential of the photoreceptor cell. A single unit of light is called a photon, which is described in physics as a packet of energy with properties of both a particle and a wave. The energy of a photon is represented by its wavelength, with each wavelength of visible light corresponding to a particular color. Visible light is electromagnetic radiation with a wavelength between 380 and 720 nm. Wavelengths of electromagnetic radiation longer than 720 nm fall into the infrared range, whereas wavelengths shorter than 380 nm fall into the ultraviolet range. Light with a wavelength of 380 nm is blue whereas light with a wavelength of 720 nm is dark red. All other colors fall between red and blue at various points along the wavelength scale. Opsin pigments are actually transmembrane proteins that contain a cofactor known as retinal. Retinal is a hydrocarbon molecule related to vitamin A. When a photon hits retinal, the long hydrocarbon chain of the molecule is biochemically altered. Specifically, photons cause some of the double-bonded carbons within the chain to switch from a cis to a trans conformation. This process is called photoisomerization. Before interacting with a photon, retinal’s flexible double-bonded carbons are in the cis conformation. This molecule is referred to as 11-cis-retinal. A photon interacting with the molecule causes the flexible double-bonded carbons to change to the trans- conformation, forming all-trans-retinal, which has a straight hydrocarbon chain (Figure 14.17). The shape change of retinal in the photoreceptors initiates visual transduction in the retina. Activation of retinal and the opsin proteins result in activation of a G protein. The G protein changes the membrane potential of the photoreceptor cell, which then releases less neurotransmitter into the outer synaptic layer of the retina. Until the retinal molecule is changed back to the 11-cis-retinal shape, the opsin cannot respond to light energy, which is called bleaching. When a large group of photopigments is bleached, the retina will send information as if opposing visual information is being perceived. After a bright flash of light, afterimages are usually seen in negative. The photoisomerization is reversed by a series of enzymatic changes so that the retinal responds to more light energy. Figure 14.17 Retinal Isomers The retinal molecule has two isomers, (a) one before a photon interacts with it and (b) one that is altered through photoisomerization. The opsins are sensitive to limited wavelengths of light. Rhodopsin, the photopigment in rods, is most sensitive to light at a wavelength of 498 nm. The three color opsins have peak sensitivities of 564 nm, 534 nm, and 420 nm corresponding roughly to the primary colors of red, green, and blue (Figure 14.18). The absorbance of rhodopsin in the rods is much more sensitive than in the cone opsins; specifically, rods are sensitive to vision in low light conditions, and cones are sensitive to brighter conditions. In normal sunlight, rhodopsin will be constantly bleached while the cones are active. In a darkened room, there is not enough light to activate cone opsins, and vision is entirely dependent on rods. Rods are so sensitive to light that a single photon can result in an action potential from a rod’s corresponding RGC. The three types of cone opsins, being sensitive to different wavelengths of light, provide us with color vision. By comparing the activity of the three different cones, the brain can extract color information from visual stimuli. For example, a bright blue light that has a wavelength of approximately 450 nm would activate the “red” cones minimally, the “green” cones marginally, and the “blue” cones predominantly. The relative activation of the three different cones is calculated by the brain, which perceives the color as blue. However, cones cannot react to low-intensity light, and rods do not sense the color of light. Therefore, our low-light vision is—in essence—in grayscale. In other words, in a dark room, everything appears as a shade of gray. If you think that you can see colors in the dark, it is most likely because your brain knows what color something is and is relying on that memory. Figure 14.18 Comparison of Color Sensitivity of Photopigments Comparing the peak sensitivity and absorbance spectra of the four photopigments suggests that they are most sensitive to particular wavelengths. INTERACTIVE LINK Watch this video to learn more about a transverse section through the brain that depicts the visual pathway from the eye to the occipital cortex. The first half of the pathway is the projection from the RGCs through the optic nerve to the lateral geniculate nucleus in the thalamus on either side. This first fiber in the pathway synapses on a thalamic cell that then projects to the visual cortex in the occipital lobe where “seeing,” or visual perception, takes place. This video gives an abbreviated overview of the visual system by concentrating on the pathway from the eyes to the occipital lobe. The video makes the statement (at 0:45) that “specialized cells in the retina called ganglion cells convert the light rays into electrical signals.” What aspect of retinal processing is simplified by that statement? Explain your answer. Sensory Nerves Once any sensory cell transduces a stimulus into a nerve impulse, that impulse has to travel along axons to reach the CNS. In many of the special senses, the axons leaving the sensory receptors have a topographical arrangement, meaning that the location of the sensory receptor relates to the location of the axon in the nerve. For example, in the retina, axons from RGCs in the fovea are located at the center of the optic nerve, where they are surrounded by axons from the more peripheral RGCs. Spinal Nerves Generally, spinal nerves contain afferent axons from sensory receptors in the periphery, such as from the skin, mixed with efferent axons travelling to the muscles or other effector organs. As the spinal nerve nears the spinal cord, it splits into dorsal and ventral roots. The dorsal root contains only the axons of sensory neurons, whereas the ventral roots contain only the axons of the motor neurons. Some of the branches will synapse with local neurons in the dorsal root ganglion, posterior (dorsal) horn, or even the anterior (ventral) horn, at the level of the spinal cord where they enter. Other branches will travel a short distance up or down the spine to interact with neurons at other levels of the spinal cord. A branch may also turn into the posterior (dorsal) column of the white matter to connect with the brain. For the sake of convenience, we will use the terms ventral and dorsal in reference to structures within the spinal cord that are part of these pathways. This will help to underscore the relationships between the different components. Typically, spinal nerve systems that connect to the brain are contralateral, in that the right side of the body is connected to the left side of the brain and the left side of the body to the right side of the brain. Cranial Nerves Cranial nerves convey specific sensory information from the head and neck directly to the brain. For sensations below the neck, the right side of the body is connected to the left side of the brain and the left side of the body to the right side of the brain. Whereas spinal information is contralateral, cranial nerve systems are mostly ipsilateral, meaning that a cranial nerve on the right side of the head is connected to the right side of the brain. Some cranial nerves contain only sensory axons, such as the olfactory, optic, and vestibulocochlear nerves. Other cranial nerves contain both sensory and motor axons, including the trigeminal, facial, glossopharyngeal, and vagus nerves (however, the vagus nerve is not associated with the somatic nervous system). The general senses of somatosensation for the face travel through the trigeminal system. Central Processing - Describe the pathways that sensory systems follow into the central nervous system - Differentiate between the two major ascending pathways in the spinal cord - Describe the pathway of somatosensory input from the face and compare it to the ascending pathways in the spinal cord - Explain topographical representations of sensory information in at least two systems - Describe two pathways of visual processing and the functions associated with each Sensory Pathways Specific regions of the CNS coordinate different somatic processes using sensory inputs and motor outputs of peripheral nerves. A simple case is a reflex caused by a synapse between a dorsal sensory neuron axon and a motor neuron in the ventral horn. More complex arrangements are possible to integrate peripheral sensory information with higher processes. The important regions of the CNS that play a role in somatic processes can be separated into the spinal cord brain stem, diencephalon, cerebral cortex, and subcortical structures. Spinal Cord and Brain Stem A sensory pathway that carries peripheral sensations to the brain is referred to as an ascending pathway, or ascending tract. The various sensory modalities each follow specific pathways through the CNS. Tactile and other somatosensory stimuli activate receptors in the skin, muscles, tendons, and joints throughout the entire body. However, the somatosensory pathways are divided into two separate systems on the basis of the location of the receptor neurons. Somatosensory stimuli from below the neck pass along the sensory pathways of the spinal cord, whereas somatosensory stimuli from the head and neck travel through the cranial nerves—specifically, the trigeminal system. The dorsal column system (sometimes referred to as the dorsal column–medial lemniscus) and the spinothalamic tract are two major pathways that bring sensory information to the brain (Figure 14.19). The sensory pathways in each of these systems are composed of three successive neurons. The dorsal column system begins with the axon of a dorsal root ganglion neuron entering the dorsal root and joining the dorsal column white matter in the spinal cord. As axons of this pathway enter the dorsal column, they take on a positional arrangement so that axons from lower levels of the body position themselves medially, whereas axons from upper levels of the body position themselves laterally. The dorsal column is separated into two component tracts, the fasciculus gracilis that contains axons from the legs and lower body, and the fasciculus cuneatus that contains axons from the upper body and arms. The axons in the dorsal column terminate in the nuclei of the medulla, where each synapses with the second neuron in their respective pathway. The nucleus gracilis is the target of fibers in the fasciculus gracilis, whereas the nucleus cuneatus is the target of fibers in the fasciculus cuneatus. The second neuron in the system projects from one of the two nuclei and then decussates, or crosses the midline of the medulla. These axons then continue to ascend the brain stem as a bundle called the medial lemniscus. These axons terminate in the thalamus, where each synapses with the third neuron in their respective pathway. The third neuron in the system projects its axons to the postcentral gyrus of the cerebral cortex, where somatosensory stimuli are initially processed and the conscious perception of the stimulus occurs. The spinothalamic tract also begins with neurons in a dorsal root ganglion. These neurons extend their axons to the dorsal horn, where they synapse with the second neuron in their respective pathway. The name “spinothalamic” comes from this second neuron, which has its cell body in the spinal cord gray matter and connects to the thalamus. Axons from these second neurons then decussate within the spinal cord and ascend to the brain and enter the thalamus, where each synapses with the third neuron in its respective pathway. The neurons in the thalamus then project their axons to the spinothalamic tract, which synapses in the postcentral gyrus of the cerebral cortex. These two systems are similar in that they both begin with dorsal root ganglion cells, as with most general sensory information. The dorsal column system is primarily responsible for touch sensations and proprioception, whereas the spinothalamic tract pathway is primarily responsible for pain and temperature sensations. Another similarity is that the second neurons in both of these pathways are contralateral, because they project across the midline to the other side of the brain or spinal cord. In the dorsal column system, this decussation takes place in the brain stem; in the spinothalamic pathway, it takes place in the spinal cord at the same spinal cord level at which the information entered. The third neurons in the two pathways are essentially the same. In both, the second neuron synapses in the thalamus, and the thalamic neuron projects to the somatosensory cortex. Figure 14.19 Ascending Sensory Pathways of the Spinal Cord The dorsal column system and spinothalamic tract are the major ascending pathways that connect the periphery with the brain. The trigeminal pathway carries somatosensory information from the face, head, mouth, and nasal cavity. As with the previously discussed nerve tracts, the sensory pathways of the trigeminal pathway each involve three successive neurons. First, axons from the trigeminal ganglion enter the brain stem at the level of the pons. These axons project to one of three locations. The spinal trigeminal nucleus of the medulla receives information similar to that carried by spinothalamic tract, such as pain and temperature sensations. Other axons go to either the chief sensory nucleus in the pons or the mesencephalic nuclei in the midbrain. These nuclei receive information like that carried by the dorsal column system, such as touch, pressure, vibration, and proprioception. Axons from the second neuron decussate and ascend to the thalamus along the trigeminothalamic tract. In the thalamus, each axon synapses with the third neuron in its respective pathway. Axons from the third neuron then project from the thalamus to the primary somatosensory cortex of the cerebrum. The sensory pathway for gustation travels along the facial and glossopharyngeal cranial nerves, which synapse with neurons of the solitary nucleus in the brain stem. Axons from the solitary nucleus then project to the ventral posterior nucleus of the thalamus. Finally, axons from the ventral posterior nucleus project to the gustatory cortex of the cerebral cortex, where taste is processed and consciously perceived. The sensory pathway for audition travels along the vestibulocochlear nerve, which synapses with neurons in the cochlear nuclei of the superior medulla. Within the brain stem, input from either ear is combined to extract location information from the auditory stimuli. Whereas the initial auditory stimuli received at the cochlea strictly represent the frequency—or pitch—of the stimuli, the locations of sounds can be determined by comparing information arriving at both ears. Sound localization is a feature of central processing in the auditory nuclei of the brain stem. Sound localization is achieved by the brain calculating the interaural time difference and the interaural intensity difference. A sound originating from a specific location will arrive at each ear at different times, unless the sound is directly in front of the listener. If the sound source is slightly to the left of the listener, the sound will arrive at the left ear microseconds before it arrives at the right ear (Figure 14.20). This time difference is an example of an interaural time difference. Also, the sound will be slightly louder in the left ear than in the right ear because some of the sound waves reaching the opposite ear are blocked by the head. This is an example of an interaural intensity difference. Figure 14.20 Auditory Brain Stem Mechanisms of Sound Localization Localizing sound in the horizontal plane is achieved by processing in the medullary nuclei of the auditory system. Connections between neurons on either side are able to compare very slight differences in sound stimuli that arrive at either ear and represent interaural time and intensity differences. Auditory processing continues on to a nucleus in the midbrain called the inferior colliculus. Axons from the inferior colliculus project to two locations, the thalamus and the superior colliculus. The medial geniculate nucleus of the thalamus receives the auditory information and then projects that information to the auditory cortex in the temporal lobe of the cerebral cortex. The superior colliculus receives input from the visual and somatosensory systems, as well as the ears, to initiate stimulation of the muscles that turn the head and neck toward the auditory stimulus. Balance is coordinated through the vestibular system, the nerves of which are composed of axons from the vestibular ganglion that carries information from the utricle, saccule, and semicircular canals. The system contributes to controlling head and neck movements in response to vestibular signals. An important function of the vestibular system is coordinating eye and head movements to maintain visual attention. Most of the axons terminate in the vestibular nuclei of the medulla. Some axons project from the vestibular ganglion directly to the cerebellum, with no intervening synapse in the vestibular nuclei. The cerebellum is primarily responsible for initiating movements on the basis of equilibrium information. Neurons in the vestibular nuclei project their axons to targets in the brain stem. One target is the reticular formation, which influences respiratory and cardiovascular functions in relation to body movements. A second target of the axons of neurons in the vestibular nuclei is the spinal cord, which initiates the spinal reflexes involved with posture and balance. To assist the visual system, fibers of the vestibular nuclei project to the oculomotor, trochlear, and abducens nuclei to influence signals sent along the cranial nerves. These connections constitute the pathway of the vestibulo-ocular reflex (VOR), which compensates for head and body movement by stabilizing images on the retina (Figure 14.21). Finally, the vestibular nuclei project to the thalamus to join the proprioceptive pathway of the dorsal column system, allowing conscious perception of equilibrium. Figure 14.21 Vestibulo-ocular Reflex Connections between the vestibular system and the cranial nerves controlling eye movement keep the eyes centered on a visual stimulus, even though the head is moving. During head movement, the eye muscles move the eyes in the opposite direction as the head movement, keeping the visual stimulus centered in the field of view. The connections of the optic nerve are more complicated than those of other cranial nerves. Instead of the connections being between each eye and the brain, visual information is segregated between the left and right sides of the visual field. In addition, some of the information from one side of the visual field projects to the opposite side of the brain. Within each eye, the axons projecting from the medial side of the retina decussate at the optic chiasm. For example, the axons from the medial retina of the left eye cross over to the right side of the brain at the optic chiasm. However, within each eye, the axons projecting from the lateral side of the retina do not decussate. For example, the axons from the lateral retina of the right eye project back to the right side of the brain. Therefore the left field of view of each eye is processed on the right side of the brain, whereas the right field of view of each eye is processed on the left side of the brain (Figure 14.22). Figure 14.22 Segregation of Visual Field Information at the Optic Chiasm Contralateral visual field information from the lateral retina projects to the ipsilateral brain, whereas ipsilateral visual field information has to decussate at the optic chiasm to reach the opposite side of the brain. (Note that this is an inferior view.) A unique clinical presentation that relates to this anatomic arrangement is the loss of lateral peripheral vision, known as bilateral hemianopia. This is different from “tunnel vision” because the superior and inferior peripheral fields are not lost. Visual field deficits can be disturbing for a patient, but in this case, the cause is not within the visual system itself. A growth of the pituitary gland presses against the optic chiasm and interferes with signal transmission. However, the axons projecting to the same side of the brain are unaffected. Therefore, the patient loses the outermost areas of their field of vision and cannot see objects to their right and left. Extending from the optic chiasm, the axons of the visual system are referred to as the optic tract instead of the optic nerve. The optic tract has three major targets, two in the diencephalon and one in the midbrain. The connection between the eyes and diencephalon is demonstrated during development, in which the neural tissue of the retina differentiates from that of the diencephalon by the growth of the secondary vesicles. The connections of the retina into the CNS are a holdover from this developmental association. The majority of the connections of the optic tract are to the thalamus—specifically, the lateral geniculate nucleus. Axons from this nucleus then project to the visual cortex of the cerebrum, located in the occipital lobe. Another target of the optic tract is the superior colliculus. In addition, a very small number of RGC axons project from the optic chiasm to the suprachiasmatic nucleus of the hypothalamus. These RGCs are photosensitive, in that they respond to the presence or absence of light. Unlike the photoreceptors, however, these photosensitive RGCs cannot be used to perceive images. By simply responding to the absence or presence of light, these RGCs can send information about day length. The perceived proportion of sunlight to darkness establishes the circadian rhythm of our bodies, allowing certain physiological events to occur at approximately the same time every day. Diencephalon The diencephalon is beneath the cerebrum and includes the thalamus and hypothalamus. In the somatic nervous system, the thalamus is an important relay for communication between the cerebrum and the rest of the nervous system. The hypothalamus has both somatic and autonomic functions. In addition, the hypothalamus communicates with the limbic system, which controls emotions and memory functions. Sensory input to the thalamus comes from most of the special senses and ascending somatosensory tracts. Each sensory system is relayed through a particular nucleus in the thalamus. The thalamus is a required transfer point for most sensory tracts that reach the cerebral cortex, where conscious sensory perception begins. The one exception to this rule is the olfactory system. The olfactory tract axons from the olfactory bulb project directly to the cerebral cortex, along with the limbic system and hypothalamus. The thalamus is a collection of several nuclei that can be categorized into three anatomical groups. White matter running through the thalamus defines the three major regions of the thalamus, which are an anterior nucleus, a medial nucleus, and a lateral group of nuclei. The anterior nucleus serves as a relay between the hypothalamus and the emotion and memory-producing limbic system. The medial nuclei serve as a relay for information from the limbic system and basal ganglia to the cerebral cortex. This allows memory creation during learning, but also determines alertness. The special and somatic senses connect to the lateral nuclei, where their information is relayed to the appropriate sensory cortex of the cerebrum. Cortical Processing As described earlier, many of the sensory axons are positioned in the same way as their corresponding receptor cells in the body. This allows identification of the position of a stimulus on the basis of which receptor cells are sending information. The cerebral cortex also maintains this sensory topography in the particular areas of the cortex that correspond to the position of the receptor cells. The somatosensory cortex provides an example in which, in essence, the locations of the somatosensory receptors in the body are mapped onto the somatosensory cortex. This mapping is often depicted using a sensory homunculus (Figure 14.23). The term homunculus comes from the Latin word for “little man” and refers to a map of the human body that is laid across a portion of the cerebral cortex. In the somatosensory cortex, the external genitals, feet, and lower legs are represented on the medial face of the gyrus within the longitudinal fissure. As the gyrus curves out of the fissure and along the surface of the parietal lobe, the body map continues through the thighs, hips, trunk, shoulders, arms, and hands. The head and face are just lateral to the fingers as the gyrus approaches the lateral sulcus. The representation of the body in this topographical map is medial to lateral from the lower to upper body. It is a continuation of the topographical arrangement seen in the dorsal column system, where axons from the lower body are carried in the fasciculus gracilis, whereas axons from the upper body are carried in the fasciculus cuneatus. As the dorsal column system continues into the medial lemniscus, these relationships are maintained. Also, the head and neck axons running from the trigeminal nuclei to the thalamus run adjacent to the upper body fibers. The connections through the thalamus maintain topography such that the anatomic information is preserved. Note that this correspondence does not result in a perfectly miniature scale version of the body, but rather exaggerates the more sensitive areas of the body, such as the fingers and lower face. Less sensitive areas of the body, such as the shoulders and back, are mapped to smaller areas on the cortex. Figure 14.23 The Sensory Homunculus A cartoon representation of the sensory homunculus arranged adjacent to the cortical region in which the processing takes place. Likewise, the topographic relationship between the retina and the visual cortex is maintained throughout the visual pathway. The visual field is projected onto the two retinae, as described above, with sorting at the optic chiasm. The right peripheral visual field falls on the medial portion of the right retina and the lateral portion of the left retina. The right medial retina then projects across the midline through the optic chiasm. This results in the right visual field being processed in the left visual cortex. Likewise, the left visual field is processed in the right visual cortex (see Figure 14.22). Though the chiasm is helping to sort right and left visual information, superior and inferior visual information is maintained topographically in the visual pathway. Light from the superior visual field falls on the inferior retina, and light from the inferior visual field falls on the superior retina. This topography is maintained such that the superior region of the visual cortex processes the inferior visual field and vice versa. Therefore, the visual field information is inverted and reversed as it enters the visual cortex—up is down, and left is right. However, the cortex processes the visual information such that the final conscious perception of the visual field is correct. The topographic relationship is evident in that information from the foveal region of the retina is processed in the center of the primary visual cortex. Information from the peripheral regions of the retina are correspondingly processed toward the edges of the visual cortex. Similar to the exaggerations in the sensory homunculus of the somatosensory cortex, the foveal-processing area of the visual cortex is disproportionately larger than the areas processing peripheral vision. In an experiment performed in the 1960s, subjects wore prism glasses so that the visual field was inverted before reaching the eye. On the first day of the experiment, subjects would duck when walking up to a table, thinking it was suspended from the ceiling. However, after a few days of acclimation, the subjects behaved as if everything were represented correctly. Therefore, the visual cortex is somewhat flexible in adapting to the information it receives from our eyes (Figure 14.24). Figure 14.24 Topographic Mapping of the Retina onto the Visual Cortex The visual field projects onto the retina through the lenses and falls on the retinae as an inverted, reversed image. The topography of this image is maintained as the visual information travels through the visual pathway to the cortex. The cortex has been described as having specific regions that are responsible for processing specific information; there is the visual cortex, somatosensory cortex, gustatory cortex, etc. However, our experience of these senses is not divided. Instead, we experience what can be referred to as a seamless percept. Our perceptions of the various sensory modalities—though distinct in their content—are integrated by the brain so that we experience the world as a continuous whole. In the cerebral cortex, sensory processing begins at the primary sensory cortex, then proceeds to an association area, and finally, into a multimodal integration area. For example, the visual pathway projects from the retinae through the thalamus to the primary visual cortex in the occipital lobe. This area is primarily in the medial wall within the longitudinal fissure. Here, visual stimuli begin to be recognized as basic shapes. Edges of objects are recognized and built into more complex shapes. Also, inputs from both eyes are compared to extract depth information. Because of the overlapping field of view between the two eyes, the brain can begin to estimate the distance of stimuli based on binocular depth cues. INTERACTIVE LINK Watch this video to learn more about how the brain perceives 3-D motion. Similar to how retinal disparity offers 3-D moviegoers a way to extract 3-D information from the two-dimensional visual field projected onto the retina, the brain can extract information about movement in space by comparing what the two eyes see. If movement of a visual stimulus is leftward in one eye and rightward in the opposite eye, the brain interprets this as movement toward (or away) from the face along the midline. If both eyes see an object moving in the same direction, but at different rates, what would that mean for spatial movement? EVERYDAY CONNECTION Depth Perception, 3-D Movies, and Optical Illusions The visual field is projected onto the retinal surface, where photoreceptors transduce light energy into neural signals for the brain to interpret. The retina is a two-dimensional surface, so it does not encode three-dimensional information. However, we can perceive depth. How is that accomplished? Two ways in which we can extract depth information from the two-dimensional retinal signal are based on monocular cues and binocular cues, respectively. Monocular depth cues are those that are the result of information within the two-dimensional visual field. One object that overlaps another object has to be in front. Relative size differences are also a cue. For example, if a basketball appears larger than the basket, then the basket must be further away. On the basis of experience, we can estimate how far away the basket is. Binocular depth cues compare information represented in the two retinae because they do not see the visual field exactly the same. The centers of the two eyes are separated by a small distance, which is approximately 6 to 6.5 cm in most people. Because of this offset, visual stimuli do not fall on exactly the same spot on both retinae unless we are fixated directly on them and they fall on the fovea of each retina. All other objects in the visual field, either closer or farther away than the fixated object, will fall on different spots on the retina. When vision is fixed on an object in space, closer objects will fall on the lateral retina of each eye, and more distant objects will fall on the medial retina of either eye (Figure 14.25). This is easily observed by holding a finger up in front of your face as you look at a more distant object. You will see two images of your finger that represent the two disparate images that are falling on either retina. These depth cues, both monocular and binocular, can be exploited to make the brain think there are three dimensions in two-dimensional information. This is the basis of 3-D movies. The projected image on the screen is two dimensional, but it has disparate information embedded in it. The 3-D glasses that are available at the theater filter the information so that only one eye sees one version of what is on the screen, and the other eye sees the other version. If you take the glasses off, the image on the screen will have varying amounts of blur because both eyes are seeing both layers of information, and the third dimension will not be evident. Some optical illusions can take advantage of depth cues as well, though those are more often using monocular cues to fool the brain into seeing different parts of the scene as being at different depths. Figure 14.25 Retinal Disparity Because of the interocular distance, which results in objects of different distances falling on different spots of the two retinae, the brain can extract depth perception from the two-dimensional information of the visual field. There are two main regions that surround the primary cortex that are usually referred to as areas V2 and V3 (the primary visual cortex is area V1). These surrounding areas are the visual association cortex. The visual association regions develop more complex visual perceptions by adding color and motion information. The information processed in these areas is then sent to regions of the temporal and parietal lobes. Visual processing has two separate streams of processing: one into the temporal lobe and one into the parietal lobe. These are the ventral and dorsal streams, respectively (Figure 14.26). The ventral streamidentifies visual stimuli and their significance. Because the ventral stream uses temporal lobe structures, it begins to interact with the non-visual cortex and may be important in visual stimuli becoming part of memories. The dorsal stream locates objects in space and helps in guiding movements of the body in response to visual inputs. The dorsal stream enters the parietal lobe, where it interacts with somatosensory cortical areas that are important for our perception of the body and its movements. The dorsal stream can then influence frontal lobe activity where motor functions originate. Figure 14.26 Ventral and Dorsal Visual Streams From the primary visual cortex in the occipital lobe, visual processing continues in two streams—one into the temporal lobe and one into the parietal lobe. DISORDERS OF THE... Brain: Prosopagnosia The failures of sensory perception can be unusual and debilitating. A particular sensory deficit that inhibits an important social function of humans is prosopagnosia, or face blindness. The word comes from the Greek words prosopa, that means “faces,” and agnosia, that means “not knowing.” Some people may feel that they cannot recognize people easily by their faces. However, a person with prosopagnosia cannot recognize the most recognizable people in their respective cultures. They would not recognize the face of a celebrity, an important historical figure, or even a family member like their mother. They may not even recognize their own face. Prosopagnosia can be caused by trauma to the brain, or it can be present from birth. The exact cause of proposagnosia and the reason that it happens to some people is unclear. A study of the brains of people born with the deficit found that a specific region of the brain, the anterior fusiform gyrus of the temporal lobe, is often underdeveloped. This region of the brain is concerned with the recognition of visual stimuli and its possible association with memories. Though the evidence is not yet definitive, this region is likely to be where facial recognition occurs. Though this can be a devastating condition, people who suffer from it can get by—often by using other cues to recognize the people they see. Often, the sound of a person’s voice, or the presence of unique cues such as distinct facial features (a mole, for example) or hair color can help the sufferer recognize a familiar person. In the video on prosopagnosia provided in this section, a woman is shown having trouble recognizing celebrities, family members, and herself. In some situations, she can use other cues to help her recognize faces. INTERACTIVE LINK The inability to recognize people by their faces is a troublesome problem. It can be caused by trauma, or it may be inborn. Watch this video to learn more about a person who lost the ability to recognize faces as the result of an injury. She cannot recognize the faces of close family members or herself. What other information can a person suffering from prosopagnosia use to figure out whom they are seeing? Motor Responses - List the components of the basic processing stream for the motor system - Describe the pathway of descending motor commands from the cortex to the skeletal muscles - Compare different descending pathways, both by structure and function - Explain the initiation of movement from the neurological connections - Describe several reflex arcs and their functional roles The defining characteristic of the somatic nervous system is that it controls skeletal muscles. Somatic senses inform the nervous system about the external environment, but the response to that is through voluntary muscle movement. The term “voluntary” suggests that there is a conscious decision to make a movement. However, some aspects of the somatic system use voluntary muscles without conscious control. One example is the ability of our breathing to switch to unconscious control while we are focused on another task. However, the muscles that are responsible for the basic process of breathing are also utilized for speech, which is entirely voluntary. Cortical Responses Let’s start with sensory stimuli that have been registered through receptor cells and the information relayed to the CNS along ascending pathways. In the cerebral cortex, the initial processing of sensory perception progresses to associative processing and then integration in multimodal areas of cortex. These levels of processing can lead to the incorporation of sensory perceptions into memory, but more importantly, they lead to a response. The completion of cortical processing through the primary, associative, and integrative sensory areas initiates a similar progression of motor processing, usually in different cortical areas. Whereas the sensory cortical areas are located in the occipital, temporal, and parietal lobes, motor functions are largely controlled by the frontal lobe. The most anterior regions of the frontal lobe—the prefrontal areas—are important for executive functions, which are those cognitive functions that lead to goal-directed behaviors. These higher cognitive processes include working memory, which has been called a “mental scratch pad,” that can help organize and represent information that is not in the immediate environment. The prefrontal lobe is responsible for aspects of attention, such as inhibiting distracting thoughts and actions so that a person can focus on a goal and direct behavior toward achieving that goal. The functions of the prefrontal cortex are integral to the personality of an individual, because it is largely responsible for what a person intends to do and how they accomplish those plans. A famous case of damage to the prefrontal cortex is that of Phineas Gage, dating back to 1848. He was a railroad worker who had a metal spike impale his prefrontal cortex (Figure 14.27). He survived the accident, but according to second-hand accounts, his personality changed drastically. Friends described him as no longer acting like himself. Whereas he was a hardworking, amiable man before the accident, he turned into an irritable, temperamental, and lazy man after the accident. Many of the accounts of his change may have been inflated in the retelling, and some behavior was likely attributable to alcohol used as a pain medication. However, the accounts suggest that some aspects of his personality did change. Also, there is new evidence that though his life changed dramatically, he was able to become a functioning stagecoach driver, suggesting that the brain has the ability to recover even from major trauma such as this. Figure 14.27 Phineas Gage The victim of an accident while working on a railroad in 1848, Phineas Gage had a large iron rod impaled through the prefrontal cortex of his frontal lobe. After the accident, his personality appeared to change, but he eventually learned to cope with the trauma and lived as a coach driver even after such a traumatic event. (credit b: John M. Harlow, MD) Secondary Motor Cortices In generating motor responses, the executive functions of the prefrontal cortex will need to initiate actual movements. One way to define the prefrontal area is any region of the frontal lobe that does not elicit movement when electrically stimulated. These are primarily in the anterior part of the frontal lobe. The regions of the frontal lobe that remain are the regions of the cortex that produce movement. The prefrontal areas project into the secondary motor cortices, which include the premotor cortex and the supplemental motor area. Two important regions that assist in planning and coordinating movements are located adjacent to the primary motor cortex. The premotor cortex is more lateral, whereas the supplemental motor area is more medial and superior. The premotor area aids in controlling movements of the core muscles to maintain posture during movement, whereas the supplemental motor area is hypothesized to be responsible for planning and coordinating movement. The supplemental motor area also manages sequential movements that are based on prior experience (that is, learned movements). Neurons in these areas are most active leading up to the initiation of movement. For example, these areas might prepare the body for the movements necessary to drive a car in anticipation of a traffic light changing. Adjacent to these two regions are two specialized motor planning centers. The frontal eye fields are responsible for moving the eyes in response to visual stimuli. There are direct connections between the frontal eye fields and the superior colliculus. Also, anterior to the premotor cortex and primary motor cortex is Broca’s area. This area is responsible for controlling movements of the structures of speech production. The area is named after a French surgeon and anatomist who studied patients who could not produce speech. They did not have impairments to understanding speech, only to producing speech sounds, suggesting a damaged or underdeveloped Broca’s area. Primary Motor Cortex The primary motor cortex is located in the precentral gyrus of the frontal lobe. A neurosurgeon, Walter Penfield, described much of the basic understanding of the primary motor cortex by electrically stimulating the surface of the cerebrum. Penfield would probe the surface of the cortex while the patient was only under local anesthesia so that he could observe responses to the stimulation. This led to the belief that the precentral gyrus directly stimulated muscle movement. We now know that the primary motor cortex receives input from several areas that aid in planning movement, and its principle output stimulates spinal cord neurons to stimulate skeletal muscle contraction. The primary motor cortex is arranged in a similar fashion to the primary somatosensory cortex, in that it has a topographical map of the body, creating a motor homunculus (see Figure 14.23). The neurons responsible for musculature in the feet and lower legs are in the medial wall of the precentral gyrus, with the thighs, trunk, and shoulder at the crest of the longitudinal fissure. The hand and face are in the lateral face of the gyrus. Also, the relative space allotted for the different regions is exaggerated in muscles that have greater enervation. The greatest amount of cortical space is given to muscles that perform fine, agile movements, such as the muscles of the fingers and the lower face. The “power muscles” that perform coarser movements, such as the buttock and back muscles, occupy much less space on the motor cortex. Descending Pathways The motor output from the cortex descends into the brain stem and to the spinal cord to control the musculature through motor neurons. Neurons located in the primary motor cortex, named Betz cells, are large cortical neurons that synapse with lower motor neurons in the brain stem or in the spinal cord. The two descending pathways travelled by the axons of Betz cells are the corticobulbar tract and the corticospinal tract, respectively. Both tracts are named for their origin in the cortex and their targets—either the brain stem (the term “bulbar” refers to the brain stem as the bulb, or enlargement, at the top of the spinal cord) or the spinal cord. These two descending pathways are responsible for the conscious or voluntary movements of skeletal muscles. Any motor command from the primary motor cortex is sent down the axons of the Betz cells to activate upper motor neurons in either the cranial motor nuclei or in the ventral horn of the spinal cord. The axons of the corticobulbar tract are ipsilateral, meaning they project from the cortex to the motor nucleus on the same side of the nervous system. Conversely, the axons of the corticospinal tract are largely contralateral, meaning that they cross the midline of the brain stem or spinal cord and synapse on the opposite side of the body. Therefore, the right motor cortex of the cerebrum controls muscles on the left side of the body, and vice versa. The corticospinal tract descends from the cortex through the deep white matter of the cerebrum. It then passes between the caudate nucleus and putamen of the basal nuclei as a bundle called the internal capsule. The tract then passes through the midbrain as the cerebral peduncles, after which it burrows through the pons. Upon entering the medulla, the tracts make up the large white matter tract referred to as the pyramids (Figure 14.28). The defining landmark of the medullary-spinal border is the pyramidal decussation, which is where most of the fibers in the corticospinal tract cross over to the opposite side of the brain. At this point, the tract separates into two parts, which have control over different domains of the musculature. Figure 14.28 Corticospinal Tract The major descending tract that controls skeletal muscle movements is the corticospinal tract. It is composed of two neurons, the upper motor neuron and the lower motor neuron. The upper motor neuron has its cell body in the primary motor cortex of the frontal lobe and synapses on the lower motor neuron, which is in the ventral horn of the spinal cord and projects to the skeletal muscle in the periphery. Appendicular Control The lateral corticospinal tract is composed of the fibers that cross the midline at the pyramidal decussation (see Figure 14.28). The axons cross over from the anterior position of the pyramids in the medulla to the lateral column of the spinal cord. These axons are responsible for controlling appendicular muscles. This influence over the appendicular muscles means that the lateral corticospinal tract is responsible for moving the muscles of the arms and legs. The ventral horn in both the lower cervical spinal cord and the lumbar spinal cord both have wider ventral horns, representing the greater number of muscles controlled by these motor neurons. The cervical enlargement is particularly large because there is greater control over the fine musculature of the upper limbs, particularly of the fingers. The lumbar enlargement is not as significant in appearance because there is less fine motor control of the lower limbs. Axial Control The anterior corticospinal tract is responsible for controlling the muscles of the body trunk (see Figure 14.28). These axons do not decussate in the medulla. Instead, they remain in an anterior position as they descend the brain stem and enter the spinal cord. These axons then travel to the spinal cord level at which they synapse with a lower motor neuron. Upon reaching the appropriate level, the axons decussate, entering the ventral horn on the opposite side of the spinal cord from which they entered. In the ventral horn, these axons synapse with their corresponding lower motor neurons. The lower motor neurons are located in the medial regions of the ventral horn, because they control the axial muscles of the trunk. Because movements of the body trunk involve both sides of the body, the anterior corticospinal tract is not entirely contralateral. Some collateral branches of the tract will project into the ipsilateral ventral horn to control synergistic muscles on that side of the body, or to inhibit antagonistic muscles through interneurons within the ventral horn. Through the influence of both sides of the body, the anterior corticospinal tract can coordinate postural muscles in broad movements of the body. These coordinating axons in the anterior corticospinal tract are often considered bilateral, as they are both ipsilateral and contralateral. INTERACTIVE LINK Watch this video to learn more about the descending motor pathway for the somatic nervous system. The autonomic connections are mentioned, which are covered in another chapter. From this brief video, only some of the descending motor pathway of the somatic nervous system is described. Which division of the pathway is described and which division is left out? Extrapyramidal Controls Other descending connections between the brain and the spinal cord are called the extrapyramidal system. The name comes from the fact that this system is outside the corticospinal pathway, which includes the pyramids in the medulla. A few pathways originating from the brain stem contribute to this system. The tectospinal tract projects from the midbrain to the spinal cord and is important for postural movements that are driven by the superior colliculus. The name of the tract comes from an alternate name for the superior colliculus, which is the tectum. The reticulospinal tract connects the reticular system, a diffuse region of gray matter in the brain stem, with the spinal cord. This tract influences trunk and proximal limb muscles related to posture and locomotion. The reticulospinal tract also contributes to muscle tone and influences autonomic functions. The vestibulospinal tract connects the brain stem nuclei of the vestibular system with the spinal cord. This allows posture, movement, and balance to be modulated on the basis of equilibrium information provided by the vestibular system. The pathways of the extrapyramidal system are influenced by subcortical structures. For example, connections between the secondary motor cortices and the extrapyramidal system modulate spine and cranium movements. The basal nuclei, which are important for regulating movement initiated by the CNS, influence the extrapyramidal system as well as its thalamic feedback to the motor cortex. The conscious movement of our muscles is more complicated than simply sending a single command from the precentral gyrus down to the proper motor neurons. During the movement of any body part, our muscles relay information back to the brain, and the brain is constantly sending “revised” instructions back to the muscles. The cerebellum is important in contributing to the motor system because it compares cerebral motor commands with proprioceptive feedback. The corticospinal fibers that project to the ventral horn of the spinal cord have branches that also synapse in the pons, which project to the cerebellum. Also, the proprioceptive sensations of the dorsal column system have a collateral projection to the medulla that projects to the cerebellum. These two streams of information are compared in the cerebellar cortex. Conflicts between the motor commands sent by the cerebrum and body position information provided by the proprioceptors cause the cerebellum to stimulate the red nucleus of the midbrain. The red nucleus then sends corrective commands to the spinal cord along the rubrospinal tract. The name of this tract comes from the word for red that is seen in the English word “ruby.” A good example of how the cerebellum corrects cerebral motor commands can be illustrated by walking in water. An original motor command from the cerebrum to walk will result in a highly coordinated set of learned movements. However, in water, the body cannot actually perform a typical walking movement as instructed. The cerebellum can alter the motor command, stimulating the leg muscles to take larger steps to overcome the water resistance. The cerebellum can make the necessary changes through the rubrospinal tract. Modulating the basic command to walk also relies on spinal reflexes, but the cerebellum is responsible for calculating the appropriate response. When the cerebellum does not work properly, coordination and balance are severely affected. The most dramatic example of this is during the overconsumption of alcohol. Alcohol inhibits the ability of the cerebellum to interpret proprioceptive feedback, making it more difficult to coordinate body movements, such as walking a straight line, or guide the movement of the hand to touch the tip of the nose. INTERACTIVE LINK Visit this site to read about an elderly woman who starts to lose the ability to control fine movements, such as speech and the movement of limbs. Many of the usual causes were ruled out. It was not a stroke, Parkinson’s disease, diabetes, or thyroid dysfunction. The next most obvious cause was medication, so her pharmacist had to be consulted. The side effect of a drug meant to help her sleep had resulted in changes in motor control. What regions of the nervous system are likely to be the focus of haloperidol side effects? Ventral Horn Output The somatic nervous system provides output strictly to skeletal muscles. The lower motor neurons, which are responsible for the contraction of these muscles, are found in the ventral horn of the spinal cord. These large, multipolar neurons have a corona of dendrites surrounding the cell body and an axon that extends out of the ventral horn. This axon travels through the ventral nerve root to join the emerging spinal nerve. The axon is relatively long because it needs to reach muscles in the periphery of the body. The diameters of cell bodies may be on the order of hundreds of micrometers to support the long axon; some axons are a meter in length, such as the lumbar motor neurons that innervate muscles in the first digits of the feet. The axons will also branch to innervate multiple muscle fibers. Together, the motor neuron and all the muscle fibers that it controls make up a motor unit. Motor units vary in size. Some may contain up to 1000 muscle fibers, such as in the quadriceps, or they may only have 10 fibers, such as in an extraocular muscle. The number of muscle fibers that are part of a motor unit corresponds to the precision of control of that muscle. Also, muscles that have finer motor control have more motor units connecting to them, and this requires a larger topographical field in the primary motor cortex. Motor neuron axons connect to muscle fibers at a neuromuscular junction. This is a specialized synaptic structure at which multiple axon terminals synapse with the muscle fiber sarcolemma. The synaptic end bulbs of the motor neurons secrete acetylcholine, which binds to receptors on the sarcolemma. The binding of acetylcholine opens ligand-gated ion channels, increasing the movement of cations across the sarcolemma. This depolarizes the sarcolemma, initiating muscle contraction. Whereas other synapses result in graded potentials that must reach a threshold in the postsynaptic target, activity at the neuromuscular junction reliably leads to muscle fiber contraction with every nerve impulse received from a motor neuron. However, the strength of contraction and the number of fibers that contract can be affected by the frequency of the motor neuron impulses. Reflexes This chapter began by introducing reflexes as an example of the basic elements of the somatic nervous system. Simple somatic reflexes do not include the higher centers discussed for conscious or voluntary aspects of movement. Reflexes can be spinal or cranial, depending on the nerves and central components that are involved. The example described at the beginning of the chapter involved heat and pain sensations from a hot stove causing withdrawal of the arm through a connection in the spinal cord that leads to contraction of the biceps brachii. The description of this withdrawal reflex was simplified, for the sake of the introduction, to emphasize the parts of the somatic nervous system. But to consider reflexes fully, more attention needs to be given to this example. As you withdraw your hand from the stove, you do not want to slow that reflex down. As the biceps brachii contracts, the antagonistic triceps brachii needs to relax. Because the neuromuscular junction is strictly excitatory, the biceps will contract when the motor nerve is active. Skeletal muscles do not actively relax. Instead the motor neuron needs to “quiet down,” or be inhibited. In the hot-stove withdrawal reflex, this occurs through an interneuron in the spinal cord. The interneuron’s cell body is located in the dorsal horn of the spinal cord. The interneuron receives a synapse from the axon of the sensory neuron that detects that the hand is being burned. In response to this stimulation from the sensory neuron, the interneuron then inhibits the motor neuron that controls the triceps brachii. This is done by releasing a neurotransmitter or other signal that hyperpolarizes the motor neuron connected to the triceps brachii, making it less likely to initiate an action potential. With this motor neuron being inhibited, the triceps brachii relaxes. Without the antagonistic contraction, withdrawal from the hot stove is faster and keeps further tissue damage from occurring. Another example of a withdrawal reflex occurs when you step on a painful stimulus, like a tack or a sharp rock. The nociceptors that are activated by the painful stimulus activate the motor neurons responsible for contraction of the tibialis anterior muscle. This causes dorsiflexion of the foot. An inhibitory interneuron, activated by a collateral branch of the nociceptor fiber, will inhibit the motor neurons of the gastrocnemius and soleus muscles to cancel plantar flexion. An important difference in this reflex is that plantar flexion is most likely in progress as the foot is pressing down onto the tack. Contraction of the tibialis anterior is not the most important aspect of the reflex, as continuation of plantar flexion will result in further damage from stepping onto the tack. Another type of reflex is a stretch reflex. In this reflex, when a skeletal muscle is stretched, a muscle spindle receptor is activated. The axon from this receptor structure will cause direct contraction of the muscle. A collateral of the muscle spindle fiber will also inhibit the motor neuron of the antagonist muscles. The reflex helps to maintain muscles at a constant length. A common example of this reflex is the knee jerk that is elicited by a rubber hammer struck against the patellar ligament in a physical exam. A specialized reflex to protect the surface of the eye is the corneal reflex, or the eye blink reflex. When the cornea is stimulated by a tactile stimulus, or even by bright light in a related reflex, blinking is initiated. The sensory component travels through the trigeminal nerve, which carries somatosensory information from the face, or through the optic nerve, if the stimulus is bright light. The motor response travels through the facial nerve and innervates the orbicularis oculi on the same side. This reflex is commonly tested during a physical exam using an air puff or a gentle touch of a cotton-tipped applicator. INTERACTIVE LINK Watch this video to learn more about the reflex arc of the corneal reflex. When the right cornea senses a tactile stimulus, what happens to the left eye? Explain your answer. INTERACTIVE LINK Watch this video to learn more about newborn reflexes. Newborns have a set of reflexes that are expected to have been crucial to survival before the modern age. These reflexes disappear as the baby grows, as some of them may be unnecessary as they age. The video demonstrates a reflex called the Babinski reflex, in which the foot flexes dorsally and the toes splay out when the sole of the foot is lightly scratched. This is normal for newborns, but it is a sign of reduced myelination of the spinal tract in adults. Why would this reflex be a problem for an adult? Key Terms - alkaloid - substance, usually from a plant source, that is chemically basic with respect to pH and will stimulate bitter receptors - amacrine cell - type of cell in the retina that connects to the bipolar cells near the outer synaptic layer and provides the basis for early image processing within the retina - ampulla - in the ear, the structure at the base of a semicircular canal that contains the hair cells and cupula for transduction of rotational movement of the head - anosmia - loss of the sense of smell; usually the result of physical disruption of the first cranial nerve - anterior corticospinal tract - division of the corticospinal pathway that travels through the ventral (anterior) column of the spinal cord and controls axial musculature through the medial motor neurons in the ventral (anterior) horn - aqueous humor - watery fluid that fills the anterior chamber containing the cornea, iris, ciliary body, and lens of the eye - ascending pathway - fiber structure that relays sensory information from the periphery through the spinal cord and brain stem to other structures of the brain - association area - region of cortex connected to a primary sensory cortical area that further processes the information to generate more complex sensory perceptions - audition - sense of hearing - auricle - fleshy external structure of the ear - basilar membrane - in the ear, the floor of the cochlear duct on which the organ of Corti sits - Betz cells - output cells of the primary motor cortex that cause musculature to move through synapses on cranial and spinal motor neurons - binocular depth cues - indications of the distance of visual stimuli on the basis of slight differences in the images projected onto either retina - bipolar cell - cell type in the retina that connects the photoreceptors to the RGCs - Broca’s area - region of the frontal lobe associated with the motor commands necessary for speech production - capsaicin - molecule that activates nociceptors by interacting with a temperature-sensitive ion channel and is the basis for “hot” sensations in spicy food - cerebral peduncles - segments of the descending motor pathway that make up the white matter of the ventral midbrain - cervical enlargement - region of the ventral (anterior) horn of the spinal cord that has a larger population of motor neurons for the greater number of and finer control of muscles of the upper limb - chemoreceptor - sensory receptor cell that is sensitive to chemical stimuli, such as in taste, smell, or pain - chief sensory nucleus - component of the trigeminal nuclei that is found in the pons - choroid - highly vascular tissue in the wall of the eye that supplies the outer retina with blood - ciliary body - smooth muscle structure on the interior surface of the iris that controls the shape of the lens through the zonule fibers - circadian rhythm - internal perception of the daily cycle of light and dark based on retinal activity related to sunlight - cochlea - auditory portion of the inner ear containing structures to transduce sound stimuli - cochlear duct - space within the auditory portion of the inner ear that contains the organ of Corti and is adjacent to the scala tympani and scala vestibuli on either side - cone photoreceptor - one of the two types of retinal receptor cell that is specialized for color vision through the use of three photopigments distributed through three separate populations of cells - contralateral - word meaning “on the opposite side,” as in axons that cross the midline in a fiber tract - cornea - fibrous covering of the anterior region of the eye that is transparent so that light can pass through it - corneal reflex - protective response to stimulation of the cornea causing contraction of the orbicularis oculi muscle resulting in blinking of the eye - corticobulbar tract - connection between the cortex and the brain stem responsible for generating movement - corticospinal tract - connection between the cortex and the spinal cord responsible for generating movement - cupula - specialized structure within the base of a semicircular canal that bends the stereocilia of hair cells when the head rotates by way of the relative movement of the enclosed fluid - decussate - to cross the midline, as in fibers that project from one side of the body to the other - dorsal column system - ascending tract of the spinal cord associated with fine touch and proprioceptive sensations - dorsal stream - connections between cortical areas from the occipital to parietal lobes that are responsible for the perception of visual motion and guiding movement of the body in relation to that motion - encapsulated ending - configuration of a sensory receptor neuron with dendrites surrounded by specialized structures to aid in transduction of a particular type of sensation, such as the lamellated corpuscles in the deep dermis and subcutaneous tissue - equilibrium - sense of balance that includes sensations of position and movement of the head - executive functions - cognitive processes of the prefrontal cortex that lead to directing goal-directed behavior, which is a precursor to executing motor commands - external ear - structures on the lateral surface of the head, including the auricle and the ear canal back to the tympanic membrane - exteroceptor - sensory receptor that is positioned to interpret stimuli from the external environment, such as photoreceptors in the eye or somatosensory receptors in the skin - extraocular muscle - one of six muscles originating out of the bones of the orbit and inserting into the surface of the eye which are responsible for moving the eye - extrapyramidal system - pathways between the brain and spinal cord that are separate from the corticospinal tract and are responsible for modulating the movements generated through that primary pathway - fasciculus cuneatus - lateral division of the dorsal column system composed of fibers from sensory neurons in the upper body - fasciculus gracilis - medial division of the dorsal column system composed of fibers from sensory neurons in the lower body - fibrous tunic - outer layer of the eye primarily composed of connective tissue known as the sclera and cornea - fovea - exact center of the retina at which visual stimuli are focused for maximal acuity, where the retina is thinnest, at which there is nothing but photoreceptors - free nerve ending - configuration of a sensory receptor neuron with dendrites in the connective tissue of the organ, such as in the dermis of the skin, that are most often sensitive to chemical, thermal, and mechanical stimuli - frontal eye fields - area of the prefrontal cortex responsible for moving the eyes to attend to visual stimuli - general sense - any sensory system that is distributed throughout the body and incorporated into organs of multiple other systems, such as the walls of the digestive organs or the skin - gustation - sense of taste - gustatory receptor cells - sensory cells in the taste bud that transduce the chemical stimuli of gustation - hair cells - mechanoreceptor cells found in the inner ear that transduce stimuli for the senses of hearing and balance - incus - (also, anvil) ossicle of the middle ear that connects the malleus to the stapes - inferior colliculus - last structure in the auditory brainstem pathway that projects to the thalamus and superior colliculus - inferior oblique - extraocular muscle responsible for lateral rotation of the eye - inferior rectus - extraocular muscle responsible for looking down - inner ear - structure within the temporal bone that contains the sensory apparati of hearing and balance - inner segment - in the eye, the section of a photoreceptor that contains the nucleus and other major organelles for normal cellular functions - inner synaptic layer - layer in the retina where bipolar cells connect to RGCs - interaural intensity difference - cue used to aid sound localization in the horizontal plane that compares the relative loudness of sounds at the two ears, because the ear closer to the sound source will hear a slightly more intense sound - interaural time difference - cue used to help with sound localization in the horizontal plane that compares the relative time of arrival of sounds at the two ears, because the ear closer to the sound source will receive the stimulus microseconds before the other ear - internal capsule - segment of the descending motor pathway that passes between the caudate nucleus and the putamen - interoceptor - sensory receptor that is positioned to interpret stimuli from internal organs, such as stretch receptors in the wall of blood vessels - ipsilateral - word meaning on the same side, as in axons that do not cross the midline in a fiber tract - iris - colored portion of the anterior eye that surrounds the pupil - kinesthesia - sense of body movement based on sensations in skeletal muscles, tendons, joints, and the skin - lacrimal duct - duct in the medial corner of the orbit that drains tears into the nasal cavity - lacrimal gland - gland lateral to the orbit that produces tears to wash across the surface of the eye - lateral corticospinal tract - division of the corticospinal pathway that travels through the lateral column of the spinal cord and controls appendicular musculature through the lateral motor neurons in the ventral (anterior) horn - lateral geniculate nucleus - thalamic target of the RGCs that projects to the visual cortex - lateral rectus - extraocular muscle responsible for abduction of the eye - lens - component of the eye that focuses light on the retina - levator palpebrae superioris - muscle that causes elevation of the upper eyelid, controlled by fibers in the oculomotor nerve - lumbar enlargement - region of the ventral (anterior) horn of the spinal cord that has a larger population of motor neurons for the greater number of muscles of the lower limb - macula - enlargement at the base of a semicircular canal at which transduction of equilibrium stimuli takes place within the ampulla - malleus - (also, hammer) ossicle that is directly attached to the tympanic membrane - mechanoreceptor - receptor cell that transduces mechanical stimuli into an electrochemical signal - medial geniculate nucleus - thalamic target of the auditory brain stem that projects to the auditory cortex - medial lemniscus - fiber tract of the dorsal column system that extends from the nuclei gracilis and cuneatus to the thalamus, and decussates - medial rectus - extraocular muscle responsible for adduction of the eye - mesencephalic nucleus - component of the trigeminal nuclei that is found in the midbrain - middle ear - space within the temporal bone between the ear canal and bony labyrinth where the ossicles amplify sound waves from the tympanic membrane to the oval window - multimodal integration area - region of the cerebral cortex in which information from more than one sensory modality is processed to arrive at higher level cortical functions such as memory, learning, or cognition - neural tunic - layer of the eye that contains nervous tissue, namely the retina - nociceptor - receptor cell that senses pain stimuli - nucleus cuneatus - medullary nucleus at which first-order neurons of the dorsal column system synapse specifically from the upper body and arms - nucleus gracilis - medullary nucleus at which first-order neurons of the dorsal column system synapse specifically from the lower body and legs - odorant molecules - volatile chemicals that bind to receptor proteins in olfactory neurons to stimulate the sense of smell - olfaction - sense of smell - olfactory bulb - central target of the first cranial nerve; located on the ventral surface of the frontal lobe in the cerebrum - olfactory epithelium - region of the nasal epithelium where olfactory neurons are located - olfactory sensory neuron - receptor cell of the olfactory system, sensitive to the chemical stimuli of smell, the axons of which compose the first cranial nerve - opsin - protein that contains the photosensitive cofactor retinal for phototransduction - optic chiasm - decussation point in the visual system at which medial retina fibers cross to the other side of the brain - optic disc - spot on the retina at which RGC axons leave the eye and blood vessels of the inner retina pass - optic nerve - second cranial nerve, which is responsible visual sensation - optic tract - name for the fiber structure containing axons from the retina posterior to the optic chiasm representing their CNS location - organ of Corti - structure in the cochlea in which hair cells transduce movements from sound waves into electrochemical signals - osmoreceptor - receptor cell that senses differences in the concentrations of bodily fluids on the basis of osmotic pressure - ossicles - three small bones in the middle ear - otolith - layer of calcium carbonate crystals located on top of the otolithic membrane - otolithic membrane - gelatinous substance in the utricle and saccule of the inner ear that contains calcium carbonate crystals and into which the stereocilia of hair cells are embedded - outer segment - in the eye, the section of a photoreceptor that contains opsin molecules that transduce light stimuli - outer synaptic layer - layer in the retina at which photoreceptors connect to bipolar cells - oval window - membrane at the base of the cochlea where the stapes attaches, marking the beginning of the scala vestibuli - palpebral conjunctiva - membrane attached to the inner surface of the eyelids that covers the anterior surface of the cornea - papilla - for gustation, a bump-like projection on the surface of the tongue that contains taste buds - photoisomerization - chemical change in the retinal molecule that alters the bonding so that it switches from the 11-cis-retinal isomer to the all-trans-retinal isomer - photon - individual “packet” of light - photoreceptor - receptor cell specialized to respond to light stimuli - premotor cortex - cortical area anterior to the primary motor cortex that is responsible for planning movements - primary sensory cortex - region of the cerebral cortex that initially receives sensory input from an ascending pathway from the thalamus and begins the processing that will result in conscious perception of that modality - proprioception - sense of position and movement of the body - proprioceptor - receptor cell that senses changes in the position and kinesthetic aspects of the body - pupil - open hole at the center of the iris that light passes through into the eye - pyramidal decussation - location at which corticospinal tract fibers cross the midline and segregate into the anterior and lateral divisions of the pathway - pyramids - segment of the descending motor pathway that travels in the anterior position of the medulla - receptor cell - cell that transduces environmental stimuli into neural signals - red nucleus - midbrain nucleus that sends corrective commands to the spinal cord along the rubrospinal tract, based on disparity between an original command and the sensory feedback from movement - reticulospinal tract - extrapyramidal connections between the brain stem and spinal cord that modulate movement, contribute to posture, and regulate muscle tone - retina - nervous tissue of the eye at which phototransduction takes place - retinal - cofactor in an opsin molecule that undergoes a biochemical change when struck by a photon (pronounced with a stress on the last syllable) - retinal ganglion cell (RGC) - neuron of the retina that projects along the second cranial nerve - rhodopsin - photopigment molecule found in the rod photoreceptors - rod photoreceptor - one of the two types of retinal receptor cell that is specialized for low-light vision - round window - membrane that marks the end of the scala tympani - rubrospinal tract - descending motor control pathway, originating in the red nucleus, that mediates control of the limbs on the basis of cerebellar processing - saccule - structure of the inner ear responsible for transducing linear acceleration in the vertical plane - scala tympani - portion of the cochlea that extends from the apex to the round window - scala vestibuli - portion of the cochlea that extends from the oval window to the apex - sclera - white of the eye - semicircular canals - structures within the inner ear responsible for transducing rotational movement information - sensory homunculus - topographic representation of the body within the somatosensory cortex demonstrating the correspondence between neurons processing stimuli and sensitivity - sensory modality - a particular system for interpreting and perceiving environmental stimuli by the nervous system - solitary nucleus - medullar nucleus that receives taste information from the facial and glossopharyngeal nerves - somatosensation - general sense associated with modalities lumped together as touch - special sense - any sensory system associated with a specific organ structure, namely smell, taste, sight, hearing, and balance - spinal trigeminal nucleus - component of the trigeminal nuclei that is found in the medulla - spinothalamic tract - ascending tract of the spinal cord associated with pain and temperature sensations - spiral ganglion - location of neuronal cell bodies that transmit auditory information along the eighth cranial nerve - stapes - (also, stirrup) ossicle of the middle ear that is attached to the inner ear - stereocilia - array of apical membrane extensions in a hair cell that transduce movements when they are bent - stretch reflex - response to activation of the muscle spindle stretch receptor that causes contraction of the muscle to maintain a constant length - submodality - specific sense within a broader major sense such as sweet as a part of the sense of taste, or color as a part of vision - superior colliculus - structure in the midbrain that combines visual, auditory, and somatosensory input to coordinate spatial and topographic representations of the three sensory systems - superior oblique - extraocular muscle responsible for medial rotation of the eye - superior rectus - extraocular muscle responsible for looking up - supplemental motor area - cortical area anterior to the primary motor cortex that is responsible for planning movements - suprachiasmatic nucleus - hypothalamic target of the retina that helps to establish the circadian rhythm of the body on the basis of the presence or absence of daylight - taste buds - structures within a papilla on the tongue that contain gustatory receptor cells - tectorial membrane - component of the organ of Corti that lays over the hair cells, into which the stereocilia are embedded - tectospinal tract - extrapyramidal connections between the superior colliculus and spinal cord - thermoreceptor - sensory receptor specialized for temperature stimuli - topographical - relating to positional information - transduction - process of changing an environmental stimulus into the electrochemical signals of the nervous system - trochlea - cartilaginous structure that acts like a pulley for the superior oblique muscle - tympanic membrane - ear drum - umami - taste submodality for sensitivity to the concentration of amino acids; also called the savory sense - utricle - structure of the inner ear responsible for transducing linear acceleration in the horizontal plane - vascular tunic - middle layer of the eye primarily composed of connective tissue with a rich blood supply - ventral posterior nucleus - nucleus in the thalamus that is the target of gustatory sensations and projects to the cerebral cortex - ventral stream - connections between cortical areas from the occipital lobe to the temporal lobe that are responsible for identification of visual stimuli - vestibular ganglion - location of neuronal cell bodies that transmit equilibrium information along the eighth cranial nerve - vestibular nuclei - targets of the vestibular component of the eighth cranial nerve - vestibule - in the ear, the portion of the inner ear responsible for the sense of equilibrium - vestibulo-ocular reflex (VOR) - reflex based on connections between the vestibular system and the cranial nerves of eye movements that ensures images are stabilized on the retina as the head and body move - vestibulospinal tract - extrapyramidal connections between the vestibular nuclei in the brain stem and spinal cord that modulate movement and contribute to balance on the basis of the sense of equilibrium - visceral sense - sense associated with the internal organs - vision - special sense of sight based on transduction of light stimuli - visual acuity - property of vision related to the sharpness of focus, which varies in relation to retinal position - vitreous humor - viscous fluid that fills the posterior chamber of the eye - working memory - function of the prefrontal cortex to maintain a representation of information that is not in the immediate environment - zonule fibers - fibrous connections between the ciliary body and the lens Chapter Review 14.1 Sensory Perception The senses are olfaction (smell), gustation (taste), somatosensation (sensations associated with the skin and body), audition (hearing), equilibrium (balance), and vision. With the exception of somatosensation, this list represents the special senses, or those systems of the body that are associated with specific organs such as the tongue or eye. Somatosensation belongs to the general senses, which are those sensory structures that are distributed throughout the body and in the walls of various organs. The special senses are all primarily part of the somatic nervous system in that they are consciously perceived through cerebral processes, though some special senses contribute to autonomic function. The general senses can be divided into somatosensation, which is commonly considered touch, but includes tactile, pressure, vibration, temperature, and pain perception. The general senses also include the visceral senses, which are separate from the somatic nervous system function in that they do not normally rise to the level of conscious perception. The cells that transduce sensory stimuli into the electrochemical signals of the nervous system are classified on the basis of structural or functional aspects of the cells. The structural classifications are either based on the anatomy of the cell that is interacting with the stimulus (free nerve endings, encapsulated endings, or specialized receptor cell), or where the cell is located relative to the stimulus (interoceptor, exteroceptor, proprioceptor). Thirdly, the functional classification is based on how the cell transduces the stimulus into a neural signal. Chemoreceptors respond to chemical stimuli and are the basis for olfaction and gustation. Related to chemoreceptors are osmoreceptors and nociceptors for fluid balance and pain reception, respectively. Mechanoreceptors respond to mechanical stimuli and are the basis for most aspects of somatosensation, as well as being the basis of audition and equilibrium in the inner ear. Thermoreceptors are sensitive to temperature changes, and photoreceptors are sensitive to light energy. The nerves that convey sensory information from the periphery to the CNS are either spinal nerves, connected to the spinal cord, or cranial nerves, connected to the brain. Spinal nerves have mixed populations of fibers; some are motor fibers and some are sensory. The sensory fibers connect to the spinal cord through the dorsal root, which is attached to the dorsal root ganglion. Sensory information from the body that is conveyed through spinal nerves will project to the opposite side of the brain to be processed by the cerebral cortex. The cranial nerves can be strictly sensory fibers, such as the olfactory, optic, and vestibulocochlear nerves, or mixed sensory and motor nerves, such as the trigeminal, facial, glossopharyngeal, and vagus nerves. The cranial nerves are connected to the same side of the brain from which the sensory information originates. 14.2 Central Processing Sensory input to the brain enters through pathways that travel through either the spinal cord (for somatosensory input from the body) or the brain stem (for everything else, except the visual and olfactory systems) to reach the diencephalon. In the diencephalon, sensory pathways reach the thalamus. This is necessary for all sensory systems to reach the cerebral cortex, except for the olfactory system that is directly connected to the frontal and temporal lobes. The two major tracts in the spinal cord, originating from sensory neurons in the dorsal root ganglia, are the dorsal column system and the spinothalamic tract. The major differences between the two are in the type of information that is relayed to the brain and where the tracts decussate. The dorsal column system primarily carries information about touch and proprioception and crosses the midline in the medulla. The spinothalamic tract is primarily responsible for pain and temperature sensation and crosses the midline in the spinal cord at the level at which it enters. The trigeminal nerve adds similar sensation information from the head to these pathways. The auditory pathway passes through multiple nuclei in the brain stem in which additional information is extracted from the basic frequency stimuli processed by the cochlea. Sound localization is made possible through the activity of these brain stem structures. The vestibular system enters the brain stem and influences activity in the cerebellum, spinal cord, and cerebral cortex. The visual pathway segregates information from the two eyes so that one half of the visual field projects to the other side of the brain. Within visual cortical areas, the perception of the stimuli and their location is passed along two streams, one ventral and one dorsal. The ventral visual stream connects to structures in the temporal lobe that are important for long-term memory formation. The dorsal visual stream interacts with the somatosensory cortex in the parietal lobe, and together they can influence the activity in the frontal lobe to generate movements of the body in relation to visual information. 14.3 Motor Responses The motor components of the somatic nervous system begin with the frontal lobe of the brain, where the prefrontal cortex is responsible for higher functions such as working memory. The integrative and associate functions of the prefrontal lobe feed into the secondary motor areas, which help plan movements. The premotor cortex and supplemental motor area then feed into the primary motor cortex that initiates movements. Large Betz cells project through the corticobulbar and corticospinal tracts to synapse on lower motor neurons in the brain stem and ventral horn of the spinal cord, respectively. These connections are responsible for generating movements of skeletal muscles. The extrapyramidal system includes projections from the brain stem and higher centers that influence movement, mostly to maintain balance and posture, as well as to maintain muscle tone. The superior colliculus and red nucleus in the midbrain, the vestibular nuclei in the medulla, and the reticular formation throughout the brain stem each have tracts projecting to the spinal cord in this system. Descending input from the secondary motor cortices, basal nuclei, and cerebellum connect to the origins of these tracts in the brain stem. All of these motor pathways project to the spinal cord to synapse with motor neurons in the ventral horn of the spinal cord. These lower motor neurons are the cells that connect to skeletal muscle and cause contractions. These neurons project through the spinal nerves to connect to the muscles at neuromuscular junctions. One motor neuron connects to multiple muscle fibers within a target muscle. The number of fibers that are innervated by a single motor neuron varies on the basis of the precision necessary for that muscle and the amount of force necessary for that motor unit. The quadriceps, for example, have many fibers controlled by single motor neurons for powerful contractions that do not need to be precise. The extraocular muscles have only a small number of fibers controlled by each motor neuron because moving the eyes does not require much force, but needs to be very precise. Reflexes are the simplest circuits within the somatic nervous system. A withdrawal reflex from a painful stimulus only requires the sensory fiber that enters the spinal cord and the motor neuron that projects to a muscle. Antagonist and postural muscles can be coordinated with the withdrawal, making the connections more complex. The simple, single neuronal connection is the basis of somatic reflexes. The corneal reflex is contraction of the orbicularis oculi muscle to blink the eyelid when something touches the surface of the eye. Stretch reflexes maintain a constant length of muscles by causing a contraction of a muscle to compensate for a stretch that can be sensed by a specialized receptor called a muscle spindle. Interactive Link Questions Watch this video to learn about Dr. Danielle Reed of the Monell Chemical Senses Center in Philadelphia, PA, who became interested in science at an early age because of her sensory experiences. She recognized that her sense of taste was unique compared with other people she knew. Now, she studies the genetic differences between people and their sensitivities to taste stimuli. In the video, there is a brief image of a person sticking out their tongue, which has been covered with a colored dye. This is how Dr. Reed is able to visualize and count papillae on the surface of the tongue. People fall into two large groups known as “tasters” and “non-tasters” on the basis of the density of papillae on their tongue, which also indicates the number of taste buds. Non-tasters can taste food, but they are not as sensitive to certain tastes, such as bitterness. Dr. Reed discovered that she is a non-taster, which explains why she perceived bitterness differently than other people she knew. Are you very sensitive to tastes? Can you see any similarities among the members of your family? 2.Figure 14.9 The basilar membrane is the thin membrane that extends from the central core of the cochlea to the edge. What is anchored to this membrane so that they can be activated by movement of the fluids within the cochlea? 3.Watch this video to learn more about how the structures of the ear convert sound waves into a neural signal by moving the “hairs,” or stereocilia, of the cochlear duct. Specific locations along the length of the duct encode specific frequencies, or pitches. The brain interprets the meaning of the sounds we hear as music, speech, noise, etc. Which ear structures are responsible for the amplification and transfer of sound from the external ear to the inner ear? 4.Watch this animation to learn more about the inner ear and to see the cochlea unroll, with the base at the back of the image and the apex at the front. Specific wavelengths of sound cause specific regions of the basilar membrane to vibrate, much like the keys of a piano produce sound at different frequencies. Based on the animation, where do frequencies—from high to low pitches—cause activity in the hair cells within the cochlear duct? 5.Watch this video to learn more about a transverse section through the brain that depicts the visual pathway from the eye to the occipital cortex. The first half of the pathway is the projection from the RGCs through the optic nerve to the lateral geniculate nucleus in the thalamus on either side. This first fiber in the pathway synapses on a thalamic cell that then projects to the visual cortex in the occipital lobe where “seeing,” or visual perception, takes place. This video gives an abbreviated overview of the visual system by concentrating on the pathway from the eyes to the occipital lobe. The video makes the statement (at 0:45) that “specialized cells in the retina called ganglion cells convert the light rays into electrical signals.” What aspect of retinal processing is simplified by that statement? Explain your answer. 6.Watch this video to learn more about how the brain perceives 3-D motion. Similar to how retinal disparity offers 3-D moviegoers a way to extract 3-D information from the two-dimensional visual field projected onto the retina, the brain can extract information about movement in space by comparing what the two eyes see. If movement of a visual stimulus is leftward in one eye and rightward in the opposite eye, the brain interprets this as movement toward (or away) from the face along the midline. If both eyes see an object moving in the same direction, but at different rates, what would that mean for spatial movement? 7.The inability to recognize people by their faces is a troublesome problem. It can be caused by trauma, or it may be inborn. Watch this video to learn more about a person who lost the ability to recognize faces as the result of an injury. She cannot recognize the faces of close family members or herself. What other information can a person suffering from prosopagnosia use to figure out whom they are seeing? 8.Watch this video to learn more about the descending motor pathway for the somatic nervous system. The autonomic connections are mentioned, which are covered in another chapter. From this brief video, only some of the descending motor pathway of the somatic nervous system is described. Which division of the pathway is described and which division is left out? 9.Visit this site to read about an elderly woman who starts to lose the ability to control fine movements, such as speech and the movement of limbs. Many of the usual causes were ruled out. It was not a stroke, Parkinson’s disease, diabetes, or thyroid dysfunction. The next most obvious cause was medication, so her pharmacist had to be consulted. The side effect of a drug meant to help her sleep had resulted in changes in motor control. What regions of the nervous system are likely to be the focus of haloperidol side effects? 10.Watch this video to learn more about the reflex arc of the corneal reflex. When the right cornea senses a tactile stimulus, what happens to the left eye? Explain your answer. 11.Watch this video to learn more about newborn reflexes. Newborns have a set of reflexes that are expected to have been crucial to survival before the modern age. These reflexes disappear as the baby grows, as some of them may be unnecessary as they age. The video demonstrates a reflex called the Babinski reflex, in which the foot flexes dorsally and the toes splay out when the sole of the foot is lightly scratched. This is normal for newborns, but it is a sign of reduced myelination of the spinal tract in adults. Why would this reflex be a problem for an adult? Review Questions What type of receptor cell is responsible for transducing pain stimuli? - mechanoreceptor - nociceptor - osmoreceptor - photoreceptor Which of these cranial nerves is part of the gustatory system? - olfactory - trochlear - trigeminal - facial Which submodality of taste is sensitive to the pH of saliva? - umami - sour - bitter - sweet Axons from which neuron in the retina make up the optic nerve? - amacrine cells - photoreceptors - bipolar cells - retinal ganglion cells What type of receptor cell is involved in the sensations of sound and balance? - photoreceptor - chemoreceptor - mechanoreceptor - nociceptor Which of these sensory modalities does not pass through the ventral posterior thalamus? - gustatory - proprioception - audition - nociception Which nucleus in the medulla is connected to the inferior colliculus? - solitary nucleus - vestibular nucleus - chief sensory nucleus - cochlear nucleus Visual stimuli in the upper-left visual field will be processed in what region of the primary visual cortex? - inferior right - inferior left - superior right - superior left Which location on the body has the largest region of somatosensory cortex representing it, according to the sensory homunculus? - lips - thigh - elbow - neck Which of the following is a direct target of the vestibular ganglion? - superior colliculus - cerebellum - thalamus - optic chiasm Which region of the frontal lobe is responsible for initiating movement by directly connecting to cranial and spinal motor neurons? - prefrontal cortex - supplemental motor area - premotor cortex - primary motor cortex Which extrapyramidal tract incorporates equilibrium sensations with motor commands to aid in posture and movement? - tectospinal tract - vestibulospinal tract - reticulospinal tract - corticospinal tract Which region of gray matter in the spinal cord contains motor neurons that innervate skeletal muscles? - ventral horn - dorsal horn - lateral horn - lateral column What type of reflex can protect the foot when a painful stimulus is sensed? - stretch reflex - gag reflex - withdrawal reflex - corneal reflex What is the name for the topographical representation of the sensory input to the somatosensory cortex? - homunculus - homo sapiens - postcentral gyrus - primary cortex Critical Thinking Questions The sweetener known as stevia can replace glucose in food. What does the molecular similarity of stevia to glucose mean for the gustatory sense? 28.Why does the blind spot from the optic disc in either eye not result in a blind spot in the visual field? 29.Following a motorcycle accident, the victim loses the ability to move the right leg but has normal control over the left one, suggesting a hemisection somewhere in the thoracic region of the spinal cord. What sensory deficits would be expected in terms of touch versus pain? Explain your answer. 30.A pituitary tumor can cause perceptual losses in the lateral visual field. The pituitary gland is located directly inferior to the hypothalamus. Why would this happen? 31.The prefrontal lobotomy is a drastic—and largely out-of-practice—procedure used to disconnect that portion of the cerebral cortex from the rest of the frontal lobe and the diencephalon as a psychiatric therapy. Why would this have been thought necessary for someone with a potentially uncontrollable behavior? 32.If a reflex is a limited circuit within the somatic system, why do physical and neurological exams include them to test the health of an individual?	oercommons	2025-03-18T00:37:01.682736	null	{ "license": "Creative Commons - Attribution - https://creativecommons.org/licenses/by/4.0/", "url": "https://oercommons.org/courseware/lesson/56377/overview", "title": "Anatomy and Physiology, Regulation, Integration, and Control", "author": null }
https://oercommons.org/courseware/lesson/56378/overview	The Autonomic Nervous System Introduction Figure 15.1 Fight or Flight? Though the threats that modern humans face are not large predators, the autonomic nervous system is adapted to this type of stimulus. The modern world presents stimuli that trigger the same response. (credit: Vernon Swanepoel) CHAPTER OBJECTIVES After studying this chapter, you will be able to: - Describe the components of the autonomic nervous system - Differentiate between the structures of the sympathetic and parasympathetic divisions in the autonomic nervous system - Name the components of a visceral reflex specific to the autonomic division to which it belongs - Predict the response of a target effector to autonomic input on the basis of the released signaling molecule - Describe how the central nervous system coordinates and contributes to autonomic functions The autonomic nervous system is often associated with the “fight-or-flight response,” which refers to the preparation of the body to either run away from a threat or to stand and fight in the face of that threat. To suggest what this means, consider the (very unlikely) situation of seeing a lioness hunting out on the savannah. Though this is not a common threat that humans deal with in the modern world, it represents the type of environment in which the human species thrived and adapted. The spread of humans around the world to the present state of the modern age occurred much more quickly than any species would adapt to environmental pressures such as predators. However, the reactions modern humans have in the modern world are based on these prehistoric situations. If your boss is walking down the hallway on Friday afternoon looking for “volunteers” to come in on the weekend, your response is the same as the prehistoric human seeing the lioness running across the savannah: fight or flight. Most likely, your response to your boss—not to mention the lioness—would be flight. Run away! The autonomic system is responsible for the physiological response to make that possible, and hopefully successful. Adrenaline starts to flood your circulatory system. Your heart rate increases. Sweat glands become active. The bronchi of the lungs dilate to allow more air exchange. Pupils dilate to increase visual information. Blood pressure increases in general, and blood vessels dilate in skeletal muscles. Time to run. Similar physiological responses would occur in preparation for fighting off the threat. This response should sound a bit familiar. The autonomic nervous system is tied into emotional responses as well, and the fight-or-flight response probably sounds like a panic attack. In the modern world, these sorts of reactions are associated with anxiety as much as with response to a threat. It is engrained in the nervous system to respond like this. In fact, the adaptations of the autonomic nervous system probably predate the human species and are likely to be common to all mammals, and perhaps shared by many animals. That lioness might herself be threatened in some other situation. However, the autonomic nervous system is not just about responding to threats. Besides the fight-or-flight response, there are the responses referred to as “rest and digest.” If that lioness is successful in her hunting, then she is going to rest from the exertion. Her heart rate will slow. Breathing will return to normal. The digestive system has a big job to do. Much of the function of the autonomic system is based on the connections within an autonomic, or visceral, reflex. Divisions of the Autonomic Nervous System - Name the components that generate the sympathetic and parasympathetic responses of the autonomic nervous system - Explain the differences in output connections within the two divisions of the autonomic nervous system - Describe the signaling molecules and receptor proteins involved in communication within the two divisions of the autonomic nervous system The nervous system can be divided into two functional parts: the somatic nervous system and the autonomic nervous system. The major differences between the two systems are evident in the responses that each produces. The somatic nervous system causes contraction of skeletal muscles. The autonomic nervous system controls cardiac and smooth muscle, as well as glandular tissue. The somatic nervous system is associated with voluntary responses (though many can happen without conscious awareness, like breathing), and the autonomic nervous system is associated with involuntary responses, such as those related to homeostasis. The autonomic nervous system regulates many of the internal organs through a balance of two aspects, or divisions. In addition to the endocrine system, the autonomic nervous system is instrumental in homeostatic mechanisms in the body. The two divisions of the autonomic nervous system are the sympathetic division and the parasympathetic division. The sympathetic system is associated with the fight-or-flight response, and parasympathetic activity is referred to by the epithet of rest and digest. Homeostasis is the balance between the two systems. At each target effector, dual innervation determines activity. For example, the heart receives connections from both the sympathetic and parasympathetic divisions. One causes heart rate to increase, whereas the other causes heart rate to decrease. INTERACTIVE LINK Watch this video to learn more about adrenaline and the fight-or-flight response. When someone is said to have a rush of adrenaline, the image of bungee jumpers or skydivers usually comes to mind. But adrenaline, also known as epinephrine, is an important chemical in coordinating the body’s fight-or-flight response. In this video, you look inside the physiology of the fight-or-flight response, as envisioned for a firefighter. His body’s reaction is the result of the sympathetic division of the autonomic nervous system causing system-wide changes as it prepares for extreme responses. What two changes does adrenaline bring about to help the skeletal muscle response? Sympathetic Division of the Autonomic Nervous System To respond to a threat—to fight or to run away—the sympathetic system causes divergent effects as many different effector organs are activated together for a common purpose. More oxygen needs to be inhaled and delivered to skeletal muscle. The respiratory, cardiovascular, and musculoskeletal systems are all activated together. Additionally, sweating keeps the excess heat that comes from muscle contraction from causing the body to overheat. The digestive system shuts down so that blood is not absorbing nutrients when it should be delivering oxygen to skeletal muscles. To coordinate all these responses, the connections in the sympathetic system diverge from a limited region of the central nervous system (CNS) to a wide array of ganglia that project to the many effector organs simultaneously. The complex set of structures that compose the output of the sympathetic system make it possible for these disparate effectors to come together in a coordinated, systemic change. The sympathetic division of the autonomic nervous system influences the various organ systems of the body through connections emerging from the thoracic and upper lumbar spinal cord. It is referred to as the thoracolumbar system to reflect this anatomical basis. A central neuron in the lateral horn of any of these spinal regions projects to ganglia adjacent to the vertebral column through the ventral spinal roots. The majority of ganglia of the sympathetic system belong to a network of sympathetic chain ganglia that runs alongside the vertebral column. The ganglia appear as a series of clusters of neurons linked by axonal bridges. There are typically 23 ganglia in the chain on either side of the spinal column. Three correspond to the cervical region, 12 are in the thoracic region, four are in the lumbar region, and four correspond to the sacral region. The cervical and sacral levels are not connected to the spinal cord directly through the spinal roots, but through ascending or descending connections through the bridges within the chain. A diagram that shows the connections of the sympathetic system is somewhat like a circuit diagram that shows the electrical connections between different receptacles and devices. In Figure 15.2, the “circuits” of the sympathetic system are intentionally simplified. Figure 15.2 Connections of Sympathetic Division of the Autonomic Nervous System Neurons from the lateral horn of the spinal cord (preganglionic nerve fibers - solid lines)) project to the chain ganglia on either side of the vertebral column or to collateral (prevertebral) ganglia that are anterior to the vertebral column in the abdominal cavity. Axons from these ganglionic neurons (postganglionic nerve fibers - dotted lines) then project to target effectors throughout the body. To continue with the analogy of the circuit diagram, there are three different types of “junctions” that operate within the sympathetic system (Figure 15.3). The first type is most direct: the sympathetic nerve projects to the chain ganglion at the same level as the target effector (the organ, tissue, or gland to be innervated). An example of this type is spinal nerve T1 that synapses with the T1 chain ganglion to innervate the trachea. The fibers of this branch are called white rami communicantes(singular = ramus communicans); they are myelinated and therefore referred to as white (see Figure 15.3a). The axon from the central neuron (the preganglionic fiber shown as a solid line) synapses with the ganglionic neuron (with the postganglionic fiber shown as a dashed line). This neuron then projects to a target effector—in this case, the trachea—via gray rami communicantes, which are unmyelinated axons. In some cases, the target effectors are located superior or inferior to the spinal segment at which the preganglionic fiber emerges. With respect to the “wiring” involved, the synapse with the ganglionic neuron occurs at chain ganglia superior or inferior to the location of the central neuron. An example of this is spinal nerve T1 that innervates the eye. The spinal nerve tracks up through the chain until it reaches the superior cervical ganglion, where it synapses with the postganglionic neuron (see Figure 15.3b). The cervical ganglia are referred to as paravertebral ganglia, given their location adjacent to prevertebral ganglia in the sympathetic chain. Not all axons from the central neurons terminate in the chain ganglia. Additional branches from the ventral nerve root continue through the chain and on to one of the collateral ganglia as the greater splanchnic nerve or lesser splanchnic nerve. For example, the greater splanchnic nerve at the level of T5 synapses with a collateral ganglion outside the chain before making the connection to the postganglionic nerves that innervate the stomach (see Figure 15.3c). Collateral ganglia, also called prevertebral ganglia, are situated anterior to the vertebral column and receive inputs from splanchnic nerves as well as central sympathetic neurons. They are associated with controlling organs in the abdominal cavity, and are also considered part of the enteric nervous system. The three collateral ganglia are the celiac ganglion, the superior mesenteric ganglion, and the inferior mesenteric ganglion (see Figure 15.2). The word celiac is derived from the Latin word “coelom,” which refers to a body cavity (in this case, the abdominal cavity), and the word mesenteric refers to the digestive system. Figure 15.3 Sympathetic Connections and Chain Ganglia The axon from a central sympathetic neuron in the spinal cord can project to the periphery in a number of different ways. (a) The fiber can project out to the ganglion at the same level and synapse on a ganglionic neuron. (b) A branch can project to more superior or inferior ganglion in the chain. (c) A branch can project through the white ramus communicans, but not terminate on a ganglionic neuron in the chain. Instead, it projects through one of the splanchnic nerves to a collateral ganglion or the adrenal medulla (not pictured). An axon from the central neuron that projects to a sympathetic ganglion is referred to as a preganglionic fiber or neuron, and represents the output from the CNS to the ganglion. Because the sympathetic ganglia are adjacent to the vertebral column, preganglionic sympathetic fibers are relatively short, and they are myelinated. A postganglionic fiber—the axon from a ganglionic neuron that projects to the target effector—represents the output of a ganglion that directly influences the organ. Compared with the preganglionic fibers, postganglionic sympathetic fibers are long because of the relatively greater distance from the ganglion to the target effector. These fibers are unmyelinated. (Note that the term “postganglionic neuron” may be used to describe the projection from a ganglion to the target. The problem with that usage is that the cell body is in the ganglion, and only the fiber is postganglionic. Typically, the term neuron applies to the entire cell.) One type of preganglionic sympathetic fiber does not terminate in a ganglion. These are the axons from central sympathetic neurons that project to the adrenal medulla, the interior portion of the adrenal gland. These axons are still referred to as preganglionic fibers, but the target is not a ganglion. The adrenal medulla releases signaling molecules into the bloodstream, rather than using axons to communicate with target structures. The cells in the adrenal medulla that are contacted by the preganglionic fibers are called chromaffin cells. These cells are neurosecretory cells that develop from the neural crest along with the sympathetic ganglia, reinforcing the idea that the gland is, functionally, a sympathetic ganglion. The projections of the sympathetic division of the autonomic nervous system diverge widely, resulting in a broad influence of the system throughout the body. As a response to a threat, the sympathetic system would increase heart rate and breathing rate and cause blood flow to the skeletal muscle to increase and blood flow to the digestive system to decrease. Sweat gland secretion should also increase as part of an integrated response. All of those physiological changes are going to be required to occur together to run away from the hunting lioness, or the modern equivalent. This divergence is seen in the branching patterns of preganglionic sympathetic neurons—a single preganglionic sympathetic neuron may have 10–20 targets. An axon that leaves a central neuron of the lateral horn in the thoracolumbar spinal cord will pass through the white ramus communicans and enter the sympathetic chain, where it will branch toward a variety of targets. At the level of the spinal cord at which the preganglionic sympathetic fiber exits the spinal cord, a branch will synapse on a neuron in the adjacent chain ganglion. Some branches will extend up or down to a different level of the chain ganglia. Other branches will pass through the chain ganglia and project through one of the splanchnic nerves to a collateral ganglion. Finally, some branches may project through the splanchnic nerves to the adrenal medulla. All of these branches mean that one preganglionic neuron can influence different regions of the sympathetic system very broadly, by acting on widely distributed organs. Parasympathetic Division of the Autonomic Nervous System The parasympathetic division of the autonomic nervous system is named because its central neurons are located on either side of the thoracolumbar region of the spinal cord (para- = “beside” or “near”). The parasympathetic system can also be referred to as the craniosacral system (or outflow) because the preganglionic neurons are located in nuclei of the brain stem and the lateral horn of the sacral spinal cord. The connections, or “circuits,” of the parasympathetic division are similar to the general layout of the sympathetic division with a few specific differences (Figure 15.4). The preganglionic fibers from the cranial region travel in cranial nerves, whereas preganglionic fibers from the sacral region travel in spinal nerves. The targets of these fibers are terminal ganglia, which are located near—or even within—the target effector. These ganglia are often referred to as intramural ganglia when they are found within the walls of the target organ. The postganglionic fiber projects from the terminal ganglia a short distance to the target effector, or to the specific target tissue within the organ. Comparing the relative lengths of axons in the parasympathetic system, the preganglionic fibers are long and the postganglionic fibers are short because the ganglia are close to—and sometimes within—the target effectors. The cranial component of the parasympathetic system is based in particular nuclei of the brain stem. In the midbrain, the Edinger–Westphal nucleus is part of the oculomotor complex, and axons from those neurons travel with the fibers in the oculomotor nerve (cranial nerve III) that innervate the extraocular muscles. The preganglionic parasympathetic fibers within cranial nerve III terminate in the ciliary ganglion, which is located in the posterior orbit. The postganglionic parasympathetic fibers then project to the smooth muscle of the iris to control pupillary size. In the upper medulla, the salivatory nuclei contain neurons with axons that project through the facial and glossopharyngeal nerves to ganglia that control salivary glands. Tear production is influenced by parasympathetic fibers in the facial nerve, which activate a ganglion, and ultimately the lacrimal (tear) gland. Neurons in the dorsal nucleus of the vagus nerve and the nucleus ambiguus project through the vagus nerve (cranial nerve X) to the terminal ganglia of the thoracic and abdominal cavities. Parasympathetic preganglionic fibers primarily influence the heart, bronchi, and esophagus in the thoracic cavity and the stomach, liver, pancreas, gall bladder, and small intestine of the abdominal cavity. The postganglionic fibers from the ganglia activated by the vagus nerve are often incorporated into the structure of the organ, such as the mesenteric plexus of the digestive tract organs and the intramural ganglia. Figure 15.4 Connections of Parasympathetic Division of the Autonomic Nervous System Neurons from brain-stem nuclei, or from the lateral horn of the sacral spinal cord, project to terminal ganglia near or within the various organs of the body. Axons from these ganglionic neurons then project the short distance to those target effectors. Chemical Signaling in the Autonomic Nervous System Where an autonomic neuron connects with a target, there is a synapse. The electrical signal of the action potential causes the release of a signaling molecule, which will bind to receptor proteins on the target cell. Synapses of the autonomic system are classified as either cholinergic, meaning that acetylcholine (ACh) is released, or adrenergic, meaning that norepinephrine is released. The terms cholinergic and adrenergic refer not only to the signaling molecule that is released but also to the class of receptors that each binds. The cholinergic system includes two classes of receptor: the nicotinic receptor and the muscarinic receptor. Both receptor types bind to ACh and cause changes in the target cell. The nicotinic receptor is a ligand-gated cation channel and the muscarinic receptor is a G protein–coupled receptor. The receptors are named for, and differentiated by, other molecules that bind to them. Whereas nicotine will bind to the nicotinic receptor, and muscarine will bind to the muscarinic receptor, there is no cross-reactivity between the receptors. The situation is similar to locks and keys. Imagine two locks—one for a classroom and the other for an office—that are opened by two separate keys. The classroom key will not open the office door and the office key will not open the classroom door. This is similar to the specificity of nicotine and muscarine for their receptors. However, a master key can open multiple locks, such as a master key for the Biology Department that opens both the classroom and the office doors. This is similar to ACh that binds to both types of receptors. The molecules that define these receptors are not crucial—they are simply tools for researchers to use in the laboratory. These molecules are exogenous, meaning that they are made outside of the human body, so a researcher can use them without any confounding endogenous results (results caused by the molecules produced in the body). The adrenergic system also has two types of receptors, named the alpha (α)-adrenergic receptor and beta (β)-adrenergic receptor. Unlike cholinergic receptors, these receptor types are not classified by which drugs can bind to them. All of them are G protein–coupled receptors. There are three types of α-adrenergic receptors, termed α1, α2, and α3, and there are two types of β-adrenergic receptors, termed β1 and β2. An additional aspect of the adrenergic system is that there is a second signaling molecule called epinephrine. The chemical difference between norepinephrine and epinephrine is the addition of a methyl group (CH3) in epinephrine. The prefix “nor-” actually refers to this chemical difference, in which a methyl group is missing. The term adrenergic should remind you of the word adrenaline, which is associated with the fight-or-flight response described at the beginning of the chapter. Adrenaline and epinephrine are two names for the same molecule. The adrenal gland (in Latin, ad- = “on top of”; renal = “kidney”) secretes adrenaline. The ending “-ine” refers to the chemical being derived, or extracted, from the adrenal gland. A similar construction from Greek instead of Latin results in the word epinephrine (epi- = “above”; nephr- = “kidney”). In scientific usage, epinephrine is preferred in the United States, whereas adrenaline is preferred in Great Britain, because “adrenalin” was once a registered, proprietary drug name in the United States. Though the drug is no longer sold, the convention of referring to this molecule by the two different names persists. Similarly, norepinephrine and noradrenaline are two names for the same molecule. Having understood the cholinergic and adrenergic systems, their role in the autonomic system is relatively simple to understand. All preganglionic fibers, both sympathetic and parasympathetic, release ACh. All ganglionic neurons—the targets of these preganglionic fibers—have nicotinic receptors in their cell membranes. The nicotinic receptor is a ligand-gated cation channel that results in depolarization of the postsynaptic membrane. The postganglionic parasympathetic fibers also release ACh, but the receptors on their targets are muscarinic receptors, which are G protein–coupled receptors and do not exclusively cause depolarization of the postsynaptic membrane. Postganglionic sympathetic fibers release norepinephrine, except for fibers that project to sweat glands and to blood vessels associated with skeletal muscles, which release ACh (Table 15.1). Autonomic System Signaling Molecules \| Sympathetic \| Parasympathetic \| \| \|---\|---\|---\| \| Preganglionic \| Acetylcholine → nicotinic receptor \| Acetylcholine → nicotinic receptor \| \| Postganglionic \| Norepinephrine → α- or β-adrenergic receptors Acetylcholine → muscarinic receptor (associated with sweat glands and the blood vessels associated with skeletal muscles only \| Acetylcholine → muscarinic receptor \| Table 15.1 Signaling molecules can belong to two broad groups. Neurotransmitters are released at synapses, whereas hormones are released into the bloodstream. These are simplistic definitions, but they can help to clarify this point. Acetylcholine can be considered a neurotransmitter because it is released by axons at synapses. The adrenergic system, however, presents a challenge. Postganglionic sympathetic fibers release norepinephrine, which can be considered a neurotransmitter. But the adrenal medulla releases epinephrine and norepinephrine into circulation, so they should be considered hormones. What are referred to here as synapses may not fit the strictest definition of synapse. Some sources will refer to the connection between a postganglionic fiber and a target effector as neuroeffector junctions; neurotransmitters, as defined above, would be called neuromodulators. The structure of postganglionic connections are not the typical synaptic end bulb that is found at the neuromuscular junction, but rather are chains of swellings along the length of a postganglionic fiber called a varicosity (Figure 15.5). Figure 15.5 Autonomic Varicosities The connection between autonomic fibers and target effectors is not the same as the typical synapse, such as the neuromuscular junction. Instead of a synaptic end bulb, a neurotransmitter is released from swellings along the length of a fiber that makes an extended network of connections in the target effector. EVERYDAY CONNECTION Fight or Flight? What About Fright and Freeze? The original usage of the epithet “fight or flight” comes from a scientist named Walter Cannon who worked at Harvard in 1915. The concept of homeostasis and the functioning of the sympathetic system had been introduced in France in the previous century. Cannon expanded the idea, and introduced the idea that an animal responds to a threat by preparing to stand and fight or run away. The nature of this response was thoroughly explained in a book on the physiology of pain, hunger, fear, and rage. When students learn about the sympathetic system and the fight-or-flight response, they often stop and wonder about other responses. If you were faced with a lioness running toward you as pictured at the beginning of this chapter, would you run or would you stand your ground? Some people would say that they would freeze and not know what to do. So isn’t there really more to what the autonomic system does than fight, flight, rest, or digest. What about fear and paralysis in the face of a threat? The common epithet of “fight or flight” is being enlarged to be “fight, flight, or fright” or even “fight, flight, fright, or freeze.” Cannon’s original contribution was a catchy phrase to express some of what the nervous system does in response to a threat, but it is incomplete. The sympathetic system is responsible for the physiological responses to emotional states. The name “sympathetic” can be said to mean that (sym- = “together”; -pathos = “pain,” “suffering,” or “emotion”). INTERACTIVE LINK Watch this video to learn more about the nervous system. As described in this video, the nervous system has a way to deal with threats and stress that is separate from the conscious control of the somatic nervous system. The system comes from a time when threats were about survival, but in the modern age, these responses become part of stress and anxiety. This video describes how the autonomic system is only part of the response to threats, or stressors. What other organ system gets involved, and what part of the brain coordinates the two systems for the entire response, including epinephrine (adrenaline) and cortisol? Autonomic Reflexes and Homeostasis - Compare the structure of somatic and autonomic reflex arcs - Explain the differences in sympathetic and parasympathetic reflexes - Differentiate between short and long reflexes - Determine the effect of the autonomic nervous system on the regulation of the various organ systems on the basis of the signaling molecules involved - Describe the effects of drugs that affect autonomic function The autonomic nervous system regulates organ systems through circuits that resemble the reflexes described in the somatic nervous system. The main difference between the somatic and autonomic systems is in what target tissues are effectors. Somatic responses are solely based on skeletal muscle contraction. The autonomic system, however, targets cardiac and smooth muscle, as well as glandular tissue. Whereas the basic circuit is a reflex arc, there are differences in the structure of those reflexes for the somatic and autonomic systems. The Structure of Reflexes One difference between a somatic reflex, such as the withdrawal reflex, and a visceral reflex, which is an autonomic reflex, is in the efferent branch. The output of a somatic reflex is the lower motor neuron in the ventral horn of the spinal cord that projects directly to a skeletal muscle to cause its contraction. The output of a visceral reflex is a two-step pathway starting with the preganglionic fiber emerging from a lateral horn neuron in the spinal cord, or a cranial nucleus neuron in the brain stem, to a ganglion—followed by the postganglionic fiber projecting to a target effector. The other part of a reflex, the afferent branch, is often the same between the two systems. Sensory neurons receiving input from the periphery—with cell bodies in the sensory ganglia, either of a cranial nerve or a dorsal root ganglion adjacent to the spinal cord—project into the CNS to initiate the reflex (Figure 15.6). The Latin root “effere” means “to carry.” Adding the prefix “ef-” suggests the meaning “to carry away,” whereas adding the prefix “af-” suggests “to carry toward or inward.” Figure 15.6 Comparison of Somatic and Visceral Reflexes The afferent inputs to somatic and visceral reflexes are essentially the same, whereas the efferent branches are different. Somatic reflexes, for instance, involve a direct connection from the ventral horn of the spinal cord to the skeletal muscle. Visceral reflexes involve a projection from the central neuron to a ganglion, followed by a second projection from the ganglion to the target effector. Afferent Branch The afferent branch of a reflex arc does differ between somatic and visceral reflexes in some instances. Many of the inputs to visceral reflexes are from special or somatic senses, but particular senses are associated with the viscera that are not part of the conscious perception of the environment through the somatic nervous system. For example, there is a specific type of mechanoreceptor, called a baroreceptor, in the walls of the aorta and carotid sinuses that senses the stretch of those organs when blood volume or pressure increases. You do not have a conscious perception of having high blood pressure, but that is an important afferent branch of the cardiovascular and, particularly, vasomotor reflexes. The sensory neuron is essentially the same as any other general sensory neuron. The baroreceptor apparatus is part of the ending of a unipolar neuron that has a cell body in a sensory ganglion. The baroreceptors from the carotid arteries have axons in the glossopharyngeal nerve, and those from the aorta have axons in the vagus nerve. Though visceral senses are not primarily a part of conscious perception, those sensations sometimes make it to conscious awareness. If a visceral sense is strong enough, it will be perceived. The sensory homunculus—the representation of the body in the primary somatosensory cortex—only has a small region allotted for the perception of internal stimuli. If you swallow a large bolus of food, for instance, you will probably feel the lump of that food as it pushes through your esophagus, or even if your stomach is distended after a large meal. If you inhale especially cold air, you can feel it as it enters your larynx and trachea. These sensations are not the same as feeling high blood pressure or blood sugar levels. When particularly strong visceral sensations rise to the level of conscious perception, the sensations are often felt in unexpected places. For example, strong visceral sensations of the heart will be felt as pain in the left shoulder and left arm. This irregular pattern of projection of conscious perception of visceral sensations is called referred pain. Depending on the organ system affected, the referred pain will project to different areas of the body (Figure 15.7). The location of referred pain is not random, but a definitive explanation of the mechanism has not been established. The most broadly accepted theory for this phenomenon is that the visceral sensory fibers enter into the same level of the spinal cord as the somatosensory fibers of the referred pain location. By this explanation, the visceral sensory fibers from the mediastinal region, where the heart is located, would enter the spinal cord at the same level as the spinal nerves from the shoulder and arm, so the brain misinterprets the sensations from the mediastinal region as being from the axillary and brachial regions. Projections from the medial and inferior divisions of the cervical ganglia do enter the spinal cord at the middle to lower cervical levels, which is where the somatosensory fibers enter. Figure 15.7 Referred Pain Chart Conscious perception of visceral sensations map to specific regions of the body, as shown in this chart. Some sensations are felt locally, whereas others are perceived as affecting areas that are quite distant from the involved organ. DISORDERS OF THE... Nervous System: Kehr’s Sign Kehr’s sign is the presentation of pain in the left shoulder, chest, and neck regions following rupture of the spleen. The spleen is in the upper-left abdominopelvic quadrant, but the pain is more in the shoulder and neck. How can this be? The sympathetic fibers connected to the spleen are from the celiac ganglion, which would be from the mid-thoracic to lower thoracic region whereas parasympathetic fibers are found in the vagus nerve, which connects in the medulla of the brain stem. However, the neck and shoulder would connect to the spinal cord at the mid-cervical level of the spinal cord. These connections do not fit with the expected correspondence of visceral and somatosensory fibers entering at the same level of the spinal cord. The incorrect assumption would be that the visceral sensations are coming from the spleen directly. In fact, the visceral fibers are coming from the diaphragm. The nerve connecting to the diaphragm takes a special route. The phrenic nerve is connected to the spinal cord at cervical levels 3 to 5. The motor fibers that make up this nerve are responsible for the muscle contractions that drive ventilation. These fibers have left the spinal cord to enter the phrenic nerve, meaning that spinal cord damage below the mid-cervical level is not fatal by making ventilation impossible. Therefore, the visceral fibers from the diaphragm enter the spinal cord at the same level as the somatosensory fibers from the neck and shoulder. The diaphragm plays a role in Kehr’s sign because the spleen is just inferior to the diaphragm in the upper-left quadrant of the abdominopelvic cavity. When the spleen ruptures, blood spills into this region. The accumulating hemorrhage then puts pressure on the diaphragm. The visceral sensation is actually in the diaphragm, so the referred pain is in a region of the body that corresponds to the diaphragm, not the spleen. Efferent Branch The efferent branch of the visceral reflex arc begins with the projection from the central neuron along the preganglionic fiber. This fiber then makes a synapse on the ganglionic neuron that projects to the target effector. The effector organs that are the targets of the autonomic system range from the iris and ciliary body of the eye to the urinary bladder and reproductive organs. The thoracolumbar output, through the various sympathetic ganglia, reaches all of these organs. The cranial component of the parasympathetic system projects from the eye to part of the intestines. The sacral component picks up with the majority of the large intestine and the pelvic organs of the urinary and reproductive systems. Short and Long Reflexes Somatic reflexes involve sensory neurons that connect sensory receptors to the CNS and motor neurons that project back out to the skeletal muscles. Visceral reflexes that involve the thoracolumbar or craniosacral systems share similar connections. However, there are reflexes that do not need to involve any CNS components. A long reflex has afferent branches that enter the spinal cord or brain and involve the efferent branches, as previously explained. A short reflex is completely peripheral and only involves the local integration of sensory input with motor output (Figure 15.8). Figure 15.8 Short and Long Reflexes Sensory input can stimulate either a short or a long reflex. A sensory neuron can project to the CNS or to an autonomic ganglion. The short reflex involves the direct stimulation of a postganglionic fiber by the sensory neuron, whereas the long reflex involves integration in the spinal cord or brain. The difference between short and long reflexes is in the involvement of the CNS. Somatic reflexes always involve the CNS, even in a monosynaptic reflex in which the sensory neuron directly activates the motor neuron. That synapse is in the spinal cord or brain stem, so it has to involve the CNS. However, in the autonomic system there is the possibility that the CNS is not involved. Because the efferent branch of a visceral reflex involves two neurons—the central neuron and the ganglionic neuron—a “short circuit” can be possible. If a sensory neuron projects directly to the ganglionic neuron and causes it to activate the effector target, then the CNS is not involved. A division of the nervous system that is related to the autonomic nervous system is the enteric nervous system. The word enteric refers to the digestive organs, so this represents the nervous tissue that is part of the digestive system. There are a few myenteric plexuses in which the nervous tissue in the wall of the digestive tract organs can directly influence digestive function. If stretch receptors in the stomach are activated by the filling and distension of the stomach, a short reflex will directly activate the smooth muscle fibers of the stomach wall to increase motility to digest the excessive food in the stomach. No CNS involvement is needed because the stretch receptor is directly activating a neuron in the wall of the stomach that causes the smooth muscle to contract. That neuron, connected to the smooth muscle, is a postganglionic parasympathetic neuron that can be controlled by a fiber found in the vagus nerve. INTERACTIVE LINK Read this article to learn about a teenager who experiences a series of spells that suggest a stroke. He undergoes endless tests and seeks input from multiple doctors. In the end, one expert, one question, and a simple blood pressure cuff answers the question. Why would the heart have to beat faster when the teenager changes his body position from lying down to sitting, and then to standing? Balance in Competing Autonomic Reflex Arcs The autonomic nervous system is important for homeostasis because its two divisions compete at the target effector. The balance of homeostasis is attributable to the competing inputs from the sympathetic and parasympathetic divisions (dual innervation). At the level of the target effector, the signal of which system is sending the message is strictly chemical. A signaling molecule binds to a receptor that causes changes in the target cell, which in turn causes the tissue or organ to respond to the changing conditions of the body. Competing Neurotransmitters The postganglionic fibers of the sympathetic and parasympathetic divisions both release neurotransmitters that bind to receptors on their targets. Postganglionic sympathetic fibers release norepinephrine, with a minor exception, whereas postganglionic parasympathetic fibers release ACh. For any given target, the difference in which division of the autonomic nervous system is exerting control is just in what chemical binds to its receptors. The target cells will have adrenergic and muscarinic receptors. If norepinephrine is released, it will bind to the adrenergic receptors present on the target cell, and if ACh is released, it will bind to the muscarinic receptors on the target cell. In the sympathetic system, there are exceptions to this pattern of dual innervation. The postganglionic sympathetic fibers that contact the blood vessels within skeletal muscle and that contact sweat glands do not release norepinephrine, they release ACh. This does not create any problem because there is no parasympathetic input to the sweat glands. Sweat glands have muscarinic receptors and produce and secrete sweat in response to the presence of ACh. At most of the other targets of the autonomic system, the effector response is based on which neurotransmitter is released and what receptor is present. For example, regions of the heart that establish heart rate are contacted by postganglionic fibers from both systems. If norepinephrine is released onto those cells, it binds to an adrenergic receptor that causes the cells to depolarize faster, and the heart rate increases. If ACh is released onto those cells, it binds to a muscarinic receptor that causes the cells to hyperpolarize so that they cannot reach threshold as easily, and the heart rate slows. Without this parasympathetic input, the heart would work at a rate of approximately 100 beats per minute (bpm). The sympathetic system speeds that up, as it would during exercise, to 120–140 bpm, for example. The parasympathetic system slows it down to the resting heart rate of 60–80 bpm. Another example is in the control of pupillary size (Figure 15.9). The afferent branch responds to light hitting the retina. Photoreceptors are activated, and the signal is transferred to the retinal ganglion cells that send an action potential along the optic nerve into the diencephalon. If light levels are low, the sympathetic system sends a signal out through the upper thoracic spinal cord to the superior cervical ganglion of the sympathetic chain. The postganglionic fiber then projects to the iris, where it releases norepinephrine onto the radial fibers of the iris (a smooth muscle). When those fibers contract, the pupil dilates—increasing the amount of light hitting the retina. If light levels are too high, the parasympathetic system sends a signal out from the Eddinger–Westphal nucleus through the oculomotor nerve. This fiber synapses in the ciliary ganglion in the posterior orbit. The postganglionic fiber then projects to the iris, where it releases ACh onto the circular fibers of the iris—another smooth muscle. When those fibers contract, the pupil constricts to limit the amount of light hitting the retina. Figure 15.9 Autonomic Control of Pupillary Size Activation of the pupillary reflex comes from the amount of light activating the retinal ganglion cells, as sent along the optic nerve. The output of the sympathetic system projects through the superior cervical ganglion, whereas the parasympathetic system originates out of the midbrain and projects through the oculomotor nerve to the ciliary ganglion, which then projects to the iris. The postganglionic fibers of either division release neurotransmitters onto the smooth muscles of the iris to cause changes in the pupillary size. Norepinephrine results in dilation and ACh results in constriction. In this example, the autonomic system is controlling how much light hits the retina. It is a homeostatic reflex mechanism that keeps the activation of photoreceptors within certain limits. In the context of avoiding a threat like the lioness on the savannah, the sympathetic response for fight or flight will increase pupillary diameter so that more light hits the retina and more visual information is available for running away. Likewise, the parasympathetic response of rest reduces the amount of light reaching the retina, allowing the photoreceptors to cycle through bleaching and be regenerated for further visual perception; this is what the homeostatic process is attempting to maintain. INTERACTIVE LINK Watch this video to learn about the pupillary reflexes. The pupillary light reflex involves sensory input through the optic nerve and motor response through the oculomotor nerve to the ciliary ganglion, which projects to the circular fibers of the iris. As shown in this short animation, pupils will constrict to limit the amount of light falling on the retina under bright lighting conditions. What constitutes the afferent and efferent branches of the competing reflex (dilation)? Autonomic Tone Organ systems are balanced between the input from the sympathetic and parasympathetic divisions. When something upsets that balance, the homeostatic mechanisms strive to return it to its regular state. For each organ system, there may be more of a sympathetic or parasympathetic tendency to the resting state, which is known as the autonomic tone of the system. For example, the heart rate was described above. Because the resting heart rate is the result of the parasympathetic system slowing the heart down from its intrinsic rate of 100 bpm, the heart can be said to be in parasympathetic tone. In a similar fashion, another aspect of the cardiovascular system is primarily under sympathetic control. Blood pressure is partially determined by the contraction of smooth muscle in the walls of blood vessels. These tissues have adrenergic receptors that respond to the release of norepinephrine from postganglionic sympathetic fibers by constricting and increasing blood pressure. The hormones released from the adrenal medulla—epinephrine and norepinephrine—will also bind to these receptors. Those hormones travel through the bloodstream where they can easily interact with the receptors in the vessel walls. The parasympathetic system has no significant input to the systemic blood vessels, so the sympathetic system determines their tone. There are a limited number of blood vessels that respond to sympathetic input in a different fashion. Blood vessels in skeletal muscle, particularly those in the lower limbs, are more likely to dilate. It does not have an overall effect on blood pressure to alter the tone of the vessels, but rather allows for blood flow to increase for those skeletal muscles that will be active in the fight-or-flight response. The blood vessels that have a parasympathetic projection are limited to those in the erectile tissue of the reproductive organs. Acetylcholine released by these postganglionic parasympathetic fibers cause the vessels to dilate, leading to the engorgement of the erectile tissue. HOMEOSTATIC IMBALANCES Orthostatic Hypotension Have you ever stood up quickly and felt dizzy for a moment? This is because, for one reason or another, blood is not getting to your brain so it is briefly deprived of oxygen. When you change position from sitting or lying down to standing, your cardiovascular system has to adjust for a new challenge, keeping blood pumping up into the head while gravity is pulling more and more blood down into the legs. The reason for this is a sympathetic reflex that maintains the output of the heart in response to postural change. When a person stands up, proprioceptors indicate that the body is changing position. A signal goes to the CNS, which then sends a signal to the upper thoracic spinal cord neurons of the sympathetic division. The sympathetic system then causes the heart to beat faster and the blood vessels to constrict. Both changes will make it possible for the cardiovascular system to maintain the rate of blood delivery to the brain. Blood is being pumped superiorly through the internal branch of the carotid arteries into the brain, against the force of gravity. Gravity is not increasing while standing, but blood is more likely to flow down into the legs as they are extended for standing. This sympathetic reflex keeps the brain well oxygenated so that cognitive and other neural processes are not interrupted. Sometimes this does not work properly. If the sympathetic system cannot increase cardiac output, then blood pressure into the brain will decrease, and a brief neurological loss can be felt. This can be brief, as a slight “wooziness” when standing up too quickly, or a loss of balance and neurological impairment for a period of time. The name for this is orthostatic hypotension, which means that blood pressure goes below the homeostatic set point when standing. It can be the result of standing up faster than the reflex can occur, which may be referred to as a benign “head rush,” or it may be the result of an underlying cause. There are two basic reasons that orthostatic hypotension can occur. First, blood volume is too low and the sympathetic reflex is not effective. This hypovolemia may be the result of dehydration or medications that affect fluid balance, such as diuretics or vasodilators. Both of these medications are meant to lower blood pressure, which may be necessary in the case of systemic hypertension, and regulation of the medications may alleviate the problem. Sometimes increasing fluid intake or water retention through salt intake can improve the situation. The second underlying cause of orthostatic hypotension is autonomic failure. There are several disorders that result in compromised sympathetic functions. The disorders range from diabetes to multiple system atrophy (a loss of control over many systems in the body), and addressing the underlying condition can improve the hypotension. For example, with diabetes, peripheral nerve damage can occur, which would affect the postganglionic sympathetic fibers. Getting blood glucose levels under control can improve neurological deficits associated with diabetes. Central Control - Describe the role of higher centers of the brain in autonomic regulation - Explain the connection of the hypothalamus to homeostasis - Describe the regions of the CNS that link the autonomic system with emotion - Describe the pathways important to descending control of the autonomic system The pupillary light reflex (Figure 15.10) begins when light hits the retina and causes a signal to travel along the optic nerve. This is visual sensation, because the afferent branch of this reflex is simply sharing the special sense pathway. Bright light hitting the retina leads to the parasympathetic response, through the oculomotor nerve, followed by the postganglionic fiber from the ciliary ganglion, which stimulates the circular fibers of the iris to contract and constrict the pupil. When light hits the retina in one eye, both pupils contract. When that light is removed, both pupils dilate again back to the resting position. When the stimulus is unilateral (presented to only one eye), the response is bilateral (both eyes). The same is not true for somatic reflexes. If you touch a hot radiator, you only pull that arm back, not both. Central control of autonomic reflexes is different than for somatic reflexes. The hypothalamus, along with other CNS locations, controls the autonomic system. Figure 15.10 Pupillary Reflex Pathways The pupil is under competing autonomic control in response to light levels hitting the retina. The sympathetic system will dilate the pupil when the retina is not receiving enough light, and the parasympathetic system will constrict the pupil when too much light hits the retina. Forebrain Structures Autonomic control is based on the visceral reflexes, composed of the afferent and efferent branches. These homeostatic mechanisms are based on the balance between the two divisions of the autonomic system, which results in tone for various organs that is based on the predominant input from the sympathetic or parasympathetic systems. Coordinating that balance requires integration that begins with forebrain structures like the hypothalamus and continues into the brain stem and spinal cord. The Hypothalamus The hypothalamus is the control center for many homeostatic mechanisms. It regulates both autonomic function and endocrine function. The roles it plays in the pupillary reflexes demonstrates the importance of this control center. The optic nerve projects primarily to the thalamus, which is the necessary relay to the occipital cortex for conscious visual perception. Another projection of the optic nerve, however, goes to the hypothalamus. The hypothalamus then uses this visual system input to drive the pupillary reflexes. If the retina is activated by high levels of light, the hypothalamus stimulates the parasympathetic response. If the optic nerve message shows that low levels of light are falling on the retina, the hypothalamus activates the sympathetic response. Output from the hypothalamus follows two main tracts, the dorsal longitudinal fasciculus and the medial forebrain bundle (Figure 15.11). Along these two tracts, the hypothalamus can influence the Eddinger–Westphal nucleus of the oculomotor complex or the lateral horns of the thoracic spinal cord. Figure 15.11 Fiber Tracts of the Central Autonomic System The hypothalamus is the source of most of the central control of autonomic function. It receives input from cerebral structures and projects to brain stem and spinal cord structures to regulate the balance of sympathetic and parasympathetic input to the organ systems of the body. The main pathways for this are the medial forebrain bundle and the dorsal longitudinal fasciculus. These two tracts connect the hypothalamus with the major parasympathetic nuclei in the brain stem and the preganglionic (central) neurons of the thoracolumbar spinal cord. The hypothalamus also receives input from other areas of the forebrain through the medial forebrain bundle. The olfactory cortex, the septal nuclei of the basal forebrain, and the amygdala project into the hypothalamus through the medial forebrain bundle. These forebrain structures inform the hypothalamus about the state of the nervous system and can influence the regulatory processes of homeostasis. A good example of this is found in the amygdala, which is found beneath the cerebral cortex of the temporal lobe and plays a role in our ability to remember and feel emotions. The Amygdala The amygdala is a group of nuclei in the medial region of the temporal lobe that is part of the limbic lobe (Figure 15.12). The limbic lobe includes structures that are involved in emotional responses, as well as structures that contribute to memory function. The limbic lobe has strong connections with the hypothalamus and influences the state of its activity on the basis of emotional state. For example, when you are anxious or scared, the amygdala will send signals to the hypothalamus along the medial forebrain bundle that will stimulate the sympathetic fight-or-flight response. The hypothalamus will also stimulate the release of stress hormones through its control of the endocrine system in response to amygdala input. Figure 15.12 The Limbic Lobe Structures arranged around the edge of the cerebrum constitute the limbic lobe, which includes the amygdala, hippocampus, and cingulate gyrus, and connects to the hypothalamus. The Medulla The medulla contains nuclei referred to as the cardiovascular center, which controls the smooth and cardiac muscle of the cardiovascular system through autonomic connections. When the homeostasis of the cardiovascular system shifts, such as when blood pressure changes, the coordination of the autonomic system can be accomplished within this region. Furthermore, when descending inputs from the hypothalamus stimulate this area, the sympathetic system can increase activity in the cardiovascular system, such as in response to anxiety or stress. The preganglionic sympathetic fibers that are responsible for increasing heart rate are referred to as the cardiac accelerator nerves, whereas the preganglionic sympathetic fibers responsible for constricting blood vessels compose the vasomotor nerves. Several brain stem nuclei are important for the visceral control of major organ systems. One brain stem nucleus involved in cardiovascular function is the solitary nucleus. It receives sensory input about blood pressure and cardiac function from the glossopharyngeal and vagus nerves, and its output will activate sympathetic stimulation of the heart or blood vessels through the upper thoracic lateral horn. Another brain stem nucleus important for visceral control is the dorsal motor nucleus of the vagus nerve, which is the motor nucleus for the parasympathetic functions ascribed to the vagus nerve, including decreasing the heart rate, relaxing bronchial tubes in the lungs, and activating digestive function through the enteric nervous system. The nucleus ambiguus, which is named for its ambiguous histology, also contributes to the parasympathetic output of the vagus nerve and targets muscles in the pharynx and larynx for swallowing and speech, as well as contributing to the parasympathetic tone of the heart along with the dorsal motor nucleus of the vagus. EVERYDAY CONNECTION Exercise and the Autonomic System In addition to its association with the fight-or-flight response and rest-and-digest functions, the autonomic system is responsible for certain everyday functions. For example, it comes into play when homeostatic mechanisms dynamically change, such as the physiological changes that accompany exercise. Getting on the treadmill and putting in a good workout will cause the heart rate to increase, breathing to be stronger and deeper, sweat glands to activate, and the digestive system to suspend activity. These are the same physiological changes associated with the fight-or-flight response, but there is nothing chasing you on that treadmill. This is not a simple homeostatic mechanism at work because “maintaining the internal environment” would mean getting all those changes back to their set points. Instead, the sympathetic system has become active during exercise so that your body can cope with what is happening. A homeostatic mechanism is dealing with the conscious decision to push the body away from a resting state. The heart, actually, is moving away from its homeostatic set point. Without any input from the autonomic system, the heart would beat at approximately 100 bpm, and the parasympathetic system slows that down to the resting rate of approximately 70 bpm. But in the middle of a good workout, you should see your heart rate at 120–140 bpm. You could say that the body is stressed because of what you are doing to it. Homeostatic mechanisms are trying to keep blood pH in the normal range, or to keep body temperature under control, but those are in response to the choice to exercise. INTERACTIVE LINK Watch this video to learn about physical responses to emotion. The autonomic system, which is important for regulating the homeostasis of the organ systems, is also responsible for our physiological responses to emotions such as fear. The video summarizes the extent of the body’s reactions and describes several effects of the autonomic system in response to fear. On the basis of what you have already studied about autonomic function, which effect would you expect to be associated with parasympathetic, rather than sympathetic, activity? Drugs that Affect the Autonomic System - List the classes of pharmaceuticals that interact with the autonomic nervous system - Differentiate between cholinergic and adrenergic compounds - Differentiate between sympathomimetic and sympatholytic drugs - Relate the consequences of nicotine abuse with respect to autonomic control of the cardiovascular system An important way to understand the effects of native neurochemicals in the autonomic system is in considering the effects of pharmaceutical drugs. This can be considered in terms of how drugs change autonomic function. These effects will primarily be based on how drugs act at the receptors of the autonomic system neurochemistry. The signaling molecules of the nervous system interact with proteins in the cell membranes of various target cells. In fact, no effect can be attributed to just the signaling molecules themselves without considering the receptors. A chemical that the body produces to interact with those receptors is called an endogenous chemical, whereas a chemical introduced to the system from outside is an exogenous chemical. Exogenous chemicals may be of a natural origin, such as a plant extract, or they may be synthetically produced in a pharmaceutical laboratory. Broad Autonomic Effects One important drug that affects the autonomic system broadly is not a pharmaceutical therapeutic agent associated with the system. This drug is nicotine. The effects of nicotine on the autonomic nervous system are important in considering the role smoking can play in health. All ganglionic neurons of the autonomic system, in both sympathetic and parasympathetic ganglia, are activated by ACh released from preganglionic fibers. The ACh receptors on these neurons are of the nicotinic type, meaning that they are ligand-gated ion channels. When the neurotransmitter released from the preganglionic fiber binds to the receptor protein, a channel opens to allow positive ions to cross the cell membrane. The result is depolarization of the ganglia. Nicotine acts as an ACh analog at these synapses, so when someone takes in the drug, it binds to these ACh receptors and activates the ganglionic neurons, causing them to depolarize. Ganglia of both divisions are activated equally by the drug. For many target organs in the body, this results in no net change. The competing inputs to the system cancel each other out and nothing significant happens. For example, the sympathetic system will cause sphincters in the digestive tract to contract, limiting digestive propulsion, but the parasympathetic system will cause the contraction of other muscles in the digestive tract, which will try to push the contents of the digestive system along. The end result is that the food does not really move along and the digestive system has not appreciably changed. The system in which this can be problematic is in the cardiovascular system, which is why smoking is a risk factor for cardiovascular disease. First, there is no significant parasympathetic regulation of blood pressure. Only a limited number of blood vessels are affected by parasympathetic input, so nicotine will preferentially cause the vascular tone to become more sympathetic, which means blood pressure will be increased. Second, the autonomic control of the heart is special. Unlike skeletal or smooth muscles, cardiac muscle is intrinsically active, meaning that it generates its own action potentials. The autonomic system does not cause the heart to beat, it just speeds it up (sympathetic) or slows it down (parasympathetic). The mechanisms for this are not mutually exclusive, so the heart receives conflicting signals, and the rhythm of the heart can be affected (Figure 15.13). Figure 15.13 Autonomic Connections to Heart and Blood Vessels The nicotinic receptor is found on all autonomic ganglia, but the cardiovascular connections are particular, and do not conform to the usual competitive projections that would just cancel each other out when stimulated by nicotine. The opposing signals to the heart would both depolarize and hyperpolarize the heart cells that establish the rhythm of the heartbeat, likely causing arrhythmia. Only the sympathetic system governs systemic blood pressure so nicotine would cause an increase. Sympathetic Effect The neurochemistry of the sympathetic system is based on the adrenergic system. Norepinephrine and epinephrine influence target effectors by binding to the α-adrenergic or β-adrenergic receptors. Drugs that affect the sympathetic system affect these chemical systems. The drugs can be classified by whether they enhance the functions of the sympathetic system or interrupt those functions. A drug that enhances adrenergic function is known as a sympathomimetic drug, whereas a drug that interrupts adrenergic function is a sympatholytic drug. Sympathomimetic Drugs When the sympathetic system is not functioning correctly or the body is in a state of homeostatic imbalance, these drugs act at postganglionic terminals and synapses in the sympathetic efferent pathway. These drugs either bind to particular adrenergic receptors and mimic norepinephrine at the synapses between sympathetic postganglionic fibers and their targets, or they increase the production and release of norepinephrine from postganglionic fibers. Also, to increase the effectiveness of adrenergic chemicals released from the fibers, some of these drugs may block the removal or reuptake of the neurotransmitter from the synapse. A common sympathomimetic drug is phenylephrine, which is a common component of decongestants. It can also be used to dilate the pupil and to raise blood pressure. Phenylephrine is known as an α1-adrenergic agonist, meaning that it binds to a specific adrenergic receptor, stimulating a response. In this role, phenylephrine will bind to the adrenergic receptors in bronchioles of the lungs and cause them to dilate. By opening these structures, accumulated mucus can be cleared out of the lower respiratory tract. Phenylephrine is often paired with other pharmaceuticals, such as analgesics, as in the “sinus” version of many over-the-counter drugs, such as Tylenol Sinus® or Excedrin Sinus®, or in expectorants for chest congestion such as in Robitussin CF®. A related molecule, called pseudoephedrine, was much more commonly used in these applications than was phenylephrine, until the molecule became useful in the illicit production of amphetamines. Phenylephrine is not as effective as a drug because it can be partially broken down in the digestive tract before it is ever absorbed. Like the adrenergic agents, phenylephrine is effective in dilating the pupil, known as mydriasis (Figure 15.14). Phenylephrine is used during an eye exam in an ophthalmologist’s or optometrist’s office for this purpose. It can also be used to increase blood pressure in situations in which cardiac function is compromised, such as under anesthesia or during septic shock. Figure 15.14 Mydriasis The sympathetic system causes pupillary dilation when norepinephrine binds to an adrenergic receptor in the radial fibers of the iris smooth muscle. Phenylephrine mimics this action by binding to the same receptor when drops are applied onto the surface of the eye in a doctor’s office. (credit: Corey Theiss) Other drugs that enhance adrenergic function are not associated with therapeutic uses, but affect the functions of the sympathetic system in a similar fashion. Cocaine primarily interferes with the uptake of dopamine at the synapse and can also increase adrenergic function. Caffeine is an antagonist to a different neurotransmitter receptor, called the adenosine receptor. Adenosine will suppress adrenergic activity, specifically the release of norepinephrine at synapses, so caffeine indirectly increases adrenergic activity. There is some evidence that caffeine can aid in the therapeutic use of drugs, perhaps by potentiating (increasing) sympathetic function, as is suggested by the inclusion of caffeine in over-the-counter analgesics such as Excedrin®. Sympatholytic Drugs Drugs that interfere with sympathetic function are referred to as sympatholytic, or sympathoplegic, drugs. They primarily work as an antagonist to the adrenergic receptors. They block the ability of norepinephrine or epinephrine to bind to the receptors so that the effect is “cut” or “takes a blow,” to refer to the endings “-lytic” and “-plegic,” respectively. The various drugs of this class will be specific to α-adrenergic or β-adrenergic receptors, or to their receptor subtypes. Possibly the most familiar type of sympatholytic drug are the β-blockers. These drugs are often used to treat cardiovascular disease because they block the β-receptors associated with vasoconstriction and cardioacceleration. By allowing blood vessels to dilate, or keeping heart rate from increasing, these drugs can improve cardiac function in a compromised system, such as for a person with congestive heart failure or who has previously suffered a heart attack. A couple of common versions of β-blockers are metoprolol, which specifically blocks the β1-receptor, and propanolol, which nonspecifically blocks β-receptors. There are other drugs that are α-blockers and can affect the sympathetic system in a similar way. Other uses for sympatholytic drugs are as antianxiety medications. A common example of this is clonidine, which is an α-agonist. The sympathetic system is tied to anxiety to the point that the sympathetic response can be referred to as “fight, flight, or fright.” Clonidine is used for other treatments aside from hypertension and anxiety, including pain conditions and attention deficit hyperactivity disorder. Parasympathetic Effects Drugs affecting parasympathetic functions can be classified into those that increase or decrease activity at postganglionic terminals. Parasympathetic postganglionic fibers release ACh, and the receptors on the targets are muscarinic receptors. There are several types of muscarinic receptors, M1–M5, but the drugs are not usually specific to the specific types. Parasympathetic drugs can be either muscarinic agonists or antagonists, or have indirect effects on the cholinergic system. Drugs that enhance cholinergic effects are called parasympathomimetic drugs, whereas those that inhibit cholinergic effects are referred to as anticholinergic drugs. Pilocarpine is a nonspecific muscarinic agonist commonly used to treat disorders of the eye. It reverses mydriasis, such as is caused by phenylephrine, and can be administered after an eye exam. Along with constricting the pupil through the smooth muscle of the iris, pilocarpine will also cause the ciliary muscle to contract. This will open perforations at the base of the cornea, allowing for the drainage of aqueous humor from the anterior compartment of the eye and, therefore, reducing intraocular pressure related to glaucoma. Atropine and scopolamine are part of a class of muscarinic antagonists that come from the Atropa genus of plants that include belladonna or deadly nightshade (Figure 15.15). The name of one of these plants, belladonna, refers to the fact that extracts from this plant were used cosmetically for dilating the pupil. The active chemicals from this plant block the muscarinic receptors in the iris and allow the pupil to dilate, which is considered attractive because it makes the eyes appear larger. Humans are instinctively attracted to anything with larger eyes, which comes from the fact that the ratio of eye-to-head size is different in infants (or baby animals) and can elicit an emotional response. The cosmetic use of belladonna extract was essentially acting on this response. Atropine is no longer used in this cosmetic capacity for reasons related to the other name for the plant, which is deadly nightshade. Suppression of parasympathetic function, especially when it becomes systemic, can be fatal. Autonomic regulation is disrupted and anticholinergic symptoms develop. The berries of this plant are highly toxic, but can be mistaken for other berries. The antidote for atropine or scopolamine poisoning is pilocarpine. Figure 15.15 Belladonna Plant The plant from the genus Atropa, which is known as belladonna or deadly nightshade, was used cosmetically to dilate pupils, but can be fatal when ingested. The berries on the plant may seem attractive as a fruit, but they contain the same anticholinergic compounds as the rest of the plant. Sympathetic and Parasympathetic Effects of Different Drug Types \| Drug type \| Example(s) \| Sympathetic effect \| Parasympathetic effect \| Overall result \| \|---\|---\|---\|---\|---\| \| Nicotinic agonists \| Nicotine \| Mimic ACh at preganglionic synapses, causing activation of postganglionic fibers and the release of norepinephrine onto the target organ \| Mimic ACh at preganglionic synapses, causing activation of postganglionic fibers and the release of ACh onto the target organ \| Most conflicting signals cancel each other out, but cardiovascular system is susceptible to hypertension and arrhythmias \| \| Sympathomimetic drugs \| Phenylephrine \| Bind to adrenergic receptors or mimics sympathetic action in some other way \| No effect \| Increase sympathetic tone \| \| Sympatholytic drugs \| β-blockers such as propanolol or metoprolol; α-agonists such as clonidine \| Block binding to adrenergic drug or decrease adrenergic signals \| No effect \| Increase parasympathetic tone \| \| Parasymphatho-mimetics/muscarinic agonists \| Pilocarpine \| No effect, except on sweat glands \| Bind to muscarinic receptor, similar to ACh \| Increase parasympathetic tone \| \| Anticholinergics/muscarinic antagonists \| Atropine, scopolamine, dimenhydrinate \| No effect \| Block muscarinic receptors and parasympathetic function \| Increase sympathetic tone \| Table 15.2 DISORDERS OF THE... Autonomic Nervous System Approximately 33 percent of people experience a mild problem with motion sickness, whereas up to 66 percent experience motion sickness under extreme conditions, such as being on a tossing boat with no view of the horizon. Connections between regions in the brain stem and the autonomic system result in the symptoms of nausea, cold sweats, and vomiting. The part of the brain responsible for vomiting, or emesis, is known as the area postrema. It is located next to the fourth ventricle and is not restricted by the blood–brain barrier, which allows it to respond to chemicals in the bloodstream—namely, toxins that will stimulate emesis. There are significant connections between this area, the solitary nucleus, and the dorsal motor nucleus of the vagus nerve. These autonomic system and nuclei connections are associated with the symptoms of motion sickness. Motion sickness is the result of conflicting information from the visual and vestibular systems. If motion is perceived by the visual system without the complementary vestibular stimuli, or through vestibular stimuli without visual confirmation, the brain stimulates emesis and the associated symptoms. The area postrema, by itself, appears to be able to stimulate emesis in response to toxins in the blood, but it is also connected to the autonomic system and can trigger a similar response to motion. Autonomic drugs are used to combat motion sickness. Though it is often described as a dangerous and deadly drug, scopolamine is used to treat motion sickness. A popular treatment for motion sickness is the transdermal scopolamine patch. Scopolamine is one of the substances derived from the Atropa genus along with atropine. At higher doses, those substances are thought to be poisonous and can lead to an extreme sympathetic syndrome. However, the transdermal patch regulates the release of the drug, and the concentration is kept very low so that the dangers are avoided. For those who are concerned about using “The Most Dangerous Drug,” as some websites will call it, antihistamines such as dimenhydrinate (Dramamine®) can be used. INTERACTIVE LINK Watch this video to learn about the side effects of 3-D movies. As discussed in this video, movies that are shot in 3-D can cause motion sickness, which elicits the autonomic symptoms of nausea and sweating. The disconnection between the perceived motion on the screen and the lack of any change in equilibrium stimulates these symptoms. Why do you think sitting close to the screen or right in the middle of the theater makes motion sickness during a 3-D movie worse? Key Terms - acetylcholine (ACh) - neurotransmitter that binds at a motor end-plate to trigger depolarization - adrenal medulla - interior portion of the adrenal (or suprarenal) gland that releases epinephrine and norepinephrine into the bloodstream as hormones - adrenergic - synapse where norepinephrine is released, which binds to α- or β-adrenergic receptors - afferent branch - component of a reflex arc that represents the input from a sensory neuron, for either a special or general sense - agonist - any exogenous substance that binds to a receptor and produces a similar effect to the endogenous ligand - alpha (α)-adrenergic receptor - one of the receptors to which epinephrine and norepinephrine bind, which comes in three subtypes: α1, α2, and α3 - antagonist - any exogenous substance that binds to a receptor and produces an opposing effect to the endogenous ligand - anticholinergic drugs - drugs that interrupt or reduce the function of the parasympathetic system - autonomic tone - tendency of an organ system to be governed by one division of the autonomic nervous system over the other, such as heart rate being lowered by parasympathetic input at rest - baroreceptor - mechanoreceptor that senses the stretch of blood vessels to indicate changes in blood pressure - beta (β)-adrenergic receptor - one of the receptors to which epinephrine and norepinephrine bind, which comes in two subtypes: β1 and β2 - cardiac accelerator nerves - preganglionic sympathetic fibers that cause the heart rate to increase when the cardiovascular center in the medulla initiates a signal - cardiovascular center - region in the medulla that controls the cardiovascular system through cardiac accelerator nerves and vasomotor nerves, which are components of the sympathetic division of the autonomic nervous system - celiac ganglion - one of the collateral ganglia of the sympathetic system that projects to the digestive system - central neuron - specifically referring to the cell body of a neuron in the autonomic system that is located in the central nervous system, specifically the lateral horn of the spinal cord or a brain stem nucleus - cholinergic - synapse at which acetylcholine is released and binds to the nicotinic or muscarinic receptor - chromaffin cells - neuroendocrine cells of the adrenal medulla that release epinephrine and norepinephrine into the bloodstream as part of sympathetic system activity - ciliary ganglion - one of the terminal ganglia of the parasympathetic system, located in the posterior orbit, axons from which project to the iris - collateral ganglia - ganglia outside of the sympathetic chain that are targets of sympathetic preganglionic fibers, which are the celiac, inferior mesenteric, and superior mesenteric ganglia - craniosacral system - alternate name for the parasympathetic division of the autonomic nervous system that is based on the anatomical location of central neurons in brain-stem nuclei and the lateral horn of the sacral spinal cord; also referred to as craniosacral outflow - dorsal longitudinal fasciculus - major output pathway of the hypothalamus that descends through the gray matter of the brain stem and into the spinal cord - dorsal nucleus of the vagus nerve - location of parasympathetic neurons that project through the vagus nerve to terminal ganglia in the thoracic and abdominal cavities - Eddinger–Westphal nucleus - location of parasympathetic neurons that project to the ciliary ganglion - efferent branch - component of a reflex arc that represents the output, with the target being an effector, such as muscle or glandular tissue - endogenous - describes substance made in the human body - endogenous chemical - substance produced and released within the body to interact with a receptor protein - epinephrine - signaling molecule released from the adrenal medulla into the bloodstream as part of the sympathetic response - exogenous - describes substance made outside of the human body - exogenous chemical - substance from a source outside the body, whether it be another organism such as a plant or from the synthetic processes of a laboratory, that binds to a transmembrane receptor protein - fight-or-flight response - set of responses induced by sympathetic activity that lead to either fleeing a threat or standing up to it, which in the modern world is often associated with anxious feelings - G protein–coupled receptor - membrane protein complex that consists of a receptor protein that binds to a signaling molecule—a G protein—that is activated by that binding and in turn activates an effector protein (enzyme) that creates a second-messenger molecule in the cytoplasm of the target cell - ganglionic neuron - specifically refers to the cell body of a neuron in the autonomic system that is located in a ganglion - gray rami communicantes - (singular = ramus communicans) unmyelinated structures that provide a short connection from a sympathetic chain ganglion to the spinal nerve that contains the postganglionic sympathetic fiber - greater splanchnic nerve - nerve that contains fibers of the central sympathetic neurons that do not synapse in the chain ganglia but project onto the celiac ganglion - inferior mesenteric ganglion - one of the collateral ganglia of the sympathetic system that projects to the digestive system - intramural ganglia - terminal ganglia of the parasympathetic system that are found within the walls of the target effector - lesser splanchnic nerve - nerve that contains fibers of the central sympathetic neurons that do not synapse in the chain ganglia but project onto the inferior mesenteric ganglion - ligand-gated cation channel - ion channel, such as the nicotinic receptor, that is specific to positively charged ions and opens when a molecule such as a neurotransmitter binds to it - limbic lobe - structures arranged around the edges of the cerebrum that are involved in memory and emotion - long reflex - reflex arc that includes the central nervous system - medial forebrain bundle - fiber pathway that extends anteriorly into the basal forebrain, passes through the hypothalamus, and extends into the brain stem and spinal cord - mesenteric plexus - nervous tissue within the wall of the digestive tract that contains neurons that are the targets of autonomic preganglionic fibers and that project to the smooth muscle and glandular tissues in the digestive organ - muscarinic receptor - type of acetylcholine receptor protein that is characterized by also binding to muscarine and is a metabotropic receptor - mydriasis - dilation of the pupil; typically the result of disease, trauma, or drugs - nicotinic receptor - type of acetylcholine receptor protein that is characterized by also binding to nicotine and is an ionotropic receptor - norepinephrine - signaling molecule released as a neurotransmitter by most postganglionic sympathetic fibers as part of the sympathetic response, or as a hormone into the bloodstream from the adrenal medulla - nucleus ambiguus - brain-stem nucleus that contains neurons that project through the vagus nerve to terminal ganglia in the thoracic cavity; specifically associated with the heart - parasympathetic division - division of the autonomic nervous system responsible for restful and digestive functions - parasympathomimetic drugs - drugs that enhance or mimic the function of the parasympathetic system - paravertebral ganglia - autonomic ganglia superior to the sympathetic chain ganglia - postganglionic fiber - axon from a ganglionic neuron in the autonomic nervous system that projects to and synapses with the target effector; sometimes referred to as a postganglionic neuron - preganglionic fiber - axon from a central neuron in the autonomic nervous system that projects to and synapses with a ganglionic neuron; sometimes referred to as a preganglionic neuron - prevertebral ganglia - autonomic ganglia that are anterior to the vertebral column and functionally related to the sympathetic chain ganglia - referred pain - the conscious perception of visceral sensation projected to a different region of the body, such as the left shoulder and arm pain as a sign for a heart attack - reflex arc - circuit of a reflex that involves a sensory input and motor output, or an afferent branch and an efferent branch, and an integrating center to connect the two branches - rest and digest - set of functions associated with the parasympathetic system that lead to restful actions and digestion - short reflex - reflex arc that does not include any components of the central nervous system - somatic reflex - reflex involving skeletal muscle as the effector, under the control of the somatic nervous system - superior cervical ganglion - one of the paravertebral ganglia of the sympathetic system that projects to the head - superior mesenteric ganglion - one of the collateral ganglia of the sympathetic system that projects to the digestive system - sympathetic chain ganglia - series of ganglia adjacent to the vertebral column that receive input from central sympathetic neurons - sympathetic division - division of the autonomic nervous system associated with the fight-or-flight response - sympatholytic drug - drug that interrupts, or “lyses,” the function of the sympathetic system - sympathomimetic drug - drug that enhances or mimics the function of the sympathetic system - target effector - organ, tissue, or gland that will respond to the control of an autonomic or somatic or endocrine signal - terminal ganglia - ganglia of the parasympathetic division of the autonomic system, which are located near or within the target effector, the latter also known as intramural ganglia - thoracolumbar system - alternate name for the sympathetic division of the autonomic nervous system that is based on the anatomical location of central neurons in the lateral horn of the thoracic and upper lumbar spinal cord - varicosity - structure of some autonomic connections that is not a typical synaptic end bulb, but a string of swellings along the length of a fiber that makes a network of connections with the target effector - vasomotor nerves - preganglionic sympathetic fibers that cause the constriction of blood vessels in response to signals from the cardiovascular center - visceral reflex - reflex involving an internal organ as the effector, under the control of the autonomic nervous system - white rami communicantes - (singular = ramus communicans) myelinated structures that provide a short connection from a sympathetic chain ganglion to the spinal nerve that contains the preganglionic sympathetic fiber Chapter Review 15.1 Divisions of the Autonomic Nervous System The primary responsibilities of the autonomic nervous system are to regulate homeostatic mechanisms in the body, which is also part of what the endocrine system does. The key to understanding the autonomic system is to explore the response pathways—the output of the nervous system. The way we respond to the world around us, to manage the internal environment on the basis of the external environment, is divided between two parts of the autonomic nervous system. The sympathetic division responds to threats and produces a readiness to confront the threat or to run away: the fight-or-flight response. The parasympathetic division plays the opposite role. When the external environment does not present any immediate danger, a restful mode descends on the body, and the digestive system is more active. The sympathetic output of the nervous system originates out of the lateral horn of the thoracolumbar spinal cord. An axon from one of these central neurons projects by way of the ventral spinal nerve root and spinal nerve to a sympathetic ganglion, either in the sympathetic chain ganglia or one of the collateral locations, where it synapses on a ganglionic neuron. These preganglionic fibers release ACh, which excites the ganglionic neuron through the nicotinic receptor. The axon from the ganglionic neuron—the postganglionic fiber—then projects to a target effector where it will release norepinephrine to bind to an adrenergic receptor, causing a change in the physiology of that organ in keeping with the broad, divergent sympathetic response. The postganglionic connections to sweat glands in the skin and blood vessels supplying skeletal muscle are, however, exceptions; those fibers release ACh onto muscarinic receptors. The sympathetic system has a specialized preganglionic connection to the adrenal medulla that causes epinephrine and norepinephrine to be released into the bloodstream rather than exciting a neuron that contacts an organ directly. This hormonal component means that the sympathetic chemical signal can spread throughout the body very quickly and affect many organ systems at once. The parasympathetic output is based in the brain stem and sacral spinal cord. Neurons from particular nuclei in the brain stem or from the lateral horn of the sacral spinal cord (preganglionic neurons) project to terminal (intramural) ganglia located close to or within the wall of target effectors. These preganglionic fibers also release ACh onto nicotinic receptors to excite the ganglionic neurons. The postganglionic fibers then contact the target tissues within the organ to release ACh, which binds to muscarinic receptors to induce rest-and-digest responses. Signaling molecules utilized by the autonomic nervous system are released from axons and can be considered as either neurotransmitters (when they directly interact with the effector) or as hormones (when they are released into the bloodstream). The same molecule, such as norepinephrine, could be considered either a neurotransmitter or a hormone on the basis of whether it is released from a postganglionic sympathetic axon or from the adrenal gland. The synapses in the autonomic system are not always the typical type of connection first described in the neuromuscular junction. Instead of having synaptic end bulbs at the very end of an axonal fiber, they may have swellings—called varicosities—along the length of a fiber so that it makes a network of connections within the target tissue. 15.2 Autonomic Reflexes and Homeostasis Autonomic nervous system function is based on the visceral reflex. This reflex is similar to the somatic reflex, but the efferent branch is composed of two neurons. The central neuron projects from the spinal cord or brain stem to synapse on the ganglionic neuron that projects to the effector. The afferent branch of the somatic and visceral reflexes is very similar, as many somatic and special senses activate autonomic responses. However, there are visceral senses that do not form part of conscious perception. If a visceral sensation, such as cardiac pain, is strong enough, it will rise to the level of consciousness. However, the sensory homunculus does not provide a representation of the internal structures to the same degree as the surface of the body, so visceral sensations are often experienced as referred pain, such as feelings of pain in the left shoulder and arm in connection with a heart attack. The role of visceral reflexes is to maintain a balance of function in the organ systems of the body. The two divisions of the autonomic system each play a role in effecting change, usually in competing directions. The sympathetic system increases heart rate, whereas the parasympathetic system decreases heart rate. The sympathetic system dilates the pupil of the eye, whereas the parasympathetic system constricts the pupil. The competing inputs can contribute to the resting tone of the organ system. Heart rate is normally under parasympathetic tone, whereas blood pressure is normally under sympathetic tone. The heart rate is slowed by the autonomic system at rest, whereas blood vessels retain a slight constriction at rest. In a few systems of the body, the competing input from the two divisions is not the norm. The sympathetic tone of blood vessels is caused by the lack of parasympathetic input to the systemic circulatory system. Only certain regions receive parasympathetic input that relaxes the smooth muscle wall of the blood vessels. Sweat glands are another example, which only receive input from the sympathetic system. 15.3 Central Control The autonomic system integrates sensory information and higher cognitive processes to generate output, which balances homeostatic mechanisms. The central autonomic structure is the hypothalamus, which coordinates sympathetic and parasympathetic efferent pathways to regulate activities of the organ systems of the body. The majority of hypothalamic output travels through the medial forebrain bundle and the dorsal longitudinal fasciculus to influence brain stem and spinal components of the autonomic nervous system. The medial forebrain bundle also connects the hypothalamus with higher centers of the limbic system where emotion can influence visceral responses. The amygdala is a structure within the limbic system that influences the hypothalamus in the regulation of the autonomic system, as well as the endocrine system. These higher centers have descending control of the autonomic system through brain stem centers, primarily in the medulla, such as the cardiovascular center. This collection of medullary nuclei regulates cardiac function, as well as blood pressure. Sensory input from the heart, aorta, and carotid sinuses project to these regions of the medulla. The solitary nucleus increases sympathetic tone of the cardiovascular system through the cardiac accelerator and vasomotor nerves. The nucleus ambiguus and the dorsal motor nucleus both contribute fibers to the vagus nerve, which exerts parasympathetic control of the heart by decreasing heart rate. 15.4 Drugs that Affect the Autonomic System The autonomic system is affected by a number of exogenous agents, including some that are therapeutic and some that are illicit. These drugs affect the autonomic system by mimicking or interfering with the endogenous agents or their receptors. A survey of how different drugs affect autonomic function illustrates the role that the neurotransmitters and hormones play in autonomic function. Drugs can be thought of as chemical tools to effect changes in the system with some precision, based on where those drugs are effective. Nicotine is not a drug that is used therapeutically, except for smoking cessation. When it is introduced into the body via products, it has broad effects on the autonomic system. Nicotine carries a risk for cardiovascular disease because of these broad effects. The drug stimulates both sympathetic and parasympathetic ganglia at the preganglionic fiber synapse. For most organ systems in the body, the competing input from the two postganglionic fibers will essentially cancel each other out. However, for the cardiovascular system, the results are different. Because there is essentially no parasympathetic influence on blood pressure for the entire body, the sympathetic input is increased by nicotine, causing an increase in blood pressure. Also, the influence that the autonomic system has on the heart is not the same as for other systems. Other organs have smooth muscle or glandular tissue that is activated or inhibited by the autonomic system. Cardiac muscle is intrinsically active and is modulated by the autonomic system. The contradictory signals do not just cancel each other out, they alter the regularity of the heart rate and can cause arrhythmias. Both hypertension and arrhythmias are risk factors for heart disease. Other drugs affect one division of the autonomic system or the other. The sympathetic system is affected by drugs that mimic the actions of adrenergic molecules (norepinephrine and epinephrine) and are called sympathomimetic drugs. Drugs such as phenylephrine bind to the adrenergic receptors and stimulate target organs just as sympathetic activity would. Other drugs are sympatholytic because they block adrenergic activity and cancel the sympathetic influence on the target organ. Drugs that act on the parasympathetic system also work by either enhancing the postganglionic signal or blocking it. A muscarinic agonist (or parasympathomimetic drug) acts just like ACh released by the parasympathetic postganglionic fiber. Anticholinergic drugs block muscarinic receptors, suppressing parasympathetic interaction with the organ. Interactive Link Questions Watch this video to learn more about adrenaline and the fight-or-flight response. When someone is said to have a rush of adrenaline, the image of bungee jumpers or skydivers usually comes to mind. But adrenaline, also known as epinephrine, is an important chemical in coordinating the body’s fight-or-flight response. In this video, you look inside the physiology of the fight-or-flight response, as envisioned for a firefighter. His body’s reaction is the result of the sympathetic division of the autonomic nervous system causing system-wide changes as it prepares for extreme responses. What two changes does adrenaline bring about to help the skeletal muscle response? 2.Watch this video to learn more about the nervous system. As described in this video, the nervous system has a way to deal with threats and stress that is separate from the conscious control of the somatic nervous system. The system comes from a time when threats were about survival, but in the modern age, these responses become part of stress and anxiety. This video describes how the autonomic system is only part of the response to threats, or stressors. What other organ system gets involved, and what part of the brain coordinates the two systems for the entire response, including epinephrine (adrenaline) and cortisol? 3.Read this article to learn about a teenager who experiences a series of spells that suggest a stroke. He undergoes endless tests and seeks input from multiple doctors. In the end, one expert, one question, and a simple blood pressure cuff answers the question. Why would the heart have to beat faster when the teenager changes his body position from lying down to sitting, and then to standing? 4.Watch this video to learn about the pupillary reflexes. The pupillary light reflex involves sensory input through the optic nerve and motor response through the oculomotor nerve to the ciliary ganglion, which projects to the circular fibers of the iris. As shown in this short animation, pupils will constrict to limit the amount of light falling on the retina under bright lighting conditions. What constitutes the afferent and efferent branches of the competing reflex (dilation)? 5.Watch this video to learn about physical responses to emotion. The autonomic system, which is important for regulating the homeostasis of the organ systems, is also responsible for our physiological responses to emotions such as fear. The video summarizes the extent of the body’s reactions and describes several effects of the autonomic system in response to fear. On the basis of what you have already studied about autonomic function, which effect would you expect to be associated with parasympathetic, rather than sympathetic, activity? 6.Watch this video to learn about the side effects of 3-D movies. As discussed in this video, movies that are shot in 3-D can cause motion sickness, which elicits the autonomic symptoms of nausea and sweating. The disconnection between the perceived motion on the screen and the lack of any change in equilibrium stimulates these symptoms. Why do you think sitting close to the screen or right in the middle of the theater makes motion sickness during a 3-D movie worse? Review Questions Which of these physiological changes would not be considered part of the sympathetic fight-or-flight response? - increased heart rate - increased sweating - dilated pupils - increased stomach motility Which type of fiber could be considered the longest? - preganglionic parasympathetic - preganglionic sympathetic - postganglionic parasympathetic - postganglionic sympathetic Which signaling molecule is most likely responsible for an increase in digestive activity? - epinephrine - norepinephrine - acetylcholine - adrenaline Which of these cranial nerves contains preganglionic parasympathetic fibers? - optic, CN II - facial, CN VII - trigeminal, CN V - hypoglossal, CN XII Which of the following is not a target of a sympathetic preganglionic fiber? - intermural ganglion - collateral ganglion - adrenal gland - chain ganglion Which of the following represents a sensory input that is not part of both the somatic and autonomic systems? - vision - taste - baroreception - proprioception What is the term for a reflex that does not include a CNS component? - long reflex - visceral reflex - somatic reflex - short reflex What neurotransmitter will result in constriction of the pupil? - norepinephrine - acetylcholine - epinephrine - serotonin What gland produces a secretion that causes fight-or-flight responses in effectors? - adrenal medulla - salivatory gland - reproductive gland - thymus Which of the following is an incorrect pairing? - norepinephrine dilates the pupil - epinephrine increases blood pressure - acetylcholine decreases digestion - norepinephrine increases heart rate Which of these locations in the forebrain is the master control center for homeostasis through the autonomic and endocrine systems? - hypothalamus - thalamus - amygdala - cerebral cortex Which nerve projects to the hypothalamus to indicate the level of light stimuli in the retina? - glossopharyngeal - oculomotor - optic - vagus What region of the limbic lobe is responsible for generating stress responses via the hypothalamus? - hippocampus - amygdala - mammillary bodies - prefrontal cortex What is another name for the preganglionic sympathetic fibers that project to the heart? - solitary tract - vasomotor nerve - vagus nerve - cardiac accelerator nerve What central fiber tract connects forebrain and brain stem structures with the hypothalamus? - cardiac accelerator nerve - medial forebrain bundle - dorsal longitudinal fasciculus - corticospinal tract A drug that affects both divisions of the autonomic system is going to bind to, or block, which type of neurotransmitter receptor? - nicotinic - muscarinic - α-adrenergic - β-adrenergic A drug is called an agonist if it ________. - blocks a receptor - interferes with neurotransmitter reuptake - acts like the endogenous neurotransmitter by binding to its receptor - blocks the voltage-gated calcium ion channel Which type of drug would be an antidote to atropine poisoning? - nicotinic agonist - anticholinergic - muscarinic agonist - α-blocker Which kind of drug would have anti-anxiety effects? - nicotinic agonist - anticholinergic - muscarinic agonist - α-blocker Which type of drug could be used to treat asthma by opening airways wider? - sympatholytic drug - sympathomimetic drug - anticholinergic drug - parasympathomimetic drug Critical Thinking Questions In the context of a lioness hunting on the savannah, why would the sympathetic system not activate the digestive system? 28.A target effector, such as the heart, receives input from the sympathetic and parasympathetic systems. What is the actual difference between the sympathetic and parasympathetic divisions at the level of those connections (i.e., at the synapse)? 29.Damage to internal organs will present as pain associated with a particular surface area of the body. Why would something like irritation to the diaphragm, which is between the thoracic and abdominal cavities, feel like pain in the shoulder or neck? 30.Medical practice is paying more attention to the autonomic system in considering disease states. Why would autonomic tone be important in considering cardiovascular disease? 31.Horner’s syndrome is a condition that presents with changes in one eye, such as pupillary constriction and dropping of eyelids, as well as decreased sweating in the face. Why could a tumor in the thoracic cavity have an effect on these autonomic functions? 32.The cardiovascular center is responsible for regulating the heart and blood vessels through homeostatic mechanisms. What tone does each component of the cardiovascular system have? What connections does the cardiovascular center invoke to keep these two systems in their resting tone? 33.Why does smoking increase the risk of heart disease? Provide two reasons based on autonomic function. 34.Why might topical, cosmetic application of atropine or scopolamine from the belladonna plant not cause fatal poisoning, as would occur with ingestion of the plant?	oercommons	2025-03-18T00:37:01.780772	null	{ "license": "Creative Commons - Attribution - https://creativecommons.org/licenses/by/4.0/", "url": "https://oercommons.org/courseware/lesson/56378/overview", "title": "Anatomy and Physiology, Regulation, Integration, and Control", "author": null }
https://oercommons.org/courseware/lesson/56379/overview	The Neurological Exam Introduction Figure 16.1 Neurological Exam Health care professionals, such as this air force nurse, can rapidly assess the neurological functions of a patient using the neurological exam. One part of the exam is the inspection of the oral cavity and pharynx, which enables the doctor to not only inspect the tissues for signs of infection, but also provides a means to test the functions of the cranial nerves associated with the oral cavity. (credit: U.S. Department of Defense) CHAPTER OBJECTIVES After studying this chapter, you will be able to: - Describe the major sections of the neurological exam - Outline the benefits of rapidly assessing neurological function - Relate anatomical structures of the nervous system to specific functions - Diagram the connections of the nervous system to the musculature and integument involved in primary sensorimotor responses - Compare and contrast the somatic and visceral reflexes with respect to how they are assessed through the neurological exam A man arrives at the hospital after feeling faint and complaining of a “pins-and-needles” feeling all along one side of his body. The most likely explanation is that he has suffered a stroke, which has caused a loss of oxygen to a particular part of the central nervous system (CNS). The problem is finding where in the entire nervous system the stroke has occurred. By checking reflexes, sensory responses, and motor control, a health care provider can focus on what abilities the patient may have lost as a result of the stroke and can use this information to determine where the injury occurred. In the emergency department of the hospital, this kind of rapid assessment of neurological function is key to treating trauma to the nervous system. In the classroom, the neurological exam is a valuable tool for learning the anatomy and physiology of the nervous system because it allows you to relate the functions of the system to particular locations in the nervous system. As a student of anatomy and physiology, you may be planning to go into an allied health field, perhaps nursing or physical therapy. You could be in the emergency department treating a patient such as the one just described. An important part of this course is to understand the nervous system. This can be especially challenging because you need to learn about the nervous system using your own nervous system. The first chapter in this unit about the nervous system began with a quote: “If the human brain were simple enough for us to understand, we would be too simple to understand it.” However, you are being asked to understand aspects of it. A healthcare provider can pinpoint problems with the nervous system in minutes by running through the series of tasks to test neurological function that are described in this chapter. You can use the same approach, though not as quickly, to learn about neurological function and its relationship to the structures of the nervous system. Nervous tissue is different from other tissues in that it is not classified into separate tissue types. It does contain two types of cells, neurons and glia, but it is all just nervous tissue. White matter and gray matter are not types of nervous tissue, but indications of different specializations within the nervous tissue. However, not all nervous tissue performs the same function. Furthermore, specific functions are not wholly localized to individual brain structures in the way that other bodily functions occur strictly within specific organs. In the CNS, we must consider the connections between cells over broad areas, not just the function of cells in one particular nucleus or region. In a broad sense, the nervous system is responsible for the majority of electrochemical signaling in the body, but the use of those signals is different in various regions. The nervous system is made up of the brain and spinal cord as the central organs, and the ganglia and nerves as organs in the periphery. The brain and spinal cord can be thought of as a collection of smaller organs, most of which would be the nuclei (such as the oculomotor nuclei), but white matter structures play an important role (such as the corpus callosum). Studying the nervous system requires an understanding of the varied physiology of the nervous system. For example, the hypothalamus plays a very different role than the visual cortex. The neurological exam provides a way to elicit behavior that represents those varied functions. Overview of the Neurological Exam - List the major sections of the neurological exam - Explain the connection between location and function in the nervous system - Explain the benefit of a rapid assessment for neurological function in a clinical setting - List the causes of neurological deficits - Describe the different ischemic events in the nervous system The neurological exam is a clinical assessment tool used to determine what specific parts of the CNS are affected by damage or disease. It can be performed in a short time—sometimes as quickly as 5 minutes—to establish neurological function. In the emergency department, this rapid assessment can make the difference with respect to proper treatment and the extent of recovery that is possible. The exam is a series of subtests separated into five major sections. The first of these is the mental status exam, which assesses the higher cognitive functions such as memory, orientation, and language. Then there is the cranial nerve exam, which tests the function of the 12 cranial nerves and, therefore, the central and peripheral structures associated with them. The cranial nerve exam tests the sensory and motor functions of each of the nerves, as applicable. Two major sections, the sensory exam and the motor exam, test the sensory and motor functions associated with spinal nerves. Finally, the coordination exam tests the ability to perform complex and coordinated movements. The gait exam, which is often considered a sixth major exam, specifically assesses the motor function of walking and can be considered part of the coordination exam because walking is a coordinated movement. Neuroanatomy and the Neurological Exam Localization of function is the concept that circumscribed locations are responsible for specific functions. The neurological exam highlights this relationship. For example, the cognitive functions that are assessed in the mental status exam are based on functions in the cerebrum, mostly in the cerebral cortex. Several of the subtests examine language function. Deficits in neurological function uncovered by these examinations usually point to damage to the left cerebral cortex. In the majority of individuals, language function is localized to the left hemisphere between the superior temporal lobe and the posterior frontal lobe, including the intervening connections through the inferior parietal lobe. The five major sections of the neurological exam are related to the major regions of the CNS (Figure 16.2). The mental status exam assesses functions related to the cerebrum. The cranial nerve exam is for the nerves that connect to the diencephalon and brain stem (as well as the olfactory connections to the forebrain). The coordination exam and the related gait exam primarily assess the functions of the cerebellum. The motor and sensory exams are associated with the spinal cord and its connections through the spinal nerves. Figure 16.2 Anatomical Underpinnings of the Neurological Exam The different regions of the CNS relate to the major sections of the neurological exam: the mental status exam, cranial nerve exam, sensory exam, motor exam, and coordination exam (including the gait exam). Part of the power of the neurological exam is this link between structure and function. Testing the various functions represented in the exam allows an accurate estimation of where the nervous system may be damaged. Consider the patient described in the chapter introduction. In the emergency department, he is given a quick exam to find where the deficit may be localized. Knowledge of where the damage occurred will lead to the most effective therapy. In rapid succession, he is asked to smile, raise his eyebrows, stick out his tongue, and shrug his shoulders. The doctor tests muscular strength by providing resistance against his arms and legs while he tries to lift them. With his eyes closed, he has to indicate when he feels the tip of a pen touch his legs, arms, fingers, and face. He follows the tip of a pen as the doctor moves it through the visual field and finally toward his face. A formal mental status exam is not needed at this point; the patient will demonstrate any possible deficits in that area during normal interactions with the interviewer. If cognitive or language deficits are apparent, the interviewer can pursue mental status in more depth. All of this takes place in less than 5 minutes. The patient reports that he feels pins and needles in his left arm and leg, and has trouble feeling the tip of the pen when he is touched on those limbs. This suggests a problem with the sensory systems between the spinal cord and the brain. The emergency department has a lead to follow before a CT scan is performed. He is put on aspirin therapy to limit the possibility of blood clots forming, in case the cause is an embolus—an obstruction such as a blood clot that blocks the flow of blood in an artery or vein. INTERACTIVE LINK Watch this video to see a demonstration of the neurological exam—a series of tests that can be performed rapidly when a patient is initially brought into an emergency department. The exam can be repeated on a regular basis to keep a record of how and if neurological function changes over time. In what order were the sections of the neurological exam tested in this video, and which section seemed to be left out? Causes of Neurological Deficits Damage to the nervous system can be limited to individual structures or can be distributed across broad areas of the brain and spinal cord. Localized, limited injury to the nervous system is most often the result of circulatory problems. Neurons are very sensitive to oxygen deprivation and will start to deteriorate within 1 or 2 minutes, and permanent damage (cell death) could result within a few hours. The loss of blood flow to part of the brain is known as a stroke, or a cerebrovascular accident (CVA). There are two main types of stroke, depending on how the blood supply is compromised: ischemic and hemorrhagic. An ischemic stroke is the loss of blood flow to an area because vessels are blocked or narrowed. This is often caused by an embolus, which may be a blood clot or fat deposit. Ischemia may also be the result of thickening of the blood vessel wall, or a drop in blood volume in the brain known as hypovolemia. A related type of CVA is known as a transient ischemic attack (TIA), which is similar to a stroke although it does not last as long. The diagnostic definition of a stroke includes effects that last at least 24 hours. Any stroke symptoms that are resolved within a 24-hour period because of restoration of adequate blood flow are classified as a TIA. A hemorrhagic stroke is bleeding into the brain because of a damaged blood vessel. Accumulated blood fills a region of the cranial vault and presses against the tissue in the brain (Figure 16.3). Physical pressure on the brain can cause the loss of function, as well as the squeezing of local arteries resulting in compromised blood flow beyond the site of the hemorrhage. As blood pools in the nervous tissue and the vasculature is damaged, the blood-brain barrier can break down and allow additional fluid to accumulate in the region, which is known as edema. Figure 16.3 Hemorrhagic Stroke (a) A hemorrhage into the tissue of the cerebrum results in a large accumulation of blood with an additional edema in the adjacent tissue. The hemorrhagic area causes the entire brain to be disfigured as suggested here by the lateral ventricles being squeezed into the opposite hemisphere. (b) A CT scan shows an intraparenchymal hemorrhage within the parietal lobe. (credit b: James Heilman) Whereas hemorrhagic stroke may involve bleeding into a large region of the CNS, such as into the deep white matter of a cerebral hemisphere, other events can cause widespread damage and loss of neurological functions. Infectious diseases can lead to loss of function throughout the CNS as components of nervous tissue, specifically astrocytes and microglia, react to the disease. Blunt force trauma, such as from a motor vehicle accident, can physically damage the CNS. A class of disorders that affect the nervous system are the neurodegenerative diseases: Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, amyotrophic lateral sclerosis (ALS), Creutzfeld–Jacob disease, multiple sclerosis (MS), and other disorders that are the result of nervous tissue degeneration. In diseases like Alzheimer’s, Parkinson’s, or ALS, neurons die; in diseases like MS, myelin is affected. Some of these disorders affect motor function, and others present with dementia. How patients with these disorders perform in the neurological exam varies, but is often broad in its effects, such as memory deficits that compromise many aspects of the mental status exam, or movement deficits that compromise aspects of the cranial nerve exam, the motor exam, or the coordination exam. The causes of these disorders are also varied. Some are the result of genetics, such as Huntington’s disease, or the result of autoimmunity, such as MS; others are not entirely understood, such as Alzheimer’s and Parkinson’s diseases. Current research suggests that many of these diseases are related in how the degeneration takes place and may be treated by common therapies. Finally, a common cause of neurological changes is observed in developmental disorders. Whether the result of genetic factors or the environment during development, there are certain situations that result in neurological functions being different from the expected norms. Developmental disorders are difficult to define because they are caused by defects that existed in the past and disrupted the normal development of the CNS. These defects probably involve multiple environmental and genetic factors—most of the time, we don’t know what the cause is other than that it is more complex than just one factor. Furthermore, each defect on its own may not be a problem, but when several are added together, they can disrupt growth processes that are not well understand in the first place. For instance, it is possible for a stroke to damage a specific region of the brain and lead to the loss of the ability to recognize faces (prosopagnosia). The link between cell death in the fusiform gyrus and the symptom is relatively easy to understand. In contrast, similar deficits can be seen in children with the developmental disorder, autism spectrum disorder (ASD). However, these children do not lack a fusiform gyrus, nor is there any damage or defect visible to this brain region. We conclude, rather poorly, that this brain region is not connected properly to other brain regions. Infection, trauma, and congenital disorders can all lead to significant signs, as identified through the neurological exam. It is important to differentiate between an acute event, such as stroke, and a chronic or global condition such as blunt force trauma. Responses seen in the neurological exam can help. A loss of language function observed in all its aspects is more likely a global event as opposed to a discrete loss of one function, such as not being able to say certain types of words. A concern, however, is that a specific function—such as controlling the muscles of speech—may mask other language functions. The various subtests within the mental status exam can address these finer points and help clarify the underlying cause of the neurological loss. INTERACTIVE LINK Watch this video for an introduction to the neurological exam. Studying the neurological exam can give insight into how structure and function in the nervous system are interdependent. This is a tool both in the clinic and in the classroom, but for different reasons. In the clinic, this is a powerful but simple tool to assess a patient’s neurological function. In the classroom, it is a different way to think about the nervous system. Though medical technology provides noninvasive imaging and real-time functional data, the presenter says these cannot replace the history at the core of the medical examination. What does history mean in the context of medical practice? The Mental Status Exam - Describe the relationship of mental status exam results to cerebral functions - Explain the categorization of regions of the cortex based on anatomy and physiology - Differentiate between primary, association, and integration areas of the cerebral cortex - Provide examples of localization of function related to the cerebral cortex In the clinical setting, the set of subtests known as the mental status exam helps us understand the relationship of the brain to the body. Ultimately, this is accomplished by assessing behavior. Tremors related to intentional movements, incoordination, or the neglect of one side of the body can be indicative of failures of the connections of the cerebrum either within the hemispheres, or from the cerebrum to other portions of the nervous system. There is no strict test for what the cerebrum does alone, but rather in what it does through its control of the rest of the CNS, the peripheral nervous system (PNS), and the musculature. Sometimes eliciting a behavior is as simple as asking a question. Asking a patient to state his or her name is not only to verify that the file folder in a health care provider’s hands is the correct one, but also to be sure that the patient is aware, oriented, and capable of interacting with another person. If the answer to “What is your name?” is “Santa Claus,” the person may have a problem understanding reality. If the person just stares at the examiner with a confused look on their face, the person may have a problem understanding or producing speech. Functions of the Cerebral Cortex The cerebrum is the seat of many of the higher mental functions, such as memory and learning, language, and conscious perception, which are the subjects of subtests of the mental status exam. The cerebral cortex is the thin layer of gray matter on the outside of the cerebrum. It is approximately a millimeter thick in most regions and highly folded to fit within the limited space of the cranial vault. These higher functions are distributed across various regions of the cortex, and specific locations can be said to be responsible for particular functions. There is a limited set of regions, for example, that are involved in language function, and they can be subdivided on the basis of the particular part of language function that each governs. The basis for parceling out areas of the cortex and attributing them to various functions has its root in pure anatomical underpinnings. The German neurologist and histologist Korbinian Brodmann, who made a careful study of the cytoarchitecture of the cerebrum around the turn of the nineteenth century, described approximately 50 regions of the cortex that differed enough from each other to be considered separate areas (Figure 16.4). Brodmann made preparations of many different regions of the cerebral cortex to view with a microscope. He compared the size, shape, and number of neurons to find anatomical differences in the various parts of the cerebral cortex. Continued investigation into these anatomical areas over the subsequent 100 or more years has demonstrated a strong correlation between the structures and the functions attributed to those structures. For example, the first three areas in Brodmann’s list—which are in the postcentral gyrus—compose the primary somatosensory cortex. Within this area, finer separation can be made on the basis of the concept of the sensory homunculus, as well as the different submodalities of somatosensation such as touch, vibration, pain, temperature, or proprioception. Today, we more frequently refer to these regions by their function (i.e., primary sensory cortex) than by the number Brodmann assigned to them, but in some situations the use of Brodmann numbers persists. Figure 16.4 Brodmann's Areas of the Cerebral Cortex On the basis of cytoarchitecture, the anatomist Korbinian Brodmann described the extensive array of cortical regions, as illustrated in his figure. Subsequent investigations found that these areas corresponded very well to functional differences in the cerebral cortex. (credit: modification of work by “Looie496”/Wikimedia Commons, based on original work by Korvinian Brodmann) Area 17, as Brodmann described it, is also known as the primary visual cortex. Adjacent to that are areas 18 and 19, which constitute subsequent regions of visual processing. Area 22 is the primary auditory cortex, and it is followed by area 23, which further processes auditory information. Area 4 is the primary motor cortex in the precentral gyrus, whereas area 6 is the premotor cortex. These areas suggest some specialization within the cortex for functional processing, both in sensory and motor regions. The fact that Brodmann’s areas correlate so closely to functional localization in the cerebral cortex demonstrates the strong link between structure and function in these regions. Areas 1, 2, 3, 4, 17, and 22 are each described as primary cortical areas. The adjoining regions are each referred to as association areas. Primary areas are where sensory information is initially received from the thalamus for conscious perception, or—in the case of the primary motor cortex—where descending commands are sent down to the brain stem or spinal cord to execute movements (Figure 16.5). Figure 16.5 Types of Cortical Areas The cerebral cortex can be described as containing three types of processing regions: primary, association, and integration areas. The primary cortical areas are where sensory information is initially processed, or where motor commands emerge to go to the brain stem or spinal cord. Association areas are adjacent to primary areas and further process the modality-specific input. Multimodal integration areas are found where the modality-specific regions meet; they can process multiple modalities together or different modalities on the basis of similar functions, such as spatial processing in vision or somatosensation. A number of other regions, which extend beyond these primary or association areas of the cortex, are referred to as integrative areas. These areas are found in the spaces between the domains for particular sensory or motor functions, and they integrate multisensory information, or process sensory or motor information in more complex ways. Consider, for example, the posterior parietal cortex that lies between the somatosensory cortex and visual cortex regions. This has been ascribed to the coordination of visual and motor functions, such as reaching to pick up a glass. The somatosensory function that would be part of this is the proprioceptive feedback from moving the arm and hand. The weight of the glass, based on what it contains, will influence how those movements are executed. Cognitive Abilities Assessment of cerebral functions is directed at cognitive abilities. The abilities assessed through the mental status exam can be separated into four groups: orientation and memory, language and speech, sensorium, and judgment and abstract reasoning. Orientation and Memory Orientation is the patient’s awareness of his or her immediate circumstances. It is awareness of time, not in terms of the clock, but of the date and what is occurring around the patient. It is awareness of place, such that a patient should know where he or she is and why. It is also awareness of who the patient is—recognizing personal identity and being able to relate that to the examiner. The initial tests of orientation are based on the questions, “Do you know what the date is?” or “Do you know where you are?” or “What is your name?” Further understanding of a patient’s awareness of orientation can come from questions that address remote memory, such as “Who is the President of the United States?”, or asking what happened on a specific date. There are also specific tasks to address memory. One is the three-word recall test. The patient is given three words to recall, such as book, clock, and shovel. After a short interval, during which other parts of the interview continue, the patient is asked to recall the three words. Other tasks that assess memory—aside from those related to orientation—have the patient recite the months of the year in reverse order to avoid the overlearned sequence and focus on the memory of the months in an order, or to spell common words backwards, or to recite a list of numbers back. Memory is largely a function of the temporal lobe, along with structures beneath the cerebral cortex such as the hippocampus and the amygdala. The storage of memory requires these structures of the medial temporal lobe. A famous case of a man who had both medial temporal lobes removed to treat intractable epilepsy provided insight into the relationship between the structures of the brain and the function of memory. Henry Molaison, who was referred to as patient HM when he was alive, had epilepsy localized to both of his medial temporal lobes. In 1953, a bilateral lobectomy was performed that alleviated the epilepsy but resulted in the inability for HM to form new memories—a condition called anterograde amnesia. HM was able to recall most events from before his surgery, although there was a partial loss of earlier memories, which is referred to as retrograde amnesia. HM became the subject of extensive studies into how memory works. What he was unable to do was form new memories of what happened to him, what are now called episodic memory. Episodic memory is autobiographical in nature, such as remembering riding a bicycle as a child around the neighborhood, as opposed to the procedural memory of how to ride a bike. HM also retained his short-term memory, such as what is tested by the three-word task described above. After a brief period, those memories would dissipate or decay and not be stored in the long-term because the medial temporal lobe structures were removed. The difference in short-term, procedural, and episodic memory, as evidenced by patient HM, suggests that there are different parts of the brain responsible for those functions. The long-term storage of episodic memory requires the hippocampus and related medial temporal structures, and the location of those memories is in the multimodal integration areas of the cerebral cortex. However, short-term memory—also called working or active memory—is localized to the prefrontal lobe. Because patient HM had only lost his medial temporal lobe—and lost very little of his previous memories, and did not lose the ability to form new short-term memories—it was concluded that the function of the hippocampus, and adjacent structures in the medial temporal lobe, is to move (or consolidate) short-term memories (in the pre-frontal lobe) to long-term memory (in the temporal lobe). The prefrontal cortex can also be tested for the ability to organize information. In one subtest of the mental status exam called set generation, the patient is asked to generate a list of words that all start with the same letter, but not to include proper nouns or names. The expectation is that a person can generate such a list of at least 10 words within 1 minute. Many people can likely do this much more quickly, but the standard separates the accepted normal from those with compromised prefrontal cortices. INTERACTIVE LINK Read this article to learn about a young man who texts his fiancée in a panic as he finds that he is having trouble remembering things. At the hospital, a neurologist administers the mental status exam, which is mostly normal except for the three-word recall test. The young man could not recall them even 30 seconds after hearing them and repeating them back to the doctor. An undiscovered mass in the mediastinum region was found to be Hodgkin’s lymphoma, a type of cancer that affects the immune system and likely caused antibodies to attack the nervous system. The patient eventually regained his ability to remember, though the events in the hospital were always elusive. Considering that the effects on memory were temporary, but resulted in the loss of the specific events of the hospital stay, what regions of the brain were likely to have been affected by the antibodies and what type of memory does that represent? Language and Speech Language is, arguably, a very human aspect of neurological function. There are certainly strides being made in understanding communication in other species, but much of what makes the human experience seemingly unique is its basis in language. Any understanding of our species is necessarily reflective, as suggested by the question “What am I?” And the fundamental answer to this question is suggested by the famous quote by René Descartes: “Cogito Ergo Sum” (translated from Latin as “I think, therefore I am”). Formulating an understanding of yourself is largely describing who you are to yourself. It is a confusing topic to delve into, but language is certainly at the core of what it means to be self-aware. The neurological exam has two specific subtests that address language. One measures the ability of the patient to understand language by asking them to follow a set of instructions to perform an action, such as “touch your right finger to your left elbow and then to your right knee.” Another subtest assesses the fluency and coherency of language by having the patient generate descriptions of objects or scenes depicted in drawings, and by reciting sentences or explaining a written passage. Language, however, is important in so many ways in the neurological exam. The patient needs to know what to do, whether it is as simple as explaining how the knee-jerk reflex is going to be performed, or asking a question such as “What is your name?” Often, language deficits can be determined without specific subtests; if a person cannot reply to a question properly, there may be a problem with the reception of language. An important example of multimodal integrative areas is associated with language function (Figure 16.6). Adjacent to the auditory association cortex, at the end of the lateral sulcus just anterior to the visual cortex, is Wernicke’s area. In the lateral aspect of the frontal lobe, just anterior to the region of the motor cortex associated with the head and neck, is Broca’s area. Both regions were originally described on the basis of losses of speech and language, which is called aphasia. The aphasia associated with Broca’s area is known as an expressive aphasia, which means that speech production is compromised. This type of aphasia is often described as non-fluency because the ability to say some words leads to broken or halting speech. Grammar can also appear to be lost. The aphasia associated with Wernicke’s area is known as a receptive aphasia, which is not a loss of speech production, but a loss of understanding of content. Patients, after recovering from acute forms of this aphasia, report not being able to understand what is said to them or what they are saying themselves, but they often cannot keep from talking. The two regions are connected by white matter tracts that run between the posterior temporal lobe and the lateral aspect of the frontal lobe. Conduction aphasia associated with damage to this connection refers to the problem of connecting the understanding of language to the production of speech. This is a very rare condition, but is likely to present as an inability to faithfully repeat spoken language. Figure 16.6 Broca's and Wernicke's Areas Two important integration areas of the cerebral cortex associated with language function are Broca’s and Wernicke’s areas. The two areas are connected through the deep white matter running from the posterior temporal lobe to the frontal lobe. Sensorium Those parts of the brain involved in the reception and interpretation of sensory stimuli are referred to collectively as the sensorium. The cerebral cortex has several regions that are necessary for sensory perception. From the primary cortical areas of the somatosensory, visual, auditory, and gustatory senses to the association areas that process information in these modalities, the cerebral cortex is the seat of conscious sensory perception. In contrast, sensory information can also be processed by deeper brain regions, which we may vaguely describe as subconscious—for instance, we are not constantly aware of the proprioceptive information that the cerebellum uses to maintain balance. Several of the subtests can reveal activity associated with these sensory modalities, such as being able to hear a question or see a picture. Two subtests assess specific functions of these cortical areas. The first is praxis, a practical exercise in which the patient performs a task completely on the basis of verbal description without any demonstration from the examiner. For example, the patient can be told to take their left hand and place it palm down on their left thigh, then flip it over so the palm is facing up, and then repeat this four times. The examiner describes the activity without any movements on their part to suggest how the movements are to be performed. The patient needs to understand the instructions, transform them into movements, and use sensory feedback, both visual and proprioceptive, to perform the movements correctly. The second subtest for sensory perception is gnosis, which involves two tasks. The first task, known as stereognosis, involves the naming of objects strictly on the basis of the somatosensory information that comes from manipulating them. The patient keeps their eyes closed and is given a common object, such as a coin, that they have to identify. The patient should be able to indicate the particular type of coin, such as a dime versus a penny, or a nickel versus a quarter, on the basis of the sensory cues involved. For example, the size, thickness, or weight of the coin may be an indication, or to differentiate the pairs of coins suggested here, the smooth or corrugated edge of the coin will correspond to the particular denomination. The second task, graphesthesia, is to recognize numbers or letters written on the palm of the hand with a dull pointer, such as a pen cap. Praxis and gnosis are related to the conscious perception and cortical processing of sensory information. Being able to transform verbal commands into a sequence of motor responses, or to manipulate and recognize a common object and associate it with a name for that object. Both subtests have language components because language function is integral to these functions. The relationship between the words that describe actions, or the nouns that represent objects, and the cerebral location of these concepts is suggested to be localized to particular cortical areas. Certain aphasias can be characterized by a deficit of verbs or nouns, known as V impairment or N impairment, or may be classified as V–N dissociation. Patients have difficulty using one type of word over the other. To describe what is happening in a photograph as part of the expressive language subtest, a patient will use active- or image-based language. The lack of one or the other of these components of language can relate to the ability to use verbs or nouns. Damage to the region at which the frontal and temporal lobes meet, including the region known as the insula, is associated with V impairment; damage to the middle and inferior temporal lobe is associated with N impairment. Judgment and Abstract Reasoning Planning and producing responses requires an ability to make sense of the world around us. Making judgments and reasoning in the abstract are necessary to produce movements as part of larger responses. For example, when your alarm goes off, do you hit the snooze button or jump out of bed? Is 10 extra minutes in bed worth the extra rush to get ready for your day? Will hitting the snooze button multiple times lead to feeling more rested or result in a panic as you run late? How you mentally process these questions can affect your whole day. The prefrontal cortex is responsible for the functions responsible for planning and making decisions. In the mental status exam, the subtest that assesses judgment and reasoning is directed at three aspects of frontal lobe function. First, the examiner asks questions about problem solving, such as “If you see a house on fire, what would you do?” The patient is also asked to interpret common proverbs, such as “Don’t look a gift horse in the mouth.” Additionally, pairs of words are compared for similarities, such as apple and orange, or lamp and cabinet. The prefrontal cortex is composed of the regions of the frontal lobe that are not directly related to specific motor functions. The most posterior region of the frontal lobe, the precentral gyrus, is the primary motor cortex. Anterior to that are the premotor cortex, Broca’s area, and the frontal eye fields, which are all related to planning certain types of movements. Anterior to what could be described as motor association areas are the regions of the prefrontal cortex. They are the regions in which judgment, abstract reasoning, and working memory are localized. The antecedents to planning certain movements are judging whether those movements should be made, as in the example of deciding whether to hit the snooze button. To an extent, the prefrontal cortex may be related to personality. The neurological exam does not necessarily assess personality, but it can be within the realm of neurology or psychiatry. A clinical situation that suggests this link between the prefrontal cortex and personality comes from the story of Phineas Gage, the railroad worker from the mid-1800s who had a metal spike impale his prefrontal cortex. There are suggestions that the steel rod led to changes in his personality. A man who was a quiet, dependable railroad worker became a raucous, irritable drunkard. Later anecdotal evidence from his life suggests that he was able to support himself, although he had to relocate and take on a different career as a stagecoach driver. A psychiatric practice to deal with various disorders was the prefrontal lobotomy. This procedure was common in the 1940s and early 1950s, until antipsychotic drugs became available. The connections between the prefrontal cortex and other regions of the brain were severed. The disorders associated with this procedure included some aspects of what are now referred to as personality disorders, but also included mood disorders and psychoses. Depictions of lobotomies in popular media suggest a link between cutting the white matter of the prefrontal cortex and changes in a patient’s mood and personality, though this correlation is not well understood. EVERYDAY CONNECTION Left Brain, Right Brain Popular media often refer to right-brained and left-brained people, as if the brain were two independent halves that work differently for different people. This is a popular misinterpretation of an important neurological phenomenon. As an extreme measure to deal with a debilitating condition, the corpus callosum may be sectioned to overcome intractable epilepsy. When the connections between the two cerebral hemispheres are cut, interesting effects can be observed. If a person with an intact corpus callosum is asked to put their hands in their pockets and describe what is there on the basis of what their hands feel, they might say that they have keys in their right pocket and loose change in the left. They may even be able to count the coins in their pocket and say if they can afford to buy a candy bar from the vending machine. If a person with a sectioned corpus callosum is given the same instructions, they will do something quite peculiar. They will only put their right hand in their pocket and say they have keys there. They will not even move their left hand, much less report that there is loose change in the left pocket. The reason for this is that the language functions of the cerebral cortex are localized to the left hemisphere in 95 percent of the population. Additionally, the left hemisphere is connected to the right side of the body through the corticospinal tract and the ascending tracts of the spinal cord. Motor commands from the precentral gyrus control the opposite side of the body, whereas sensory information processed by the postcentral gyrus is received from the opposite side of the body. For a verbal command to initiate movement of the right arm and hand, the left side of the brain needs to be connected by the corpus callosum. Language is processed in the left side of the brain and directly influences the left brain and right arm motor functions, but is sent to influence the right brain and left arm motor functions through the corpus callosum. Likewise, the left-handed sensory perception of what is in the left pocket travels across the corpus callosum from the right brain, so no verbal report on those contents would be possible if the hand happened to be in the pocket. INTERACTIVE LINK Watch the video titled “The Man With Two Brains” to see the neuroscientist Michael Gazzaniga introduce a patient he has worked with for years who has had his corpus callosum cut, separating his two cerebral hemispheres. A few tests are run to demonstrate how this manifests in tests of cerebral function. Unlike normal people, this patient can perform two independent tasks at the same time because the lines of communication between the right and left sides of his brain have been removed. Whereas a person with an intact corpus callosum cannot overcome the dominance of one hemisphere over the other, this patient can. If the left cerebral hemisphere is dominant in the majority of people, why would right-handedness be most common? The Mental Status Exam The cerebrum, particularly the cerebral cortex, is the location of important cognitive functions that are the focus of the mental status exam. The regionalization of the cortex, initially described on the basis of anatomical evidence of cytoarchitecture, reveals the distribution of functionally distinct areas. Cortical regions can be described as primary sensory or motor areas, association areas, or multimodal integration areas. The functions attributed to these regions include attention, memory, language, speech, sensation, judgment, and abstract reasoning. The mental status exam addresses these cognitive abilities through a series of subtests designed to elicit particular behaviors ascribed to these functions. The loss of neurological function can illustrate the location of damage to the cerebrum. Memory functions are attributed to the temporal lobe, particularly the medial temporal lobe structures known as the hippocampus and amygdala, along with the adjacent cortex. Evidence of the importance of these structures comes from the side effects of a bilateral temporal lobectomy that were studied in detail in patient HM. Losses of language and speech functions, known as aphasias, are associated with damage to the important integration areas in the left hemisphere known as Broca’s or Wernicke’s areas, as well as the connections in the white matter between them. Different types of aphasia are named for the particular structures that are damaged. Assessment of the functions of the sensorium includes praxis and gnosis. The subtests related to these functions depend on multimodal integration, as well as language-dependent processing. The prefrontal cortex contains structures important for planning, judgment, reasoning, and working memory. Damage to these areas can result in changes to personality, mood, and behavior. The famous case of Phineas Gage suggests a role for this cortex in personality, as does the outdated practice of prefrontal lobectomy. The Cranial Nerve Exam - Describe the functional grouping of cranial nerves - Match the regions of the forebrain and brain stem that are connected to each cranial nerve - Suggest diagnoses that would explain certain losses of function in the cranial nerves - Relate cranial nerve deficits to damage of adjacent, unrelated structures The twelve cranial nerves are typically covered in introductory anatomy courses, and memorizing their names is facilitated by numerous mnemonics developed by students over the years of this practice. But knowing the names of the nerves in order often leaves much to be desired in understanding what the nerves do. The nerves can be categorized by functions, and subtests of the cranial nerve exam can clarify these functional groupings. Three of the nerves are strictly responsible for special senses whereas four others contain fibers for special and general senses. Three nerves are connected to the extraocular muscles resulting in the control of gaze. Four nerves connect to muscles of the face, oral cavity, and pharynx, controlling facial expressions, mastication, swallowing, and speech. Four nerves make up the cranial component of the parasympathetic nervous system responsible for pupillary constriction, salivation, and the regulation of the organs of the thoracic and upper abdominal cavities. Finally, one nerve controls the muscles of the neck, assisting with spinal control of the movement of the head and neck. The cranial nerve exam allows directed tests of forebrain and brain stem structures. The twelve cranial nerves serve the head and neck. The vagus nerve (cranial nerve X) has autonomic functions in the thoracic and superior abdominal cavities. The special senses are served through the cranial nerves, as well as the general senses of the head and neck. The movement of the eyes, face, tongue, throat, and neck are all under the control of cranial nerves. Preganglionic parasympathetic nerve fibers that control pupillary size, salivary glands, and the thoracic and upper abdominal viscera are found in four of the nerves. Tests of these functions can provide insight into damage to specific regions of the brain stem and may uncover deficits in adjacent regions. Sensory Nerves The olfactory, optic, and vestibulocochlear nerves (cranial nerves I, II, and VIII) are dedicated to four of the special senses: smell, vision, equilibrium, and hearing, respectively. Taste sensation is relayed to the brain stem through fibers of the facial and glossopharyngeal nerves. The trigeminal nerve is a mixed nerve that carries the general somatic senses from the head, similar to those coming through spinal nerves from the rest of the body. Testing smell is straightforward, as common smells are presented to one nostril at a time. The patient should be able to recognize the smell of coffee or mint, indicating the proper functioning of the olfactory system. Loss of the sense of smell is called anosmia and can be lost following blunt trauma to the head or through aging. The short axons of the first cranial nerve regenerate on a regular basis. The neurons in the olfactory epithelium have a limited life span, and new cells grow to replace the ones that die off. The axons from these neurons grow back into the CNS by following the existing axons—representing one of the few examples of such growth in the mature nervous system. If all of the fibers are sheared when the brain moves within the cranium, such as in a motor vehicle accident, then no axons can find their way back to the olfactory bulb to re-establish connections. If the nerve is not completely severed, the anosmia may be temporary as new neurons can eventually reconnect. Olfaction is not the pre-eminent sense, but its loss can be quite detrimental. The enjoyment of food is largely based on our sense of smell. Anosmia means that food will not seem to have the same taste, though the gustatory sense is intact, and food will often be described as being bland. However, the taste of food can be improved by adding ingredients (e.g., salt) that stimulate the gustatory sense. Testing vision relies on the tests that are common in an optometry office. The Snellen chart (Figure 16.7) demonstrates visual acuity by presenting standard Roman letters in a variety of sizes. The result of this test is a rough generalization of the acuity of a person based on the normal accepted acuity, such that a letter that subtends a visual angle of 5 minutes of an arc at 20 feet can be seen. To have 20/60 vision, for example, means that the smallest letters that a person can see at a 20-foot distance could be seen by a person with normal acuity from 60 feet away. Testing the extent of the visual field means that the examiner can establish the boundaries of peripheral vision as simply as holding their hands out to either side and asking the patient when the fingers are no longer visible without moving the eyes to track them. If it is necessary, further tests can establish the perceptions in the visual fields. Physical inspection of the optic disk, or where the optic nerve emerges from the eye, can be accomplished by looking through the pupil with an ophthalmoscope. Figure 16.7 The Snellen Chart The Snellen chart for visual acuity presents a limited number of Roman letters in lines of decreasing size. The line with letters that subtend 5 minutes of an arc from 20 feet represents the smallest letters that a person with normal acuity should be able to read at that distance. The different sizes of letters in the other lines represent rough approximations of what a person of normal acuity can read at different distances. For example, the line that represents 20/200 vision would have larger letters so that they are legible to the person with normal acuity at 200 feet. The optic nerves from both sides enter the cranium through the respective optic canals and meet at the optic chiasm at which fibers sort such that the two halves of the visual field are processed by the opposite sides of the brain. Deficits in visual field perception often suggest damage along the length of the optic pathway between the orbit and the diencephalon. For example, loss of peripheral vision may be the result of a pituitary tumor pressing on the optic chiasm (Figure 16.8). The pituitary, seated in the sella turcica of the sphenoid bone, is directly inferior to the optic chiasm. The axons that decussate in the chiasm are from the medial retinae of either eye, and therefore carry information from the peripheral visual field. Figure 16.8 Pituitary Tumor The pituitary gland is located in the sella turcica of the sphenoid bone within the cranial floor, placing it immediately inferior to the optic chiasm. If the pituitary gland develops a tumor, it can press against the fibers crossing in the chiasm. Those fibers are conveying peripheral visual information to the opposite side of the brain, so the patient will experience “tunnel vision”—meaning that only the central visual field will be perceived. The vestibulocochlear nerve (CN VIII) carries both equilibrium and auditory sensations from the inner ear to the medulla. Though the two senses are not directly related, anatomy is mirrored in the two systems. Problems with balance, such as vertigo, and deficits in hearing may both point to problems with the inner ear. Within the petrous region of the temporal bone is the bony labyrinth of the inner ear. The vestibule is the portion for equilibrium, composed of the utricle, saccule, and the three semicircular canals. The cochlea is responsible for transducing sound waves into a neural signal. The sensory nerves from these two structures travel side-by-side as the vestibulocochlear nerve, though they are really separate divisions. They both emerge from the inner ear, pass through the internal auditory meatus, and synapse in nuclei of the superior medulla. Though they are part of distinct sensory systems, the vestibular nuclei and the cochlear nuclei are close neighbors with adjacent inputs. Deficits in one or both systems could occur from damage that encompasses structures close to both. Damage to structures near the two nuclei can result in deficits to one or both systems. Balance or hearing deficits may be the result of damage to the middle or inner ear structures. Ménière's disease is a disorder that can affect both equilibrium and audition in a variety of ways. The patient can suffer from vertigo, a low-frequency ringing in the ears, or a loss of hearing. From patient to patient, the exact presentation of the disease can be different. Additionally, within a single patient, the symptoms and signs may change as the disease progresses. Use of the neurological exam subtests for the vestibulocochlear nerve illuminates the changes a patient may go through. The disease appears to be the result of accumulation, or over-production, of fluid in the inner ear, in either the vestibule or cochlea. Tests of equilibrium are important for coordination and gait and are related to other aspects of the neurological exam. The vestibulo-ocular reflex involves the cranial nerves for gaze control. Balance and equilibrium, as tested by the Romberg test, are part of spinal and cerebellar processes and involved in those components of the neurological exam, as discussed later. Hearing is tested by using a tuning fork in a couple of different ways. The Rinne test involves using a tuning fork to distinguish between conductive hearing and sensorineural hearing. Conductive hearing relies on vibrations being conducted through the ossicles of the middle ear. Sensorineural hearing is the transmission of sound stimuli through the neural components of the inner ear and cranial nerve. A vibrating tuning fork is placed on the mastoid process and the patient indicates when the sound produced from this is no longer present. Then the fork is immediately moved to just next to the ear canal so the sound travels through the air. If the sound is not heard through the ear, meaning the sound is conducted better through the temporal bone than through the ossicles, a conductive hearing deficit is present. The Weber test also uses a tuning fork to differentiate between conductive versus sensorineural hearing loss. In this test, the tuning fork is placed at the top of the skull, and the sound of the tuning fork reaches both inner ears by travelling through bone. In a healthy patient, the sound would appear equally loud in both ears. With unilateral conductive hearing loss, however, the tuning fork sounds louder in the ear with hearing loss. This is because the sound of the tuning fork has to compete with background noise coming from the outer ear, but in conductive hearing loss, the background noise is blocked in the damaged ear, allowing the tuning fork to sound relatively louder in that ear. With unilateral sensorineural hearing loss, however, damage to the cochlea or associated nervous tissue means that the tuning fork sounds quieter in that ear. The trigeminal system of the head and neck is the equivalent of the ascending spinal cord systems of the dorsal column and the spinothalamic pathways. Somatosensation of the face is conveyed along the nerve to enter the brain stem at the level of the pons. Synapses of those axons, however, are distributed across nuclei found throughout the brain stem. The mesencephalic nucleus processes proprioceptive information of the face, which is the movement and position of facial muscles. It is the sensory component of the jaw-jerk reflex, a stretch reflex of the masseter muscle. The chief nucleus, located in the pons, receives information about light touch as well as proprioceptive information about the mandible, which are both relayed to the thalamus and, ultimately, to the postcentral gyrus of the parietal lobe. The spinal trigeminal nucleus, located in the medulla, receives information about crude touch, pain, and temperature to be relayed to the thalamus and cortex. Essentially, the projection through the chief nucleus is analogous to the dorsal column pathway for the body, and the projection through the spinal trigeminal nucleus is analogous to the spinothalamic pathway. Subtests for the sensory component of the trigeminal system are the same as those for the sensory exam targeting the spinal nerves. The primary sensory subtest for the trigeminal system is sensory discrimination. A cotton-tipped applicator, which is cotton attached to the end of a thin wooden stick, can be used easily for this. The wood of the applicator can be snapped so that a pointed end is opposite the soft cotton-tipped end. The cotton end provides a touch stimulus, while the pointed end provides a painful, or sharp, stimulus. While the patient’s eyes are closed, the examiner touches the two ends of the applicator to the patient’s face, alternating randomly between them. The patient must identify whether the stimulus is sharp or dull. These stimuli are processed by the trigeminal system separately. Contact with the cotton tip of the applicator is a light touch, relayed by the chief nucleus, but contact with the pointed end of the applicator is a painful stimulus relayed by the spinal trigeminal nucleus. Failure to discriminate these stimuli can localize problems within the brain stem. If a patient cannot recognize a painful stimulus, that might indicate damage to the spinal trigeminal nucleus in the medulla. The medulla also contains important regions that regulate the cardiovascular, respiratory, and digestive systems, as well as being the pathway for ascending and descending tracts between the brain and spinal cord. Damage, such as a stroke, that results in changes in sensory discrimination may indicate these unrelated regions are affected as well. Gaze Control The three nerves that control the extraocular muscles are the oculomotor, trochlear, and abducens nerves, which are the third, fourth, and sixth cranial nerves. As the name suggests, the abducens nerve is responsible for abducting the eye, which it controls through contraction of the lateral rectus muscle. The trochlear nerve controls the superior oblique muscle to rotate the eye along its axis in the orbit medially, which is called intorsion, and is a component of focusing the eyes on an object close to the face. The oculomotor nerve controls all the other extraocular muscles, as well as a muscle of the upper eyelid. Movements of the two eyes need to be coordinated to locate and track visual stimuli accurately. When moving the eyes to locate an object in the horizontal plane, or to track movement horizontally in the visual field, the lateral rectus muscle of one eye and medial rectus muscle of the other eye are both active. The lateral rectus is controlled by neurons of the abducens nucleus in the superior medulla, whereas the medial rectus is controlled by neurons in the oculomotor nucleus of the midbrain. Coordinated movement of both eyes through different nuclei requires integrated processing through the brain stem. In the midbrain, the superior colliculus integrates visual stimuli with motor responses to initiate eye movements. The paramedian pontine reticular formation (PPRF) will initiate a rapid eye movement, or saccade, to bring the eyes to bear on a visual stimulus quickly. These areas are connected to the oculomotor, trochlear, and abducens nuclei by the medial longitudinal fasciculus (MLF) that runs through the majority of the brain stem. The MLF allows for conjugate gaze, or the movement of the eyes in the same direction, during horizontal movements that require the lateral and medial rectus muscles. Control of conjugate gaze strictly in the vertical direction is contained within the oculomotor complex. To elevate the eyes, the oculomotor nerve on either side stimulates the contraction of both superior rectus muscles; to depress the eyes, the oculomotor nerve on either side stimulates the contraction of both inferior rectus muscles. Purely vertical movements of the eyes are not very common. Movements are often at an angle, so some horizontal components are necessary, adding the medial and lateral rectus muscles to the movement. The rapid movement of the eyes used to locate and direct the fovea onto visual stimuli is called a saccade. Notice that the paths that are traced in Figure 16.9 are not strictly vertical. The movements between the nose and the mouth are closest, but still have a slant to them. Also, the superior and inferior rectus muscles are not perfectly oriented with the line of sight. The origin for both muscles is medial to their insertions, so elevation and depression may require the lateral rectus muscles to compensate for the slight adduction inherent in the contraction of those muscles, requiring MLF activity as well. Figure 16.9 Saccadic Eye Movements Saccades are rapid, conjugate movements of the eyes to survey a complicated visual stimulus, or to follow a moving visual stimulus. This image represents the shifts in gaze typical of a person studying a face. Notice the concentration of gaze on the major features of the face and the large number of paths traced between the eyes or around the mouth. Testing eye movement is simply a matter of having the patient track the tip of a pen as it is passed through the visual field. This may appear similar to testing visual field deficits related to the optic nerve, but the difference is that the patient is asked to not move the eyes while the examiner moves a stimulus into the peripheral visual field. Here, the extent of movement is the point of the test. The examiner is watching for conjugate movements representing proper function of the related nuclei and the MLF. Failure of one eye to abduct while the other adducts in a horizontal movement is referred to as internuclear ophthalmoplegia. When this occurs, the patient will experience diplopia, or double vision, as the two eyes are temporarily pointed at different stimuli. Diplopia is not restricted to failure of the lateral rectus, because any of the extraocular muscles may fail to move one eye in perfect conjugation with the other. The final aspect of testing eye movements is to move the tip of the pen in toward the patient’s face. As visual stimuli move closer to the face, the two medial recti muscles cause the eyes to move in the one nonconjugate movement that is part of gaze control. When the two eyes move to look at something closer to the face, they both adduct, which is referred to as convergence. To keep the stimulus in focus, the eye also needs to change the shape of the lens, which is controlled through the parasympathetic fibers of the oculomotor nerve. The change in focal power of the eye is referred to as accommodation. Accommodation ability changes with age; focusing on nearer objects, such as the written text of a book or on a computer screen, may require corrective lenses later in life. Coordination of the skeletal muscles for convergence and coordination of the smooth muscles of the ciliary body for accommodation are referred to as the accommodation–convergence reflex. A crucial function of the cranial nerves is to keep visual stimuli centered on the fovea of the retina. The vestibulo-ocular reflex (VOR) coordinates all of the components (Figure 16.10), both sensory and motor, that make this possible. If the head rotates in one direction—for example, to the right—the horizontal pair of semicircular canals in the inner ear indicate the movement by increased activity on the right and decreased activity on the left. The information is sent to the abducens nuclei and oculomotor nuclei on either side to coordinate the lateral and medial rectus muscles. The left lateral rectus and right medial rectus muscles will contract, rotating the eyes in the opposite direction of the head, while nuclei controlling the right lateral rectus and left medial rectus muscles will be inhibited to reduce antagonism of the contracting muscles. These actions stabilize the visual field by compensating for the head rotation with opposite rotation of the eyes in the orbits. Deficits in the VOR may be related to vestibular damage, such as in Ménière’s disease, or from dorsal brain stem damage that would affect the eye movement nuclei or their connections through the MLF. Figure 16.10 Vestibulo-ocular Reflex If the head is turned in one direction, the coordination of that movement with the fixation of the eyes on a visual stimulus involves a circuit that ties the vestibular sense with the eye movement nuclei through the MLF. Nerves of the Face and Oral Cavity An iconic part of a doctor’s visit is the inspection of the oral cavity and pharynx, suggested by the directive to “open your mouth and say ‘ah.’” This is followed by inspection, with the aid of a tongue depressor, of the back of the mouth, or the opening of the oral cavity into the pharynx known as the fauces. Whereas this portion of a medical exam inspects for signs of infection, such as in tonsillitis, it is also the means to test the functions of the cranial nerves that are associated with the oral cavity. The facial and glossopharyngeal nerves convey gustatory stimulation to the brain. Testing this is as simple as introducing salty, sour, bitter, or sweet stimuli to either side of the tongue. The patient should respond to the taste stimulus before retracting the tongue into the mouth. Stimuli applied to specific locations on the tongue will dissolve into the saliva and may stimulate taste buds connected to either the left or right of the nerves, masking any lateral deficits. Along with taste, the glossopharyngeal nerve relays general sensations from the pharyngeal walls. These sensations, along with certain taste stimuli, can stimulate the gag reflex. If the examiner moves the tongue depressor to contact the lateral wall of the fauces, this should elicit the gag reflex. Stimulation of either side of the fauces should elicit an equivalent response. The motor response, through contraction of the muscles of the pharynx, is mediated through the vagus nerve. Normally, the vagus nerve is considered autonomic in nature. The vagus nerve directly stimulates the contraction of skeletal muscles in the pharynx and larynx to contribute to the swallowing and speech functions. Further testing of vagus motor function has the patient repeating consonant sounds that require movement of the muscles around the fauces. The patient is asked to say “lah-kah-pah” or a similar set of alternating sounds while the examiner observes the movements of the soft palate and arches between the palate and tongue. The facial and glossopharyngeal nerves are also responsible for the initiation of salivation. Neurons in the salivary nuclei of the medulla project through these two nerves as preganglionic fibers, and synapse in ganglia located in the head. The parasympathetic fibers of the facial nerve synapse in the pterygopalatine ganglion, which projects to the submandibular gland and sublingual gland. The parasympathetic fibers of the glossopharyngeal nerve synapse in the otic ganglion, which projects to the parotid gland. Salivation in response to food in the oral cavity is based on a visceral reflex arc within the facial or glossopharyngeal nerves. Other stimuli that stimulate salivation are coordinated through the hypothalamus, such as the smell and sight of food. The hypoglossal nerve is the motor nerve that controls the muscles of the tongue, except for the palatoglossus muscle, which is controlled by the vagus nerve. There are two sets of muscles of the tongue. The extrinsic muscles of the tongue are connected to other structures, whereas the intrinsic muscles of the tongue are completely contained within the lingual tissues. While examining the oral cavity, movement of the tongue will indicate whether hypoglossal function is impaired. The test for hypoglossal function is the “stick out your tongue” part of the exam. The genioglossus muscle is responsible for protrusion of the tongue. If the hypoglossal nerves on both sides are working properly, then the tongue will stick straight out. If the nerve on one side has a deficit, the tongue will stick out to that side—pointing to the side with damage. Loss of function of the tongue can interfere with speech and swallowing. Additionally, because the location of the hypoglossal nerve and nucleus is near the cardiovascular center, inspiratory and expiratory areas for respiration, and the vagus nuclei that regulate digestive functions, a tongue that protrudes incorrectly can suggest damage in adjacent structures that have nothing to do with controlling the tongue. INTERACTIVE LINK Watch this short video to see an examination of the facial nerve using some simple tests. The facial nerve controls the muscles of facial expression. Severe deficits will be obvious in watching someone use those muscles for normal control. One side of the face might not move like the other side. But directed tests, especially for contraction against resistance, require a formal testing of the muscles. The muscles of the upper and lower face need to be tested. The strength test in this video involves the patient squeezing her eyes shut and the examiner trying to pry her eyes open. Why does the examiner ask her to try a second time? Motor Nerves of the Neck The accessory nerve, also referred to as the spinal accessory nerve, innervates the sternocleidomastoid and trapezius muscles (Figure 16.11). When both the sternocleidomastoids contract, the head flexes forward; individually, they cause rotation to the opposite side. The trapezius can act as an antagonist, causing extension and hyperextension of the neck. These two superficial muscles are important for changing the position of the head. Both muscles also receive input from cervical spinal nerves. Along with the spinal accessory nerve, these nerves contribute to elevating the scapula and clavicle through the trapezius, which is tested by asking the patient to shrug both shoulders, and watching for asymmetry. For the sternocleidomastoid, those spinal nerves are primarily sensory projections, whereas the trapezius also has lateral insertions to the clavicle and scapula, and receives motor input from the spinal cord. Calling the nerve the spinal accessory nerve suggests that it is aiding the spinal nerves. Though that is not precisely how the name originated, it does help make the association between the function of this nerve in controlling these muscles and the role these muscles play in movements of the trunk or shoulders. Figure 16.11 Muscles Controlled by the Accessory Nerve The accessory nerve innervates the sternocleidomastoid and trapezius muscles, both of which attach to the head and to the trunk and shoulders. They can act as antagonists in head flexion and extension, and as synergists in lateral flexion toward the shoulder. To test these muscles, the patient is asked to flex and extend the neck or shrug the shoulders against resistance, testing the strength of the muscles. Lateral flexion of the neck toward the shoulder tests both at the same time. Any difference on one side versus the other would suggest damage on the weaker side. These strength tests are common for the skeletal muscles controlled by spinal nerves and are a significant component of the motor exam. Deficits associated with the accessory nerve may have an effect on orienting the head, as described with the VOR. HOMEOSTATIC IMBALANCES The Pupillary Light Response The autonomic control of pupillary size in response to a bright light involves the sensory input of the optic nerve and the parasympathetic motor output of the oculomotor nerve. When light hits the retina, specialized photosensitive ganglion cells send a signal along the optic nerve to the pretectal nucleus in the superior midbrain. A neuron from this nucleus projects to the Eddinger–Westphal nuclei in the oculomotor complex in both sides of the midbrain. Neurons in this nucleus give rise to the preganglionic parasympathetic fibers that project through the oculomotor nerve to the ciliary ganglion in the posterior orbit. The postganglionic parasympathetic fibers from the ganglion project to the iris, where they release acetylcholine onto circular fibers that constrict the pupil to reduce the amount of light hitting the retina. The sympathetic nervous system is responsible for dilating the pupil when light levels are low. Shining light in one eye will elicit constriction of both pupils. The efferent limb of the pupillary light reflex is bilateral. Light shined in one eye causes a constriction of that pupil, as well as constriction of the contralateral pupil. Shining a penlight in the eye of a patient is a very artificial situation, as both eyes are normally exposed to the same light sources. Testing this reflex can illustrate whether the optic nerve or the oculomotor nerve is damaged. If shining the light in one eye results in no changes in pupillary size but shining light in the opposite eye elicits a normal, bilateral response, the damage is associated with the optic nerve on the nonresponsive side. If light in either eye elicits a response in only one eye, the problem is with the oculomotor system. If light in the right eye only causes the left pupil to constrict, the direct reflex is lost and the consensual reflex is intact, which means that the right oculomotor nerve (or Eddinger–Westphal nucleus) is damaged. Damage to the right oculomotor connections will be evident when light is shined in the left eye. In that case, the direct reflex is intact but the consensual reflex is lost, meaning that the left pupil will constrict while the right does not. The Cranial Nerve Exam The cranial nerves can be separated into four major groups associated with the subtests of the cranial nerve exam. First are the sensory nerves, then the nerves that control eye movement, the nerves of the oral cavity and superior pharynx, and the nerve that controls movements of the neck. The olfactory, optic, and vestibulocochlear nerves are strictly sensory nerves for smell, sight, and balance and hearing, whereas the trigeminal, facial, and glossopharyngeal nerves carry somatosensation of the face, and taste—separated between the anterior two-thirds of the tongue and the posterior one-third. Special senses are tested by presenting the particular stimuli to each receptive organ. General senses can be tested through sensory discrimination of touch versus painful stimuli. The oculomotor, trochlear, and abducens nerves control the extraocular muscles and are connected by the medial longitudinal fasciculus to coordinate gaze. Testing conjugate gaze is as simple as having the patient follow a visual target, like a pen tip, through the visual field ending with an approach toward the face to test convergence and accommodation. Along with the vestibular functions of the eighth nerve, the vestibulo-ocular reflex stabilizes gaze during head movements by coordinating equilibrium sensations with the eye movement systems. The trigeminal nerve controls the muscles of chewing, which are tested for stretch reflexes. Motor functions of the facial nerve are usually obvious if facial expressions are compromised, but can be tested by having the patient raise their eyebrows, smile, and frown. Movements of the tongue, soft palate, or superior pharynx can be observed directly while the patient swallows, while the gag reflex is elicited, or while the patient says repetitive consonant sounds. The motor control of the gag reflex is largely controlled by fibers in the vagus nerve and constitutes a test of that nerve because the parasympathetic functions of that nerve are involved in visceral regulation, such as regulating the heartbeat and digestion. Movement of the head and neck using the sternocleidomastoid and trapezius muscles is controlled by the accessory nerve. Flexing of the neck and strength testing of those muscles reviews the function of that nerve. The Sensory and Motor Exams - Describe the arrangement of sensory and motor regions in the spinal cord - Relate damage in the spinal cord to sensory or motor deficits - Differentiate between upper motor neuron and lower motor neuron diseases - Describe the clinical indications of common reflexes Connections between the body and the CNS occur through the spinal cord. The cranial nerves connect the head and neck directly to the brain, but the spinal cord receives sensory input and sends motor commands out to the body through the spinal nerves. Whereas the brain develops into a complex series of nuclei and fiber tracts, the spinal cord remains relatively simple in its configuration (Figure 16.12). From the initial neural tube early in embryonic development, the spinal cord retains a tube-like structure with gray matter surrounding the small central canal and white matter on the surface in three columns. The dorsal, or posterior, horns of the gray matter are mainly devoted to sensory functions whereas the ventral, or anterior, and lateral horns are associated with motor functions. In the white matter, the dorsal column relays sensory information to the brain, and the anterior column is almost exclusively relaying motor commands to the ventral horn motor neurons. The lateral column, however, conveys both sensory and motor information between the spinal cord and brain. Figure 16.12 Locations of Spinal Fiber Tracts Sensory Modalities and Location The general senses are distributed throughout the body, relying on nervous tissue incorporated into various organs. Somatic senses are incorporated mostly into the skin, muscles, or tendons, whereas the visceral senses come from nervous tissue incorporated into the majority of organs such as the heart or stomach. The somatic senses are those that usually make up the conscious perception of the how the body interacts with the environment. The visceral senses are most often below the limit of conscious perception because they are involved in homeostatic regulation through the autonomic nervous system. The sensory exam tests the somatic senses, meaning those that are consciously perceived. Testing of the senses begins with examining the regions known as dermatomes that connect to the cortical region where somatosensation is perceived in the postcentral gyrus. To test the sensory fields, a simple stimulus of the light touch of the soft end of a cotton-tipped applicator is applied at various locations on the skin. The spinal nerves, which contain sensory fibers with dendritic endings in the skin, connect with the skin in a topographically organized manner, illustrated as dermatomes (Figure 16.13). For example, the fibers of eighth cervical nerve innervate the medial surface of the forearm and extend out to the fingers. In addition to testing perception at different positions on the skin, it is necessary to test sensory perception within the dermatome from distal to proximal locations in the appendages, or lateral to medial locations in the trunk. In testing the eighth cervical nerve, the patient would be asked if the touch of the cotton to the fingers or the medial forearm was perceptible, and whether there were any differences in the sensations. Figure 16.13 Dermatomes The surface of the skin can be divided into topographic regions that relate to the location of sensory endings in the skin based on the spinal nerve that contains those fibers. (credit: modification of work by Mikael Häggström) Other modalities of somatosensation can be tested using a few simple tools. The perception of pain can be tested using the broken end of the cotton-tipped applicator. The perception of vibratory stimuli can be testing using an oscillating tuning fork placed against prominent bone features such as the distal head of the ulna on the medial aspect of the elbow. When the tuning fork is still, the metal against the skin can be perceived as a cold stimulus. Using the cotton tip of the applicator, or even just a fingertip, the perception of tactile movement can be assessed as the stimulus is drawn across the skin for approximately 2–3 cm. The patient would be asked in what direction the stimulus is moving. All of these tests are repeated in distal and proximal locations and for different dermatomes to assess the spatial specificity of perception. The sense of position and motion, proprioception, is tested by moving the fingers or toes and asking the patient if they sense the movement. If the distal locations are not perceived, the test is repeated at increasingly proximal joints. The various stimuli used to test sensory input assess the function of the major ascending tracts of the spinal cord. The dorsal column pathway conveys fine touch, vibration, and proprioceptive information, whereas the spinothalamic pathway primarily conveys pain and temperature. Testing these stimuli provides information about whether these two major ascending pathways are functioning properly. Within the spinal cord, the two systems are segregated. The dorsal column information ascends ipsilateral to the source of the stimulus and decussates in the medulla, whereas the spinothalamic pathway decussates at the level of entry and ascends contralaterally. The differing sensory stimuli are segregated in the spinal cord so that the various subtests for these stimuli can distinguish which ascending pathway may be damaged in certain situations. Whereas the basic sensory stimuli are assessed in the subtests directed at each submodality of somatosensation, testing the ability to discriminate sensations is important. Pairing the light touch and pain subtests together makes it possible to compare the two submodalities at the same time, and therefore the two major ascending tracts at the same time. Mistaking painful stimuli for light touch, or vice versa, may point to errors in ascending projections, such as in a hemisection of the spinal cord that might come from a motor vehicle accident. Another issue of sensory discrimination is not distinguishing between different submodalities, but rather location. The two-point discrimination subtest highlights the density of sensory endings, and therefore receptive fields in the skin. The sensitivity to fine touch, which can give indications of the texture and detailed shape of objects, is highest in the fingertips. To assess the limit of this sensitivity, two-point discrimination is measured by simultaneously touching the skin in two locations, such as could be accomplished with a pair of forceps. Specialized calipers for precisely measuring the distance between points are also available. The patient is asked to indicate whether one or two stimuli are present while keeping their eyes closed. The examiner will switch between using the two points and a single point as the stimulus. Failure to recognize two points may be an indication of a dorsal column pathway deficit. Similar to two-point discrimination, but assessing laterality of perception, is double simultaneous stimulation. Two stimuli, such as the cotton tips of two applicators, are touched to the same position on both sides of the body. If one side is not perceived, this may indicate damage to the contralateral posterior parietal lobe. Because there is one of each pathway on either side of the spinal cord, they are not likely to interact. If none of the other subtests suggest particular deficits with the pathways, the deficit is likely to be in the cortex where conscious perception is based. The mental status exam contains subtests that assess other functions that are primarily localized to the parietal cortex, such as stereognosis and graphesthesia. A final subtest of sensory perception that concentrates on the sense of proprioception is known as the Romberg test. The patient is asked to stand straight with feet together. Once the patient has achieved their balance in that position, they are asked to close their eyes. Without visual feedback that the body is in a vertical orientation relative to the surrounding environment, the patient must rely on the proprioceptive stimuli of joint and muscle position, as well as information from the inner ear, to maintain balance. This test can indicate deficits in dorsal column pathway proprioception, as well as problems with proprioceptive projections to the cerebellum through the spinocerebellar tract. INTERACTIVE LINK Watch this video to see a quick demonstration of two-point discrimination. Touching a specialized caliper to the surface of the skin will measure the distance between two points that are perceived as distinct stimuli versus a single stimulus. The patient keeps their eyes closed while the examiner switches between using both points of the caliper or just one. The patient then must indicate whether one or two stimuli are in contact with the skin. Why is the distance between the caliper points closer on the fingertips as opposed to the palm of the hand? And what do you think the distance would be on the arm, or the shoulder? Muscle Strength and Voluntary Movement The skeletomotor system is largely based on the simple, two-cell projection from the precentral gyrus of the frontal lobe to the skeletal muscles. The corticospinal tract represents the neurons that send output from the primary motor cortex. These fibers travel through the deep white matter of the cerebrum, then through the midbrain and pons, into the medulla where most of them decussate, and finally through the spinal cord white matter in the lateral (crossed fibers) or anterior (uncrossed fibers) columns. These fibers synapse on motor neurons in the ventral horn. The ventral horn motor neurons then project to skeletal muscle and cause contraction. These two cells are termed the upper motor neuron (UMN) and the lower motor neuron (LMN). Voluntary movements require these two cells to be active. The motor exam tests the function of these neurons and the muscles they control. First, the muscles are inspected and palpated for signs of structural irregularities. Movement disorders may be the result of changes to the muscle tissue, such as scarring, and these possibilities need to be ruled out before testing function. Along with this inspection, muscle tone is assessed by moving the muscles through a passive range of motion. The arm is moved at the elbow and wrist, and the leg is moved at the knee and ankle. Skeletal muscle should have a resting tension representing a slight contraction of the fibers. The lack of muscle tone, known as hypotonicity or flaccidity, may indicate that the LMN is not conducting action potentials that will keep a basal level of acetylcholine in the neuromuscular junction. If muscle tone is present, muscle strength is tested by having the patient contract muscles against resistance. The examiner will ask the patient to lift the arm, for example, while the examiner is pushing down on it. This is done for both limbs, including shrugging the shoulders. Lateral differences in strength—being able to push against resistance with the right arm but not the left—would indicate a deficit in one corticospinal tract versus the other. An overall loss of strength, without laterality, could indicate a global problem with the motor system. Diseases that result in UMN lesions include cerebral palsy or MS, or it may be the result of a stroke. A sign of UMN lesion is a negative result in the subtest for pronator drift. The patient is asked to extend both arms in front of the body with the palms facing up. While keeping the eyes closed, if the patient unconsciously allows one or the other arm to slowly relax, toward the pronated position, this could indicate a failure of the motor system to maintain the supinated position. Reflexes Reflexes combine the spinal sensory and motor components with a sensory input that directly generates a motor response. The reflexes that are tested in the neurological exam are classified into two groups. A deep tendon reflex is commonly known as a stretch reflex, and is elicited by a strong tap to a tendon, such as in the knee-jerk reflex. A superficial reflex is elicited through gentle stimulation of the skin and causes contraction of the associated muscles. For the arm, the common reflexes to test are of the biceps, brachioradialis, triceps, and flexors for the digits. For the leg, the knee-jerk reflex of the quadriceps is common, as is the ankle reflex for the gastrocnemius and soleus. The tendon at the insertion for each of these muscles is struck with a rubber mallet. The muscle is quickly stretched, resulting in activation of the muscle spindle that sends a signal into the spinal cord through the dorsal root. The fiber synapses directly on the ventral horn motor neuron that activates the muscle, causing contraction. The reflexes are physiologically useful for stability. If a muscle is stretched, it reflexively contracts to return the muscle to compensate for the change in length. In the context of the neurological exam, reflexes indicate that the LMN is functioning properly. The most common superficial reflex in the neurological exam is the plantar reflex that tests for the Babinski sign on the basis of the extension or flexion of the toes at the plantar surface of the foot. The plantar reflex is commonly tested in newborn infants to establish the presence of neuromuscular function. To elicit this reflex, an examiner brushes a stimulus, usually the examiner’s fingertip, along the plantar surface of the infant’s foot. An infant would present a positive Babinski sign, meaning the foot dorsiflexes and the toes extend and splay out. As a person learns to walk, the plantar reflex changes to cause curling of the toes and a moderate plantar flexion. If superficial stimulation of the sole of the foot caused extension of the foot, keeping one’s balance would be harder. The descending input of the corticospinal tract modifies the response of the plantar reflex, meaning that a negative Babinski sign is the expected response in testing the reflex. Other superficial reflexes are not commonly tested, though a series of abdominal reflexes can target function in the lower thoracic spinal segments. INTERACTIVE LINK Watch this video to see how to test reflexes in the abdomen. Testing reflexes of the trunk is not commonly performed in the neurological exam, but if findings suggest a problem with the thoracic segments of the spinal cord, a series of superficial reflexes of the abdomen can localize function to those segments. If contraction is not observed when the skin lateral to the umbilicus (belly button) is stimulated, what level of the spinal cord may be damaged? Comparison of Upper and Lower Motor Neuron Damage Many of the tests of motor function can indicate differences that will address whether damage to the motor system is in the upper or lower motor neurons. Signs that suggest a UMN lesion include muscle weakness, strong deep tendon reflexes, decreased control of movement or slowness, pronator drift, a positive Babinski sign, spasticity, and the clasp-knife response. Spasticity is an excess contraction in resistance to stretch. It can result in hyperflexia, which is when joints are overly flexed. The clasp-knife response occurs when the patient initially resists movement, but then releases, and the joint will quickly flex like a pocket knife closing. A lesion on the LMN would result in paralysis, or at least partial loss of voluntary muscle control, which is known as paresis. The paralysis observed in LMN diseases is referred to as flaccid paralysis, referring to a complete or partial loss of muscle tone, in contrast to the loss of control in UMN lesions in which tone is retained and spasticity is exhibited. Other signs of an LMN lesion are fibrillation, fasciculation, and compromised or lost reflexes resulting from the denervation of the muscle fibers. DISORDERS OF THE... Spinal Cord In certain situations, such as a motorcycle accident, only half of the spinal cord may be damaged in what is known as a hemisection. Forceful trauma to the trunk may cause ribs or vertebrae to fracture, and debris can crush or section through part of the spinal cord. The full section of a spinal cord would result in paraplegia, or loss of voluntary motor control of the lower body, as well as loss of sensations from that point down. A hemisection, however, will leave spinal cord tracts intact on one side. The resulting condition would be hemiplegia on the side of the trauma—one leg would be paralyzed. The sensory results are more complicated. The ascending tracts in the spinal cord are segregated between the dorsal column and spinothalamic pathways. This means that the sensory deficits will be based on the particular sensory information each pathway conveys. Sensory discrimination between touch and painful stimuli will illustrate the difference in how these pathways divide these functions. On the paralyzed leg, a patient will acknowledge painful stimuli, but not fine touch or proprioceptive sensations. On the functional leg, the opposite is true. The reason for this is that the dorsal column pathway ascends ipsilateral to the sensation, so it would be damaged the same way as the lateral corticospinal tract. The spinothalamic pathway decussates immediately upon entering the spinal cord and ascends contralateral to the source; it would therefore bypass the hemisection. The motor system can indicate the loss of input to the ventral horn in the lumbar enlargement where motor neurons to the leg are found, but motor function in the trunk is less clear. The left and right anterior corticospinal tracts are directly adjacent to each other. The likelihood of trauma to the spinal cord resulting in a hemisection that affects one anterior column, but not the other, is very unlikely. Either the axial musculature will not be affected at all, or there will be bilateral losses in the trunk. Sensory discrimination can pinpoint the level of damage in the spinal cord. Below the hemisection, pain stimuli will be perceived in the damaged side, but not fine touch. The opposite is true on the other side. The pain fibers on the side with motor function cross the midline in the spinal cord and ascend in the contralateral lateral column as far as the hemisection. The dorsal column will be intact ipsilateral to the source on the intact side and reach the brain for conscious perception. The trauma would be at the level just before sensory discrimination returns to normal, helping to pinpoint the trauma. Whereas imaging technology, like magnetic resonance imaging (MRI) or computed tomography (CT) scanning, could localize the injury as well, nothing more complicated than a cotton-tipped applicator can localize the damage. That may be all that is available on the scene when moving the victim requires crucial decisions be made. The Coordination and Gait Exams - Explain the relationship between the location of the cerebellum and its function in movement - Chart the major divisions of the cerebellum - List the major connections of the cerebellum - Describe the relationship of the cerebellum to axial and appendicular musculature - Explain the prevalent causes of cerebellar ataxia The role of the cerebellum is a subject of debate. There is an obvious connection to motor function based on the clinical implications of cerebellar damage. There is also strong evidence of the cerebellar role in procedural memory. The two are not incompatible; in fact, procedural memory is motor memory, such as learning to ride a bicycle. Significant work has been performed to describe the connections within the cerebellum that result in learning. A model for this learning is classical conditioning, as shown by the famous dogs from the physiologist Ivan Pavlov’s work. This classical conditioning, which can be related to motor learning, fits with the neural connections of the cerebellum. The cerebellum is 10 percent of the mass of the brain and has varied functions that all point to a role in the motor system. Location and Connections of the Cerebellum The cerebellum is located in apposition to the dorsal surface of the brain stem, centered on the pons. The name of the pons is derived from its connection to the cerebellum. The word means “bridge” and refers to the thick bundle of myelinated axons that form a bulge on its ventral surface. Those fibers are axons that project from the gray matter of the pons into the contralateral cerebellar cortex. These fibers make up the middle cerebellar peduncle (MCP) and are the major physical connection of the cerebellum to the brain stem (Figure 16.14). Two other white matter bundles connect the cerebellum to the other regions of the brain stem. The superior cerebellar peduncle (SCP) is the connection of the cerebellum to the midbrain and forebrain. The inferior cerebellar peduncle (ICP) is the connection to the medulla. Figure 16.14 Cerebellar Penduncles The connections to the cerebellum are the three cerebellar peduncles, which are close to each other. The ICP arises from the medulla—specifically from the inferior olive, which is visible as a bulge on the ventral surface of the brain stem. The MCP is the ventral surface of the pons. The SCP projects into the midbrain. These connections can also be broadly described by their functions. The ICP conveys sensory input to the cerebellum, partially from the spinocerebellar tract, but also through fibers of the inferior olive. The MCP is part of the cortico-ponto-cerebellar pathway that connects the cerebral cortex with the cerebellum and preferentially targets the lateral regions of the cerebellum. It includes a copy of the motor commands sent from the precentral gyrus through the corticospinal tract, arising from collateral branches that synapse in the gray matter of the pons, along with input from other regions such as the visual cortex. The SCP is the major output of the cerebellum, divided between the red nucleus in the midbrain and the thalamus, which will return cerebellar processing to the motor cortex. These connections describe a circuit that compares motor commands and sensory feedback to generate a new output. These comparisons make it possible to coordinate movements. If the cerebral cortex sends a motor command to initiate walking, that command is copied by the pons and sent into the cerebellum through the MCP. Sensory feedback in the form of proprioception from the spinal cord, as well as vestibular sensations from the inner ear, enters through the ICP. If you take a step and begin to slip on the floor because it is wet, the output from the cerebellum—through the SCP—can correct for that and keep you balanced and moving. The red nucleus sends new motor commands to the spinal cord through the rubrospinal tract. The cerebellum is divided into regions that are based on the particular functions and connections involved. The midline regions of the cerebellum, the vermis and flocculonodular lobe, are involved in comparing visual information, equilibrium, and proprioceptive feedback to maintain balance and coordinate movements such as walking, or gait, through the descending output of the red nucleus (Figure 16.15). The lateral hemispheres are primarily concerned with planning motor functions through frontal lobe inputs that are returned through the thalamic projections back to the premotor and motor cortices. Processing in the midline regions targets movements of the axial musculature, whereas the lateral regions target movements of the appendicular musculature. The vermis is referred to as the spinocerebellum because it primarily receives input from the dorsal columns and spinocerebellar pathways. The flocculonodular lobe is referred to as the vestibulocerebellum because of the vestibular projection into that region. Finally, the lateral cerebellum is referred to as the cerebrocerebellum, reflecting the significant input from the cerebral cortex through the cortico-ponto-cerebellar pathway. Figure 16.15 Major Regions of the Cerebellum The cerebellum can be divided into two basic regions: the midline and the hemispheres. The midline is composed of the vermis and the flocculonodular lobe, and the hemispheres are the lateral regions. Coordination and Alternating Movement Testing for cerebellar function is the basis of the coordination exam. The subtests target appendicular musculature, controlling the limbs, and axial musculature for posture and gait. The assessment of cerebellar function will depend on the normal functioning of other systems addressed in previous sections of the neurological exam. Motor control from the cerebrum, as well as sensory input from somatic, visual, and vestibular senses, are important to cerebellar function. The subtests that address appendicular musculature, and therefore the lateral regions of the cerebellum, begin with a check for tremor. The patient extends their arms in front of them and holds the position. The examiner watches for the presence of tremors that would not be present if the muscles are relaxed. By pushing down on the arms in this position, the examiner can check for the rebound response, which is when the arms are automatically brought back to the extended position. The extension of the arms is an ongoing motor process, and the tap or push on the arms presents a change in the proprioceptive feedback. The cerebellum compares the cerebral motor command with the proprioceptive feedback and adjusts the descending input to correct. The red nucleus would send an additional signal to the LMN for the arm to increase contraction momentarily to overcome the change and regain the original position. The check reflex depends on cerebellar input to keep increased contraction from continuing after the removal of resistance. The patient flexes the elbow against resistance from the examiner to extend the elbow. When the examiner releases the arm, the patient should be able to stop the increased contraction and keep the arm from moving. A similar response would be seen if you try to pick up a coffee mug that you believe to be full but turns out to be empty. Without checking the contraction, the mug would be thrown from the overexertion of the muscles expecting to lift a heavier object. Several subtests of the cerebellum assess the ability to alternate movements, or switch between muscle groups that may be antagonistic to each other. In the finger-to-nose test, the patient touches their finger to the examiner’s finger and then to their nose, and then back to the examiner’s finger, and back to the nose. The examiner moves the target finger to assess a range of movements. A similar test for the lower extremities has the patient touch their toe to a moving target, such as the examiner’s finger. Both of these tests involve flexion and extension around a joint—the elbow or the knee and the shoulder or hip—as well as movements of the wrist and ankle. The patient must switch between the opposing muscles, like the biceps and triceps brachii, to move their finger from the target to their nose. Coordinating these movements involves the motor cortex communicating with the cerebellum through the pons and feedback through the thalamus to plan the movements. Visual cortex information is also part of the processing that occurs in the cerebrocerebellum while it is involved in guiding movements of the finger or toe. Rapid, alternating movements are tested for the upper and lower extremities. The patient is asked to touch each finger to their thumb, or to pat the palm of one hand on the back of the other, and then flip that hand over and alternate back-and-forth. To test similar function in the lower extremities, the patient touches their heel to their shin near the knee and slides it down toward the ankle, and then back again, repetitively. Rapid, alternating movements are part of speech as well. A patient is asked to repeat the nonsense consonants “lah-kah-pah” to alternate movements of the tongue, lips, and palate. All of these rapid alternations require planning from the cerebrocerebellum to coordinate movement commands that control the coordination. Posture and Gait Gait can either be considered a separate part of the neurological exam or a subtest of the coordination exam that addresses walking and balance. Testing posture and gait addresses functions of the spinocerebellum and the vestibulocerebellum because both are part of these activities. A subtest called station begins with the patient standing in a normal position to check for the placement of the feet and balance. The patient is asked to hop on one foot to assess the ability to maintain balance and posture during movement. Though the station subtest appears to be similar to the Romberg test, the difference is that the patient’s eyes are open during station. The Romberg test has the patient stand still with the eyes closed. Any changes in posture would be the result of proprioceptive deficits, and the patient is able to recover when they open their eyes. Subtests of walking begin with having the patient walk normally for a distance away from the examiner, and then turn and return to the starting position. The examiner watches for abnormal placement of the feet and the movement of the arms relative to the movement. The patient is then asked to walk with a few different variations. Tandem gait is when the patient places the heel of one foot against the toe of the other foot and walks in a straight line in that manner. Walking only on the heels or only on the toes will test additional aspects of balance. Ataxia A movement disorder of the cerebellum is referred to as ataxia. It presents as a loss of coordination in voluntary movements. Ataxia can also refer to sensory deficits that cause balance problems, primarily in proprioception and equilibrium. When the problem is observed in movement, it is ascribed to cerebellar damage. Sensory and vestibular ataxia would likely also present with problems in gait and station. Ataxia is often the result of exposure to exogenous substances, focal lesions, or a genetic disorder. Focal lesions include strokes affecting the cerebellar arteries, tumors that may impinge on the cerebellum, trauma to the back of the head and neck, or MS. Alcohol intoxication or drugs such as ketamine cause ataxia, but it is often reversible. Mercury in fish can cause ataxia as well. Hereditary conditions can lead to degeneration of the cerebellum or spinal cord, as well as malformation of the brain, or the abnormal accumulation of copper seen in Wilson’s disease. INTERACTIVE LINK Watch this short video to see a test for station. Station refers to the position a person adopts when they are standing still. The examiner would look for issues with balance, which coordinates proprioceptive, vestibular, and visual information in the cerebellum. To test the ability of a subject to maintain balance, asking them to stand or hop on one foot can be more demanding. The examiner may also push the subject to see if they can maintain balance. An abnormal finding in the test of station is if the feet are placed far apart. Why would a wide stance suggest problems with cerebellar function? EVERYDAY CONNECTION The Field Sobriety Test The neurological exam has been described as a clinical tool throughout this chapter. It is also useful in other ways. A variation of the coordination exam is the Field Sobriety Test (FST) used to assess whether drivers are under the influence of alcohol. The cerebellum is crucial for coordinated movements such as keeping balance while walking, or moving appendicular musculature on the basis of proprioceptive feedback. The cerebellum is also very sensitive to ethanol, the particular type of alcohol found in beer, wine, and liquor. Walking in a straight line involves comparing the motor command from the primary motor cortex to the proprioceptive and vestibular sensory feedback, as well as following the visual guide of the white line on the side of the road. When the cerebellum is compromised by alcohol, the cerebellum cannot coordinate these movements effectively, and maintaining balance becomes difficult. Another common aspect of the FST is to have the driver extend their arms out wide and touch their fingertip to their nose, usually with their eyes closed. The point of this is to remove the visual feedback for the movement and force the driver to rely just on proprioceptive information about the movement and position of their fingertip relative to their nose. With eyes open, the corrections to the movement of the arm might be so small as to be hard to see, but proprioceptive feedback is not as immediate and broader movements of the arm will probably be needed, particularly if the cerebellum is affected by alcohol. Reciting the alphabet backwards is not always a component of the FST, but its relationship to neurological function is interesting. There is a cognitive aspect to remembering how the alphabet goes and how to recite it backwards. That is actually a variation of the mental status subtest of repeating the months backwards. However, the cerebellum is important because speech production is a coordinated activity. The speech rapid alternating movement subtest is specifically using the consonant changes of “lah-kah-pah” to assess coordinated movements of the lips, tongue, pharynx, and palate. But the entire alphabet, especially in the nonrehearsed backwards order, pushes this type of coordinated movement quite far. It is related to the reason that speech becomes slurred when a person is intoxicated. Key Terms - accommodation - in vision, a change in the ability of the eye to focus on objects at different distances - accommodation–convergence reflex - coordination of somatic control of the medial rectus muscles of either eye with the parasympathetic control of the ciliary bodies to maintain focus while the eyes converge on visual stimuli near to the face - anterograde amnesia - inability to form new memories from a particular time forward - aphasia - loss of language function - ataxia - movement disorder related to damage of the cerebellum characterized by loss of coordination in voluntary movements - Babinski sign - dorsiflexion of the foot with extension and splaying of the toes in response to the plantar reflex, normally suppressed by corticospinal input - cerebrocerebellum - lateral regions of the cerebellum; named for the significant input from the cerebral cortex - check reflex - response to a release in resistance so that the contractions stop, or check, movement - clasp-knife response - sign of UMN disease when a patient initially resists passive movement of a muscle but will quickly release to a lower state of resistance - conduction aphasia - loss of language function related to connecting the understanding of speech with the production of speech, without either specific function being lost - conductive hearing - hearing dependent on the conduction of vibrations of the tympanic membrane through the ossicles of the middle ear - conjugate gaze - coordinated movement of the two eyes simultaneously in the same direction - convergence - in vision, the movement of the eyes so that they are both pointed at the same point in space, which increases for stimuli that are closer to the subject - coordination exam - major section of the neurological exam that assesses complex, coordinated motor functions of the cerebellum and associated motor pathways - cortico-ponto-cerebellar pathway - projection from the cerebral cortex to the cerebellum by way of the gray matter of the pons - cranial nerve exam - major section of the neurological exam that assesses sensory and motor functions of the cranial nerves and their associated central and peripheral structures - cytoarchitecture - study of a tissue based on the structure and organization of its cellular components; related to the broader term, histology - deep tendon reflex - another term for stretch reflex, based on the elicitation through deep stimulation of the tendon at the insertion - diplopia - double vision resulting from a failure in conjugate gaze - edema - fluid accumulation in tissue; often associated with circulatory deficits - embolus - obstruction in a blood vessel such as a blood clot, fatty mass, air bubble, or other foreign matter that interrupts the flow of blood to an organ or some part of the body - episodic memory - memory of specific events in an autobiographical sense - expressive aphasia - loss of the ability to produce language; usually associated with damage to Broca’s area in the frontal lobe - extrinsic muscles of the tongue - muscles that are connected to other structures, such as the hyoid bone or the mandible, and control the position of the tongue - fasciculation - small muscle twitch as a result of spontaneous activity from an LMN - fauces - opening from the oral cavity into the pharynx - fibrillation - in motor responses, a spontaneous muscle action potential that occurs in the absence of neuromuscular input, resulting from LMN lesions - flaccid paralysis - loss of voluntary muscle control and muscle tone, as the result of LMN disease - flaccidity - presentation of a loss of muscle tone, observed as floppy limbs or a lack of resistance to passive movement - flocculonodular lobe - lobe of the cerebellum that receives input from the vestibular system to help with balance and posture - gait - rhythmic pattern of alternating movements of the lower limbs during locomotion - gait exam - major section of the neurological exam that assesses the cerebellum and descending pathways in the spinal cord through the coordinated motor functions of walking; a portion of the coordination exam - gnosis - in a neurological exam, intuitive experiential knowledge tested by interacting with common objects or symbols - graphesthesia - perception of symbols, such as letters or numbers, traced in the palm of the hand - hemisection - cut through half of a structure, such as the spinal cord - hemorrhagic stroke - disruption of blood flow to the brain caused by bleeding within the cranial vault - hyperflexia - overly flexed joints - hypotonicity - low muscle tone, a sign of LMN disease - hypovolemia - decrease in blood volume - inferior cerebellar peduncle (ICP) - input to the cerebellum, largely from the inferior olive, that represents sensory feedback from the periphery - inferior olive - large nucleus in the medulla that receives input from sensory systems and projects into the cerebellar cortex - internuclear ophthalmoplegia - deficit of conjugate lateral gaze because the lateral rectus muscle of one eye does not contract resulting from damage to the abducens nerve or the MLF - intorsion - medial rotation of the eye around its axis - intrinsic muscles of the tongue - muscles that originate out of, and insert into, other tissues within the tongue and control the shape of the tongue - ischemic stroke - disruption of blood flow to the brain because blood cannot flow through blood vessels as a result of a blockage or narrowing of the vessel - jaw-jerk reflex - stretch reflex of the masseter muscle - localization of function - principle that circumscribed anatomical locations are responsible for specific functions in an organ system - medial longitudinal fasciculus (MLF) - fiber pathway that connects structures involved in the control of eye and head position, from the superior colliculus to the vestibular nuclei and cerebellum - mental status exam - major section of the neurological exam that assesses cognitive functions of the cerebrum - middle cerebellar peduncle (MCP) - large, white-matter bridge from the pons that constitutes the major input to the cerebellar cortex - motor exam - major section of the neurological exam that assesses motor functions of the spinal cord and spinal nerves - neurological exam - clinical assessment tool that can be used to quickly evaluate neurological function and determine if specific parts of the nervous system have been affected by damage or disease - paramedian pontine reticular formation (PPRF) - region of the brain stem adjacent to the motor nuclei for gaze control that coordinates rapid, conjugate eye movements - paresis - partial loss of, or impaired, voluntary muscle control - plantar reflex - superficial reflex initiated by gentle stimulation of the sole of the foot - praxis - in a neurological exam, the act of doing something using ready knowledge or skills in response to verbal instruction - procedural memory - memory of how to perform a specific task - pronator drift - sign of contralateral corticospinal lesion when the one arm will drift into a pronated position when held straight out with the palms facing upward - receptive aphasia - loss of the ability to understand received language, such as what is spoken to the subject or given in written form - red nucleus - nucleus in the midbrain that receives output from the cerebellum and projects onto the spinal cord in the rubrospinal tract - retrograde amnesia - loss of memories before a particular event - Rinne test - use of a tuning fork to test conductive hearing loss versus sensorineural hearing loss - Romberg test - test of equilibrium that requires the patient to maintain a straight, upright posture without visual feedback of position - rubrospinal tract - descending tract from the red nucleus of the midbrain that results in modification of ongoing motor programs - saccade - small, rapid movement of the eyes used to locate and direct the fovea onto visual stimuli - sensorineural hearing - hearing dependent on the transduction and propagation of auditory information through the neural components of the peripheral auditory structures - sensory exam - major section of the neurological exam that assesses sensory functions of the spinal cord and spinal nerves - short-term memory - capacity to retain information actively in the brain for a brief period of time - Snellen chart - standardized arrangement of letters in decreasing size presented to a subject at a distance of 20 feet to test visual acuity - spasticity - increased contraction of a muscle in response to resistance, often resulting in hyperflexia - spinocerebellar tract - ascending fibers that carry proprioceptive input to the cerebellum used in maintaining balance and coordinated movement - spinocerebellum - midline region of the cerebellum known as the vermis that receives proprioceptive input from the spinal cord - stereognosis - perception of common objects placed in the hand solely on the basis of manipulation of that object in the hand - stroke - (also, cerebrovascular accident (CVA)) loss of neurological function caused by an interruption of blood flow to a region of the central nervous system - superficial reflex - reflexive contraction initiated by gentle stimulation of the skin - superior cerebellar peduncle (SCP) - white-matter tract representing output of the cerebellum to the red nucleus of the midbrain - transient ischemic attack (TIA) - temporary disruption of blood flow to the brain in which symptoms occur rapidly but last only a short time - vermis - prominent ridge along the midline of the cerebellum that is referred to as the spinocerebellum - vestibulo-ocular reflex (VOR) - reflex based on connections between the vestibular system and the cranial nerves of eye movements that ensures that images are stabilized on the retina as the head and body move - vestibulocerebellum - flocculonodular lobe of the cerebellum named for the vestibular input from the eighth cranial nerve - Weber test - use of a tuning fork to test the laterality of hearing loss by placing it at several locations on the midline of the skull - Wernicke’s area - region at the posterior end of the lateral sulcus in which speech comprehension is localized Chapter Review 16.1 Overview of the Neurological Exam The neurological exam is a clinical assessment tool to determine the extent of function from the nervous system. It is divided into five major sections that each deal with a specific region of the CNS. The mental status exam is concerned with the cerebrum and assesses higher functions such as memory, language, and emotion. The cranial nerve exam tests the functions of all of the cranial nerves and, therefore, their connections to the CNS through the forebrain and brain stem. The sensory and motor exams assess those functions as they relate to the spinal cord, as well as the combination of the functions in spinal reflexes. The coordination exam targets cerebellar function in coordinated movements, including those functions associated with gait. Damage to and disease of the nervous system lead to loss of function. The location of the injury will correspond to the functional loss, as suggested by the principle of localization of function. The neurological exam provides the opportunity for a clinician to determine where damage has occurred on the basis of the function that is lost. Damage from acute injuries such as strokes may result in specific functions being lost, whereas broader effects in infection or developmental disorders may result in general losses across an entire section of the neurological exam. 16.4 The Sensory and Motor Exams The sensory and motor exams assess function related to the spinal cord and the nerves connected to it. Sensory functions are associated with the dorsal regions of the spinal cord, whereas motor function is associated with the ventral side. Localizing damage to the spinal cord is related to assessments of the peripheral projections mapped to dermatomes. Sensory tests address the various submodalities of the somatic senses: touch, temperature, vibration, pain, and proprioception. Results of the subtests can point to trauma in the spinal cord gray matter, white matter, or even in connections to the cerebral cortex. Motor tests focus on the function of the muscles and the connections of the descending motor pathway. Muscle tone and strength are tested for upper and lower extremities. Input to the muscles comes from the descending cortical input of upper motor neurons and the direct innervation of lower motor neurons. Reflexes can either be based on deep stimulation of tendons or superficial stimulation of the skin. The presence of reflexive contractions helps to differentiate motor disorders between the upper and lower motor neurons. The specific signs associated with motor disorders can establish the difference further, based on the type of paralysis, the state of muscle tone, and specific indicators such as pronator drift or the Babinski sign. 16.5 The Coordination and Gait Exams The cerebellum is an important part of motor function in the nervous system. It apparently plays a role in procedural learning, which would include motor skills such as riding a bike or throwing a football. The basis for these roles is likely to be tied into the role the cerebellum plays as a comparator for voluntary movement. The motor commands from the cerebral hemispheres travel along the corticospinal pathway, which passes through the pons. Collateral branches of these fibers synapse on neurons in the pons, which then project into the cerebellar cortex through the middle cerebellar peduncles. Ascending sensory feedback, entering through the inferior cerebellar peduncles, provides information about motor performance. The cerebellar cortex compares the command to the actual performance and can adjust the descending input to compensate for any mismatch. The output from deep cerebellar nuclei projects through the superior cerebellar peduncles to initiate descending signals from the red nucleus to the spinal cord. The primary role of the cerebellum in relation to the spinal cord is through the spinocerebellum; it controls posture and gait with significant input from the vestibular system. Deficits in cerebellar function result in ataxias, or a specific kind of movement disorder. The root cause of the ataxia may be the sensory input—either the proprioceptive input from the spinal cord or the equilibrium input from the vestibular system, or direct damage to the cerebellum by stroke, trauma, hereditary factors, or toxins. Interactive Link Questions Watch this video that provides a demonstration of the neurological exam—a series of tests that can be performed rapidly when a patient is initially brought into an emergency department. The exam can be repeated on a regular basis to keep a record of how and if neurological function changes over time. In what order were the sections of the neurological exam tested in this video, and which section seemed to be left out? 2.Watch this video for an introduction to the neurological exam. Studying the neurological exam can give insight into how structure and function in the nervous system are interdependent. This is a tool both in the clinic and in the classroom, but for different reasons. In the clinic, this is a powerful but simple tool to assess a patient’s neurological function. In the classroom, it is a different way to think about the nervous system. Though medical technology provides noninvasive imaging and real-time functional data, the presenter says these cannot replace the history at the core of the medical examination. What does history mean in the context of medical practice? 3.Read this article to learn about a young man who texts his fiancée in a panic as he finds that he is having trouble remembering things. At the hospital, a neurologist administers the mental status exam, which is mostly normal except for the three-word recall test. The young man could not recall them even 30 seconds after hearing them and repeating them back to the doctor. An undiscovered mass in the mediastinum region was found to be Hodgkin’s lymphoma, a type of cancer that affects the immune system and likely caused antibodies to attack the nervous system. The patient eventually regained his ability to remember, though the events in the hospital were always elusive. Considering that the effects on memory were temporary, but resulted in the loss of the specific events of the hospital stay, what regions of the brain were likely to have been affected by the antibodies and what type of memory does that represent? 4.Watch the video titled “The Man With Two Brains” to see the neuroscientist Michael Gazzaniga introduce a patient he has worked with for years who has had his corpus callosum cut, separating his two cerebral hemispheres. A few tests are run to demonstrate how this manifests in tests of cerebral function. Unlike normal people, this patient can perform two independent tasks at the same time because the lines of communication between the right and left sides of his brain have been removed. Whereas a person with an intact corpus callosum cannot overcome the dominance of one hemisphere over the other, this patient can. If the left cerebral hemisphere is dominant in the majority of people, why would right-handedness be most common? 5.Watch this short video to see an examination of the facial nerve using some simple tests. The facial nerve controls the muscles of facial expression. Severe deficits will be obvious in watching someone use those muscles for normal control. One side of the face might not move like the other side. But directed tests, especially for contraction against resistance, require a formal testing of the muscles. The muscles of the upper and lower face need to be tested. The strength test in this video involves the patient squeezing her eyes shut and the examiner trying to pry her eyes open. Why does the examiner ask her to try a second time? 6.Watch this video to see a quick demonstration of two-point discrimination. Touching a specialized caliper to the surface of the skin will measure the distance between two points that are perceived as distinct stimuli versus a single stimulus. The patient keeps their eyes closed while the examiner switches between using both points of the caliper or just one. The patient then must indicate whether one or two stimuli are in contact with the skin. Why is the distance between the caliper points closer on the fingertips as opposed to the palm of the hand? And what do you think the distance would be on the arm, or the shoulder? 7.Watch this video to see how to test reflexes in the abdomen. Testing reflexes of the trunk is not commonly performed in the neurological exam, but if findings suggest a problem with the thoracic segments of the spinal cord, a series of superficial reflexes of the abdomen can localize function to those segments. If contraction is not observed when the skin lateral to the umbilicus (belly button) is stimulated, what level of the spinal cord may be damaged? 8.Watch this short video to see a test for station. Station refers to the position a person adopts when they are standing still. The examiner would look for issues with balance, which coordinates proprioceptive, vestibular, and visual information in the cerebellum. To test the ability of a subject to maintain balance, asking them to stand or hop on one foot can be more demanding. The examiner may also push the subject to see if they can maintain balance. An abnormal finding in the test of station is if the feet are placed far apart. Why would a wide stance suggest problems with cerebellar function? Review Questions Which major section of the neurological exam is most likely to reveal damage to the cerebellum? - cranial nerve exam - mental status exam - sensory exam - coordination exam What function would most likely be affected by a restriction of a blood vessel in the cerebral cortex? - language - gait - facial expressions - knee-jerk reflex Which major section of the neurological exam includes subtests that are sometimes considered a separate set of tests concerned with walking? - mental status exam - cranial nerve exam - coordination exam - sensory exam Memory, emotional, language, and sensorimotor deficits together are most likely the result of what kind of damage? - stroke - developmental disorder - whiplash - gunshot wound Where is language function localized in the majority of people? - cerebellum - right cerebral hemisphere - hippocampus - left cerebral hemisphere Which of the following could be elements of cytoarchitecture, as related to Brodmann’s microscopic studies of the cerebral cortex? - connections to the cerebellum - activation by visual stimuli - number of neurons per square millimeter - number of gyri or sulci Which of the following could be a multimodal integrative area? - primary visual cortex - premotor cortex - hippocampus - Wernicke’s area Which is an example of episodic memory? - how to bake a cake - your last birthday party - how old you are - needing to wear an oven mitt to take a cake out of the oven Which type of aphasia is more like hearing a foreign language spoken? - receptive aphasia - expressive aphasia - conductive aphasia - Broca’s aphasia What region of the cerebral cortex is associated with understanding language, both from another person and the language a person generates himself or herself? - medial temporal lobe - ventromedial prefrontal cortex - superior temporal gyrus - postcentral gyrus Without olfactory sensation to complement gustatory stimuli, food will taste bland unless it is seasoned with which substance? - salt - thyme - garlic - olive oil Which of the following cranial nerves is not part of the VOR? - optic - oculomotor - abducens - vestibulocochlear Which nerve is responsible for controlling the muscles that result in the gag reflex? - trigeminal - facial - glossopharyngeal - vagus Which nerve is responsible for taste, as well as salivation, in the anterior oral cavity? - facial - glossopharyngeal - vagus - hypoglossal Which of the following nerves controls movements of the neck? - oculomotor - vestibulocochlear - spinal accessory - hypoglossal Which of the following is not part of the corticospinal pathway? - cerebellar deep white matter - midbrain - medulla - lateral column Which subtest is directed at proprioceptive sensation? - two-point discrimination - tactile movement - vibration - Romberg test What term describes the inability to lift the arm above the level of the shoulder? - paralysis - paresis - fasciculation - fibrillation Which type of reflex is the jaw-jerk reflex that is part of the cranial nerve exam for the vestibulocochlear nerve? - visceral reflex - withdrawal reflex - stretch reflex - superficial reflex Which of the following is a feature of both somatic and visceral senses? - requires cerebral input - causes skeletal muscle contraction - projects to a ganglion near the target effector - involves an axon in the ventral nerve root Which white matter structure carries information from the cerebral cortex to the cerebellum? - cerebral peduncle - superior cerebellar peduncle - middle cerebellar peduncle - inferior cerebellar peduncle Which region of the cerebellum receives proprioceptive input from the spinal cord? - vermis - left hemisphere - flocculonodular lobe - right hemisphere Which of the following tests cerebellar function related to gait? - toe-to-finger - station - lah-kah-pah - finger-to-nose Which of the following is not a cause of cerebellar ataxia? - mercury from fish - drinking alcohol - antibiotics - hereditary degeneration of the cerebellum Which of the following functions cannot be attributed to the cerebellum? - comparing motor commands and sensory feedback - associating sensory stimuli with learned behavior - coordinating complex movements - processing visual information Critical Thinking Questions Why is a rapid assessment of neurological function important in an emergency situation? 35.How is the diagnostic category of TIA different from a stroke? 36.A patient’s performance of the majority of the mental status exam subtests is in line with the expected norms, but the patient cannot repeat a string of numbers given by the examiner. What is a likely explanation? 37.A patient responds to the question “What is your name?” with a look of incomprehension. Which of the two major language areas is most likely affected and what is the name for that type of aphasia? 38.As a person ages, their ability to focus on near objects (accommodation) changes. If a person is already myopic (near-sighted), why would corrective lenses not be necessary to read a book or computer screen? 39.When a patient flexes their neck, the head tips to the right side. Also, their tongue sticks out slightly to the left when they try to stick it straight out. Where is the damage to the brain stem most likely located? 40.The location of somatosensation is based on the topographical map of sensory innervation. What does this mean? 41.Why are upper motor neuron lesions characterized by “spastic paralysis”? 42.Learning to ride a bike is a motor function dependent on the cerebellum. Why are the different regions of the cerebellum involved in this complex motor learning? 43.Alcohol intoxication can produce slurred speech. How is this related to cerebellar function?	oercommons	2025-03-18T00:37:01.887035	null	{ "license": "Creative Commons - Attribution - https://creativecommons.org/licenses/by/4.0/", "url": "https://oercommons.org/courseware/lesson/56379/overview", "title": "Anatomy and Physiology, Regulation, Integration, and Control", "author": null }
https://oercommons.org/courseware/lesson/56380/overview	The Endocrine System Introduction Figure 17.1 A Child Catches a Falling Leaf Hormones of the endocrine system coordinate and control growth, metabolism, temperature regulation, the stress response, reproduction, and many other functions. (credit: “seenthroughmylense”/flickr.com) CHAPTER OBJECTIVES After studying this chapter, you will be able to: - Identify the contributions of the endocrine system to homeostasis - Discuss the chemical composition of hormones and the mechanisms of hormone action - Summarize the site of production, regulation, and effects of the hormones of the pituitary, thyroid, parathyroid, adrenal, and pineal glands - Discuss the hormonal regulation of the reproductive system - Explain the role of the pancreatic endocrine cells in the regulation of blood glucose - Identify the hormones released by the heart, kidneys, and other organs with secondary endocrine functions - Discuss several common diseases associated with endocrine system dysfunction - Discuss the embryonic development of, and the effects of aging on, the endocrine system You may never have thought of it this way, but when you send a text message to two friends to meet you at the dining hall at six, you’re sending digital signals that (you hope) will affect their behavior—even though they are some distance away. Similarly, certain cells send chemical signals to other cells in the body that influence their behavior. This long-distance intercellular communication, coordination, and control is critical for homeostasis, and it is the fundamental function of the endocrine system. An Overview of the Endocrine System - Distinguish the types of intercellular communication, their importance, mechanisms, and effects - Identify the major organs and tissues of the endocrine system and their location in the body Communication is a process in which a sender transmits signals to one or more receivers to control and coordinate actions. In the human body, two major organ systems participate in relatively “long distance” communication: the nervous system and the endocrine system. Together, these two systems are primarily responsible for maintaining homeostasis in the body. Neural and Endocrine Signaling The nervous system uses two types of intercellular communication—electrical and chemical signaling—either by the direct action of an electrical potential, or in the latter case, through the action of chemical neurotransmitters such as serotonin or norepinephrine. Neurotransmitters act locally and rapidly. When an electrical signal in the form of an action potential arrives at the synaptic terminal, they diffuse across the synaptic cleft (the gap between a sending neuron and a receiving neuron or muscle cell). Once the neurotransmitters interact (bind) with receptors on the receiving (post-synaptic) cell, the receptor stimulation is transduced into a response such as continued electrical signaling or modification of cellular response. The target cell responds within milliseconds of receiving the chemical “message”; this response then ceases very quickly once the neural signaling ends. In this way, neural communication enables body functions that involve quick, brief actions, such as movement, sensation, and cognition.In contrast, the endocrine system uses just one method of communication: chemical signaling. These signals are sent by the endocrine organs, which secrete chemicals—the hormone—into the extracellular fluid. Hormones are transported primarily via the bloodstream throughout the body, where they bind to receptors on target cells, inducing a characteristic response. As a result, endocrine signaling requires more time than neural signaling to prompt a response in target cells, though the precise amount of time varies with different hormones. For example, the hormones released when you are confronted with a dangerous or frightening situation, called the fight-or-flight response, occur by the release of adrenal hormones—epinephrine and norepinephrine—within seconds. In contrast, it may take up to 48 hours for target cells to respond to certain reproductive hormones. INTERACTIVE LINK Visit this link to watch an animation of the events that occur when a hormone binds to a cell membrane receptor. What is the secondary messenger made by adenylyl cyclase during the activation of liver cells by epinephrine? In addition, endocrine signaling is typically less specific than neural signaling. The same hormone may play a role in a variety of different physiological processes depending on the target cells involved. For example, the hormone oxytocin promotes uterine contractions in women in labor. It is also important in breastfeeding, and may be involved in the sexual response and in feelings of emotional attachment in both males and females. In general, the nervous system involves quick responses to rapid changes in the external environment, and the endocrine system is usually slower acting—taking care of the internal environment of the body, maintaining homeostasis, and controlling reproduction (Table 17.1). So how does the fight-or-flight response that was mentioned earlier happen so quickly if hormones are usually slower acting? It is because the two systems are connected. It is the fast action of the nervous system in response to the danger in the environment that stimulates the adrenal glands to secrete their hormones. As a result, the nervous system can cause rapid endocrine responses to keep up with sudden changes in both the external and internal environments when necessary. Endocrine and Nervous Systems \| Endocrine system \| Nervous system \| \| \|---\|---\|---\| \| Signaling mechanism(s) \| Chemical \| Chemical/electrical \| \| Primary chemical signal \| Hormones \| Neurotransmitters \| \| Distance traveled \| Long or short \| Always short \| \| Response time \| Fast or slow \| Always fast \| \| Environment targeted \| Internal \| Internal and external \| Table 17.1 Structures of the Endocrine System The endocrine system consists of cells, tissues, and organs that secrete hormones as a primary or secondary function. The endocrine gland is the major player in this system. The primary function of these ductless glands is to secrete their hormones directly into the surrounding fluid. The interstitial fluid and the blood vessels then transport the hormones throughout the body. The endocrine system includes the pituitary, thyroid, parathyroid, adrenal, and pineal glands (Figure 17.2). Some of these glands have both endocrine and non-endocrine functions. For example, the pancreas contains cells that function in digestion as well as cells that secrete the hormones insulin and glucagon, which regulate blood glucose levels. The hypothalamus, thymus, heart, kidneys, stomach, small intestine, liver, skin, female ovaries, and male testes are other organs that contain cells with endocrine function. Moreover, adipose tissue has long been known to produce hormones, and recent research has revealed that even bone tissue has endocrine functions. Figure 17.2 Endocrine System Endocrine glands and cells are located throughout the body and play an important role in homeostasis. The ductless endocrine glands are not to be confused with the body’s exocrine system, whose glands release their secretions through ducts. Examples of exocrine glands include the sebaceous and sweat glands of the skin. As just noted, the pancreas also has an exocrine function: most of its cells secrete pancreatic juice through the pancreatic and accessory ducts to the lumen of the small intestine. Other Types of Chemical Signaling In endocrine signaling, hormones secreted into the extracellular fluid diffuse into the blood or lymph, and can then travel great distances throughout the body. In contrast, autocrine signaling takes place within the same cell. An autocrine (auto- = “self”) is a chemical that elicits a response in the same cell that secreted it. Interleukin-1, or IL-1, is a signaling molecule that plays an important role in inflammatory response. The cells that secrete IL-1 have receptors on their cell surface that bind these molecules, resulting in autocrine signaling. Local intercellular communication is the province of the paracrine, also called a paracrine factor, which is a chemical that induces a response in neighboring cells. Although paracrines may enter the bloodstream, their concentration is generally too low to elicit a response from distant tissues. A familiar example to those with asthma is histamine, a paracrine that is released by immune cells in the bronchial tree. Histamine causes the smooth muscle cells of the bronchi to constrict, narrowing the airways. Another example is the neurotransmitters of the nervous system, which act only locally within the synaptic cleft. CAREER CONNECTION Endocrinologist Endocrinology is a specialty in the field of medicine that focuses on the treatment of endocrine system disorders. Endocrinologists—medical doctors who specialize in this field—are experts in treating diseases associated with hormonal systems, ranging from thyroid disease to diabetes mellitus. Endocrine surgeons treat endocrine disease through the removal, or resection, of the affected endocrine gland. Patients who are referred to endocrinologists may have signs and symptoms or blood test results that suggest excessive or impaired functioning of an endocrine gland or endocrine cells. The endocrinologist may order additional blood tests to determine whether the patient’s hormonal levels are abnormal, or they may stimulate or suppress the function of the suspect endocrine gland and then have blood taken for analysis. Treatment varies according to the diagnosis. Some endocrine disorders, such as type 2 diabetes, may respond to lifestyle changes such as modest weight loss, adoption of a healthy diet, and regular physical activity. Other disorders may require medication, such as hormone replacement, and routine monitoring by the endocrinologist. These include disorders of the pituitary gland that can affect growth and disorders of the thyroid gland that can result in a variety of metabolic problems. Some patients experience health problems as a result of the normal decline in hormones that can accompany aging. These patients can consult with an endocrinologist to weigh the risks and benefits of hormone replacement therapy intended to boost their natural levels of reproductive hormones. In addition to treating patients, endocrinologists may be involved in research to improve the understanding of endocrine system disorders and develop new treatments for these diseases. Hormones - Identify the three major classes of hormones on the basis of chemical structure - Compare and contrast intracellular and cell membrane hormone receptors - Describe signaling pathways that involve cAMP and IP3 - Identify several factors that influence a target cell’s response - Discuss the role of feedback loops and humoral, hormonal, and neural stimuli in hormone control Although a given hormone may travel throughout the body in the bloodstream, it will affect the activity only of its target cells; that is, cells with receptors for that particular hormone. Once the hormone binds to the receptor, a chain of events is initiated that leads to the target cell’s response. Hormones play a critical role in the regulation of physiological processes because of the target cell responses they regulate. These responses contribute to human reproduction, growth and development of body tissues, metabolism, fluid, and electrolyte balance, sleep, and many other body functions. The major hormones of the human body and their effects are identified in Table 17.2. Endocrine Glands and Their Major Hormones \| Endocrine gland \| Associated hormones \| Chemical class \| Effect \| \|---\|---\|---\|---\| \| Pituitary (anterior) \| Growth hormone (GH) \| Protein \| Promotes growth of body tissues \| \| Pituitary (anterior) \| Prolactin (PRL) \| Peptide \| Promotes milk production \| \| Pituitary (anterior) \| Thyroid-stimulating hormone (TSH) \| Glycoprotein \| Stimulates thyroid hormone release \| \| Pituitary (anterior) \| Adrenocorticotropic hormone (ACTH) \| Peptide \| Stimulates hormone release by adrenal cortex \| \| Pituitary (anterior) \| Follicle-stimulating hormone (FSH) \| Glycoprotein \| Stimulates gamete production \| \| Pituitary (anterior) \| Luteinizing hormone (LH) \| Glycoprotein \| Stimulates androgen production by gonads \| \| Pituitary (posterior) \| Antidiuretic hormone (ADH) \| Peptide \| Stimulates water reabsorption by kidneys \| \| Pituitary (posterior) \| Oxytocin \| Peptide \| Stimulates uterine contractions during childbirth \| \| Thyroid \| Thyroxine (T4), triiodothyronine (T3) \| Amine \| Stimulate basal metabolic rate \| \| Thyroid \| Calcitonin \| Peptide \| Reduces blood Ca2+ levels \| \| Parathyroid \| Parathyroid hormone (PTH) \| Peptide \| Increases blood Ca2+ levels \| \| Adrenal (cortex) \| Aldosterone \| Steroid \| Increases blood Na+ levels \| \| Adrenal (cortex) \| Cortisol, corticosterone, cortisone \| Steroid \| Increase blood glucose levels \| \| Adrenal (medulla) \| Epinephrine, norepinephrine \| Amine \| Stimulate fight-or-flight response \| \| Pineal \| Melatonin \| Amine \| Regulates sleep cycles \| \| Pancreas \| Insulin \| Protein \| Reduces blood glucose levels \| \| Pancreas \| Glucagon \| Protein \| Increases blood glucose levels \| \| Testes \| Testosterone \| Steroid \| Stimulates development of male secondary sex characteristics and sperm production \| \| Ovaries \| Estrogens and progesterone \| Steroid \| Stimulate development of female secondary sex characteristics and prepare the body for childbirth \| Table 17.2 Types of Hormones The hormones of the human body can be divided into two major groups on the basis of their chemical structure. Hormones derived from amino acids include amines, peptides, and proteins. Those derived from lipids include steroids (Figure 17.3). These chemical groups affect a hormone’s distribution, the type of receptors it binds to, and other aspects of its function. Figure 17.3 Amine, Peptide, Protein, and Steroid Hormone Structure Amine Hormones Hormones derived from the modification of amino acids are referred to as amine hormones. Typically, the original structure of the amino acid is modified such that a –COOH, or carboxyl, group is removed, whereas the −NH+3−NH3+ Amine hormones are synthesized from the amino acids tryptophan or tyrosine. An example of a hormone derived from tryptophan is melatonin, which is secreted by the pineal gland and helps regulate circadian rhythm. Tyrosine derivatives include the metabolism-regulating thyroid hormones, as well as the catecholamines, such as epinephrine, norepinephrine, and dopamine. Epinephrine and norepinephrine are secreted by the adrenal medulla and play a role in the fight-or-flight response, whereas dopamine is secreted by the hypothalamus and inhibits the release of certain anterior pituitary hormones. Peptide and Protein Hormones Whereas the amine hormones are derived from a single amino acid, peptide and protein hormones consist of multiple amino acids that link to form an amino acid chain. Peptide hormones consist of short chains of amino acids, whereas protein hormones are longer polypeptides. Both types are synthesized like other body proteins: DNA is transcribed into mRNA, which is translated into an amino acid chain. Examples of peptide hormones include antidiuretic hormone (ADH), a pituitary hormone important in fluid balance, and atrial-natriuretic peptide, which is produced by the heart and helps to decrease blood pressure. Some examples of protein hormones include growth hormone, which is produced by the pituitary gland, and follicle-stimulating hormone (FSH), which has an attached carbohydrate group and is thus classified as a glycoprotein. FSH helps stimulate the maturation of eggs in the ovaries and sperm in the testes. Steroid Hormones The primary hormones derived from lipids are steroids. Steroid hormones are derived from the lipid cholesterol. For example, the reproductive hormones testosterone and the estrogens—which are produced by the gonads (testes and ovaries)—are steroid hormones. The adrenal glands produce the steroid hormone aldosterone, which is involved in osmoregulation, and cortisol, which plays a role in metabolism. Like cholesterol, steroid hormones are not soluble in water (they are hydrophobic). Because blood is water-based, lipid-derived hormones must travel to their target cell bound to a transport protein. This more complex structure extends the half-life of steroid hormones much longer than that of hormones derived from amino acids. A hormone’s half-life is the time required for half the concentration of the hormone to be degraded. For example, the lipid-derived hormone cortisol has a half-life of approximately 60 to 90 minutes. In contrast, the amino acid–derived hormone epinephrine has a half-life of approximately one minute. Pathways of Hormone Action The message a hormone sends is received by a hormone receptor, a protein located either inside the cell or within the cell membrane. The receptor will process the message by initiating other signaling events or cellular mechanisms that result in the target cell’s response. Hormone receptors recognize molecules with specific shapes and side groups, and respond only to those hormones that are recognized. The same type of receptor may be located on cells in different body tissues, and trigger somewhat different responses. Thus, the response triggered by a hormone depends not only on the hormone, but also on the target cell. Once the target cell receives the hormone signal, it can respond in a variety of ways. The response may include the stimulation of protein synthesis, activation or deactivation of enzymes, alteration in the permeability of the cell membrane, altered rates of mitosis and cell growth, and stimulation of the secretion of products. Moreover, a single hormone may be capable of inducing different responses in a given cell. Pathways Involving Intracellular Hormone Receptors Intracellular hormone receptors are located inside the cell. Hormones that bind to this type of receptor must be able to cross the cell membrane. Steroid hormones are derived from cholesterol and therefore can readily diffuse through the lipid bilayer of the cell membrane to reach the intracellular receptor (Figure 17.4). Thyroid hormones, which contain benzene rings studded with iodine, are also lipid-soluble and can enter the cell. The location of steroid and thyroid hormone binding differs slightly: a steroid hormone may bind to its receptor within the cytosol or within the nucleus. In either case, this binding generates a hormone-receptor complex that moves toward the chromatin in the cell nucleus and binds to a particular segment of the cell’s DNA. In contrast, thyroid hormones bind to receptors already bound to DNA. For both steroid and thyroid hormones, binding of the hormone-receptor complex with DNA triggers transcription of a target gene to mRNA, which moves to the cytosol and directs protein synthesis by ribosomes. Figure 17.4 Binding of Lipid-Soluble Hormones A steroid hormone directly initiates the production of proteins within a target cell. Steroid hormones easily diffuse through the cell membrane. The hormone binds to its receptor in the cytosol, forming a receptor–hormone complex. The receptor–hormone complex then enters the nucleus and binds to the target gene on the DNA. Transcription of the gene creates a messenger RNA that is translated into the desired protein within the cytoplasm. Pathways Involving Cell Membrane Hormone Receptors Hydrophilic, or water-soluble, hormones are unable to diffuse through the lipid bilayer of the cell membrane and must therefore pass on their message to a receptor located at the surface of the cell. Except for thyroid hormones, which are lipid-soluble, all amino acid–derived hormones bind to cell membrane receptors that are located, at least in part, on the extracellular surface of the cell membrane. Therefore, they do not directly affect the transcription of target genes, but instead initiate a signaling cascade that is carried out by a molecule called a second messenger. In this case, the hormone is called a first messenger. The second messenger used by most hormones is cyclic adenosine monophosphate (cAMP). In the cAMP second messenger system, a water-soluble hormone binds to its receptor in the cell membrane (Step 1 in Figure 17.5). This receptor is associated with an intracellular component called a G protein, and binding of the hormone activates the G-protein component (Step 2). The activated G protein in turn activates an enzyme called adenylyl cyclase, also known as adenylate cyclase (Step 3), which converts adenosine triphosphate (ATP) to cAMP (Step 4). As the second messenger, cAMP activates a type of enzyme called a protein kinase that is present in the cytosol (Step 5). Activated protein kinases initiate a phosphorylation cascade, in which multiple protein kinases phosphorylate (add a phosphate group to) numerous and various cellular proteins, including other enzymes (Step 6). Figure 17.5 Binding of Water-Soluble Hormones Water-soluble hormones cannot diffuse through the cell membrane. These hormones must bind to a surface cell-membrane receptor. The receptor then initiates a cell-signaling pathway within the cell involving G proteins, adenylyl cyclase, the secondary messenger cyclic AMP (cAMP), and protein kinases. In the final step, these protein kinases phosphorylate proteins in the cytoplasm. This activates proteins in the cell that carry out the changes specified by the hormone. The phosphorylation of cellular proteins can trigger a wide variety of effects, from nutrient metabolism to the synthesis of different hormones and other products. The effects vary according to the type of target cell, the G proteins and kinases involved, and the phosphorylation of proteins. Examples of hormones that use cAMP as a second messenger include calcitonin, which is important for bone construction and regulating blood calcium levels; glucagon, which plays a role in blood glucose levels; and thyroid-stimulating hormone, which causes the release of T3 and T4 from the thyroid gland. Overall, the phosphorylation cascade significantly increases the efficiency, speed, and specificity of the hormonal response, as thousands of signaling events can be initiated simultaneously in response to a very low concentration of hormone in the bloodstream. However, the duration of the hormone signal is short, as cAMP is quickly deactivated by the enzyme phosphodiesterase (PDE), which is located in the cytosol. The action of PDE helps to ensure that a target cell’s response ceases quickly unless new hormones arrive at the cell membrane. Importantly, there are also G proteins that decrease the levels of cAMP in the cell in response to hormone binding. For example, when growth hormone–inhibiting hormone (GHIH), also known as somatostatin, binds to its receptors in the pituitary gland, the level of cAMP decreases, thereby inhibiting the secretion of human growth hormone. Not all water-soluble hormones initiate the cAMP second messenger system. One common alternative system uses calcium ions as a second messenger. In this system, G proteins activate the enzyme phospholipase C (PLC), which functions similarly to adenylyl cyclase. Once activated, PLC cleaves a membrane-bound phospholipid into two molecules: diacylglycerol (DAG) and inositol triphosphate (IP3). Like cAMP, DAG activates protein kinases that initiate a phosphorylation cascade. At the same time, IP3 causes calcium ions to be released from storage sites within the cytosol, such as from within the smooth endoplasmic reticulum. The calcium ions then act as second messengers in two ways: they can influence enzymatic and other cellular activities directly, or they can bind to calcium-binding proteins, the most common of which is calmodulin. Upon binding calcium, calmodulin is able to modulate protein kinase within the cell. Examples of hormones that use calcium ions as a second messenger system include angiotensin II, which helps regulate blood pressure through vasoconstriction, and growth hormone–releasing hormone (GHRH), which causes the pituitary gland to release growth hormones. Factors Affecting Target Cell Response You will recall that target cells must have receptors specific to a given hormone if that hormone is to trigger a response. But several other factors influence the target cell response. For example, the presence of a significant level of a hormone circulating in the bloodstream can cause its target cells to decrease their number of receptors for that hormone. This process is called downregulation, and it allows cells to become less reactive to the excessive hormone levels. When the level of a hormone is chronically reduced, target cells engage in upregulation to increase their number of receptors. This process allows cells to be more sensitive to the hormone that is present. Cells can also alter the sensitivity of the receptors themselves to various hormones. Two or more hormones can interact to affect the response of cells in a variety of ways. The three most common types of interaction are as follows: - The permissive effect, in which the presence of one hormone enables another hormone to act. For example, thyroid hormones have complex permissive relationships with certain reproductive hormones. A dietary deficiency of iodine, a component of thyroid hormones, can therefore affect reproductive system development and functioning. - The synergistic effect, in which two hormones with similar effects produce an amplified response. In some cases, two hormones are required for an adequate response. For example, two different reproductive hormones—FSH from the pituitary gland and estrogens from the ovaries—are required for the maturation of female ova (egg cells). - The antagonistic effect, in which two hormones have opposing effects. A familiar example is the effect of two pancreatic hormones, insulin and glucagon. Insulin increases the liver’s storage of glucose as glycogen, decreasing blood glucose, whereas glucagon stimulates the breakdown of glycogen stores, increasing blood glucose. Regulation of Hormone Secretion To prevent abnormal hormone levels and a potential disease state, hormone levels must be tightly controlled. The body maintains this control by balancing hormone production and degradation. Feedback loops govern the initiation and maintenance of most hormone secretion in response to various stimuli. Role of Feedback Loops The contribution of feedback loops to homeostasis will only be briefly reviewed here. Positive feedback loops are characterized by the release of additional hormone in response to an original hormone release. The release of oxytocin during childbirth is a positive feedback loop. The initial release of oxytocin begins to signal the uterine muscles to contract, which pushes the fetus toward the cervix, causing it to stretch. This, in turn, signals the pituitary gland to release more oxytocin, causing labor contractions to intensify. The release of oxytocin decreases after the birth of the child. The more common method of hormone regulation is the negative feedback loop. Negative feedback is characterized by the inhibition of further secretion of a hormone in response to adequate levels of that hormone. This allows blood levels of the hormone to be regulated within a narrow range. An example of a negative feedback loop is the release of glucocorticoid hormones from the adrenal glands, as directed by the hypothalamus and pituitary gland. As glucocorticoid concentrations in the blood rise, the hypothalamus and pituitary gland reduce their signaling to the adrenal glands to prevent additional glucocorticoid secretion (Figure 17.6). Figure 17.6 Negative Feedback Loop The release of adrenal glucocorticoids is stimulated by the release of hormones from the hypothalamus and pituitary gland. This signaling is inhibited when glucocorticoid levels become elevated by causing negative signals to the pituitary gland and hypothalamus. Role of Endocrine Gland Stimuli Reflexes triggered by both chemical and neural stimuli control endocrine activity. These reflexes may be simple, involving only one hormone response, or they may be more complex and involve many hormones, as is the case with the hypothalamic control of various anterior pituitary–controlled hormones. Humoral stimuli are changes in blood levels of non-hormone chemicals, such as nutrients or ions, which cause the release or inhibition of a hormone to, in turn, maintain homeostasis. For example, osmoreceptors in the hypothalamus detect changes in blood osmolarity (the concentration of solutes in the blood plasma). If blood osmolarity is too high, meaning that the blood is not dilute enough, osmoreceptors signal the hypothalamus to release ADH. The hormone causes the kidneys to reabsorb more water and reduce the volume of urine produced. This reabsorption causes a reduction of the osmolarity of the blood, diluting the blood to the appropriate level. The regulation of blood glucose is another example. High blood glucose levels cause the release of insulin from the pancreas, which increases glucose uptake by cells and liver storage of glucose as glycogen. An endocrine gland may also secrete a hormone in response to the presence of another hormone produced by a different endocrine gland. Such hormonal stimuli often involve the hypothalamus, which produces releasing and inhibiting hormones that control the secretion of a variety of pituitary hormones. In addition to these chemical signals, hormones can also be released in response to neural stimuli. A common example of neural stimuli is the activation of the fight-or-flight response by the sympathetic nervous system. When an individual perceives danger, sympathetic neurons signal the adrenal glands to secrete norepinephrine and epinephrine. The two hormones dilate blood vessels, increase the heart and respiratory rate, and suppress the digestive and immune systems. These responses boost the body’s transport of oxygen to the brain and muscles, thereby improving the body’s ability to fight or flee. EVERYDAY CONNECTION Bisphenol A and Endocrine Disruption You may have heard news reports about the effects of a chemical called bisphenol A (BPA) in various types of food packaging. BPA is used in the manufacturing of hard plastics and epoxy resins. Common food-related items that may contain BPA include the lining of aluminum cans, plastic food-storage containers, drinking cups, as well as baby bottles and “sippy” cups. Other uses of BPA include medical equipment, dental fillings, and the lining of water pipes. Research suggests that BPA is an endocrine disruptor, meaning that it negatively interferes with the endocrine system, particularly during the prenatal and postnatal development period. In particular, BPA mimics the hormonal effects of estrogens and has the opposite effect—that of androgens. The U.S. Food and Drug Administration (FDA) notes in their statement about BPA safety that although traditional toxicology studies have supported the safety of low levels of exposure to BPA, recent studies using novel approaches to test for subtle effects have led to some concern about the potential effects of BPA on the brain, behavior, and prostate gland in fetuses, infants, and young children. The FDA is currently facilitating decreased use of BPA in food-related materials. Many US companies have voluntarily removed BPA from baby bottles, “sippy” cups, and the linings of infant formula cans, and most plastic reusable water bottles sold today boast that they are “BPA free.” In contrast, both Canada and the European Union have completely banned the use of BPA in baby products. The potential harmful effects of BPA have been studied in both animal models and humans and include a large variety of health effects, such as developmental delay and disease. For example, prenatal exposure to BPA during the first trimester of human pregnancy may be associated with wheezing and aggressive behavior during childhood. Adults exposed to high levels of BPA may experience altered thyroid signaling and male sexual dysfunction. BPA exposure during the prenatal or postnatal period of development in animal models has been observed to cause neurological delays, changes in brain structure and function, sexual dysfunction, asthma, and increased risk for multiple cancers. In vitro studies have also shown that BPA exposure causes molecular changes that initiate the development of cancers of the breast, prostate, and brain. Although these studies have implicated BPA in numerous ill health effects, some experts caution that some of these studies may be flawed and that more research needs to be done. In the meantime, the FDA recommends that consumers take precautions to limit their exposure to BPA. In addition to purchasing foods in packaging free of BPA, consumers should avoid carrying or storing foods or liquids in bottles with the recycling code 3 or 7. Foods and liquids should not be microwave-heated in any form of plastic: use paper, glass, or ceramics instead. The Pituitary Gland and Hypothalamus - Explain the interrelationships of the anatomy and functions of the hypothalamus and the posterior and anterior lobes of the pituitary gland - Identify the two hormones released from the posterior pituitary, their target cells, and their principal actions - Identify the six hormones produced by the anterior lobe of the pituitary gland, their target cells, their principal actions, and their regulation by the hypothalamus The hypothalamus–pituitary complex can be thought of as the “command center” of the endocrine system. This complex secretes several hormones that directly produce responses in target tissues, as well as hormones that regulate the synthesis and secretion of hormones of other glands. In addition, the hypothalamus–pituitary complex coordinates the messages of the endocrine and nervous systems. In many cases, a stimulus received by the nervous system must pass through the hypothalamus–pituitary complex to be translated into hormones that can initiate a response. The hypothalamus is a structure of the diencephalon of the brain located anterior and inferior to the thalamus (Figure 17.7). It has both neural and endocrine functions, producing and secreting many hormones. In addition, the hypothalamus is anatomically and functionally related to the pituitary gland (or hypophysis), a bean-sized organ suspended from it by a stem called the infundibulum (or pituitary stalk). The pituitary gland is cradled within the sellaturcica of the sphenoid bone of the skull. It consists of two lobes that arise from distinct parts of embryonic tissue: the posterior pituitary (neurohypophysis) is neural tissue, whereas the anterior pituitary (also known as the adenohypophysis) is glandular tissue that develops from the primitive digestive tract. The hormones secreted by the posterior and anterior pituitary, and the intermediate zone between the lobes are summarized in Table 17.3. Figure 17.7 Hypothalamus–Pituitary Complex The hypothalamus region lies inferior and anterior to the thalamus. It connects to the pituitary gland by the stalk-like infundibulum. The pituitary gland consists of an anterior and posterior lobe, with each lobe secreting different hormones in response to signals from the hypothalamus. Pituitary Hormones \| Pituitary lobe \| Associated hormones \| Chemical class \| Effect \| \|---\|---\|---\|---\| \| Anterior \| Growth hormone (GH) \| Protein \| Promotes growth of body tissues \| \| Anterior \| Prolactin (PRL) \| Peptide \| Promotes milk production from mammary glands \| \| Anterior \| Thyroid-stimulating hormone (TSH) \| Glycoprotein \| Stimulates thyroid hormone release from thyroid \| \| Anterior \| Adrenocorticotropic hormone (ACTH) \| Peptide \| Stimulates hormone release by adrenal cortex \| \| Anterior \| Follicle-stimulating hormone (FSH) \| Glycoprotein \| Stimulates gamete production in gonads \| \| Anterior \| Luteinizing hormone (LH) \| Glycoprotein \| Stimulates androgen production by gonads \| \| Posterior \| Antidiuretic hormone (ADH) \| Peptide \| Stimulates water reabsorption by kidneys \| \| Posterior \| Oxytocin \| Peptide \| Stimulates uterine contractions during childbirth \| \| Intermediate zone \| Melanocyte-stimulating hormone \| Peptide \| Stimulates melanin formation in melanocytes \| Table 17.3 Posterior Pituitary The posterior pituitary is actually an extension of the neurons of the paraventricular and supraoptic nuclei of the hypothalamus. The cell bodies of these regions rest in the hypothalamus, but their axons descend as the hypothalamic–hypophyseal tract within the infundibulum, and end in axon terminals that comprise the posterior pituitary (Figure 17.8). Figure 17.8 Posterior Pituitary Neurosecretory cells in the hypothalamus release oxytocin (OT) or ADH into the posterior lobe of the pituitary gland. These hormones are stored or released into the blood via the capillary plexus. The posterior pituitary gland does not produce hormones, but rather stores and secretes hormones produced by the hypothalamus. The paraventricular nuclei produce the hormone oxytocin, whereas the supraoptic nuclei produce ADH. These hormones travel along the axons into storage sites in the axon terminals of the posterior pituitary. In response to signals from the same hypothalamic neurons, the hormones are released from the axon terminals into the bloodstream. Oxytocin When fetal development is complete, the peptide-derived hormone oxytocin (tocia- = “childbirth”) stimulates uterine contractions and dilation of the cervix. Throughout most of pregnancy, oxytocin hormone receptors are not expressed at high levels in the uterus. Toward the end of pregnancy, the synthesis of oxytocin receptors in the uterus increases, and the smooth muscle cells of the uterus become more sensitive to its effects. Oxytocin is continually released throughout childbirth through a positive feedback mechanism. As noted earlier, oxytocin prompts uterine contractions that push the fetal head toward the cervix. In response, cervical stretching stimulates additional oxytocin to be synthesized by the hypothalamus and released from the pituitary. This increases the intensity and effectiveness of uterine contractions and prompts additional dilation of the cervix. The feedback loop continues until birth. Although the mother’s high blood levels of oxytocin begin to decrease immediately following birth, oxytocin continues to play a role in maternal and newborn health. First, oxytocin is necessary for the milk ejection reflex (commonly referred to as “let-down”) in breastfeeding women. As the newborn begins suckling, sensory receptors in the nipples transmit signals to the hypothalamus. In response, oxytocin is secreted and released into the bloodstream. Within seconds, cells in the mother’s milk ducts contract, ejecting milk into the infant’s mouth. Secondly, in both males and females, oxytocin is thought to contribute to parent–newborn bonding, known as attachment. Oxytocin is also thought to be involved in feelings of love and closeness, as well as in the sexual response. Antidiuretic Hormone (ADH) The solute concentration of the blood, or blood osmolarity, may change in response to the consumption of certain foods and fluids, as well as in response to disease, injury, medications, or other factors. Blood osmolarity is constantly monitored by osmoreceptors—specialized cells within the hypothalamus that are particularly sensitive to the concentration of sodium ions and other solutes. In response to high blood osmolarity, which can occur during dehydration or following a very salty meal, the osmoreceptors signal the posterior pituitary to release antidiuretic hormone (ADH). The target cells of ADH are located in the tubular cells of the kidneys. Its effect is to increase epithelial permeability to water, allowing increased water reabsorption. The more water reabsorbed from the filtrate, the greater the amount of water that is returned to the blood and the less that is excreted in the urine. A greater concentration of water results in a reduced concentration of solutes. ADH is also known as vasopressin because, in very high concentrations, it causes constriction of blood vessels, which increases blood pressure by increasing peripheral resistance. The release of ADH is controlled by a negative feedback loop. As blood osmolarity decreases, the hypothalamic osmoreceptors sense the change and prompt a corresponding decrease in the secretion of ADH. As a result, less water is reabsorbed from the urine filtrate. Interestingly, drugs can affect the secretion of ADH. For example, alcohol consumption inhibits the release of ADH, resulting in increased urine production that can eventually lead to dehydration and a hangover. A disease called diabetes insipidus is characterized by chronic underproduction of ADH that causes chronic dehydration. Because little ADH is produced and secreted, not enough water is reabsorbed by the kidneys. Although patients feel thirsty, and increase their fluid consumption, this doesn’t effectively decrease the solute concentration in their blood because ADH levels are not high enough to trigger water reabsorption in the kidneys. Electrolyte imbalances can occur in severe cases of diabetes insipidus. Anterior Pituitary The anterior pituitary originates from the digestive tract in the embryo and migrates toward the brain during fetal development. There are three regions: the pars distalis is the most anterior, the pars intermedia is adjacent to the posterior pituitary, and the pars tuberalis is a slender “tube” that wraps the infundibulum. Recall that the posterior pituitary does not synthesize hormones, but merely stores them. In contrast, the anterior pituitary does manufacture hormones. However, the secretion of hormones from the anterior pituitary is regulated by two classes of hormones. These hormones—secreted by the hypothalamus—are the releasing hormones that stimulate the secretion of hormones from the anterior pituitary and the inhibiting hormones that inhibit secretion. Hypothalamic hormones are secreted by neurons, but enter the anterior pituitary through blood vessels (Figure 17.9). Within the infundibulum is a bridge of capillaries that connects the hypothalamus to the anterior pituitary. This network, called the hypophyseal portal system, allows hypothalamic hormones to be transported to the anterior pituitary without first entering the systemic circulation. The system originates from the superior hypophyseal artery, which branches off the carotid arteries and transports blood to the hypothalamus. The branches of the superior hypophyseal artery form the hypophyseal portal system (see Figure 17.9). Hypothalamic releasing and inhibiting hormones travel through a primary capillary plexus to the portal veins, which carry them into the anterior pituitary. Hormones produced by the anterior pituitary (in response to releasing hormones) enter a secondary capillary plexus, and from there drain into the circulation. Figure 17.9 Anterior Pituitary The anterior pituitary manufactures seven hormones. The hypothalamus produces separate hormones that stimulate or inhibit hormone production in the anterior pituitary. Hormones from the hypothalamus reach the anterior pituitary via the hypophyseal portal system. The anterior pituitary produces seven hormones. These are the growth hormone (GH), thyroid-stimulating hormone (TSH), adrenocorticotropic hormone (ACTH), follicle-stimulating hormone (FSH), luteinizing hormone (LH), beta endorphin, and prolactin. Of the hormones of the anterior pituitary, TSH, ACTH, FSH, and LH are collectively referred to as tropic hormones (trope- = “turning”) because they turn on or off the function of other endocrine glands. Growth Hormone The endocrine system regulates the growth of the human body, protein synthesis, and cellular replication. A major hormone involved in this process is growth hormone (GH), also called somatotropin—a protein hormone produced and secreted by the anterior pituitary gland. Its primary function is anabolic; it promotes protein synthesis and tissue building through direct and indirect mechanisms (Figure 17.10). GH levels are controlled by the release of GHRH and GHIH (also known as somatostatin) from the hypothalamus. Figure 17.10 Hormonal Regulation of Growth Growth hormone (GH) directly accelerates the rate of protein synthesis in skeletal muscle and bones. Insulin-like growth factor 1 (IGF-1) is activated by growth hormone and indirectly supports the formation of new proteins in muscle cells and bone. A glucose-sparing effect occurs when GH stimulates lipolysis, or the breakdown of adipose tissue, releasing fatty acids into the blood. As a result, many tissues switch from glucose to fatty acids as their main energy source, which means that less glucose is taken up from the bloodstream. GH also initiates the diabetogenic effect in which GH stimulates the liver to break down glycogen to glucose, which is then deposited into the blood. The name “diabetogenic” is derived from the similarity in elevated blood glucose levels observed between individuals with untreated diabetes mellitus and individuals experiencing GH excess. Blood glucose levels rise as the result of a combination of glucose-sparing and diabetogenic effects. GH indirectly mediates growth and protein synthesis by triggering the liver and other tissues to produce a group of proteins called insulin-like growth factors (IGFs). These proteins enhance cellular proliferation and inhibit apoptosis, or programmed cell death. IGFs stimulate cells to increase their uptake of amino acids from the blood for protein synthesis. Skeletal muscle and cartilage cells are particularly sensitive to stimulation from IGFs. Dysfunction of the endocrine system’s control of growth can result in several disorders. For example, gigantism is a disorder in children that is caused by the secretion of abnormally large amounts of GH, resulting in excessive growth. A similar condition in adults is acromegaly, a disorder that results in the growth of bones in the face, hands, and feet in response to excessive levels of GH in individuals who have stopped growing. Abnormally low levels of GH in children can cause growth impairment—a disorder called pituitary dwarfism (also known as growth hormone deficiency). Thyroid-Stimulating Hormone The activity of the thyroid gland is regulated by thyroid-stimulating hormone (TSH), also called thyrotropin. TSH is released from the anterior pituitary in response to thyrotropin-releasing hormone (TRH) from the hypothalamus. As discussed shortly, it triggers the secretion of thyroid hormones by the thyroid gland. In a classic negative feedback loop, elevated levels of thyroid hormones in the bloodstream then trigger a drop in production of TRH and subsequently TSH. Adrenocorticotropic Hormone The adrenocorticotropic hormone (ACTH), also called corticotropin, stimulates the adrenal cortex (the more superficial “bark” of the adrenal glands) to secrete corticosteroid hormones such as cortisol. ACTH come from a precursor molecule known as pro-opiomelanotropin (POMC) which produces several biologically active molecules when cleaved, including ACTH, melanocyte-stimulating hormone, and the brain opioid peptides known as endorphins. The release of ACTH is regulated by the corticotropin-releasing hormone (CRH) from the hypothalamus in response to normal physiologic rhythms. A variety of stressors can also influence its release, and the role of ACTH in the stress response is discussed later in this chapter. Follicle-Stimulating Hormone and Luteinizing Hormone The endocrine glands secrete a variety of hormones that control the development and regulation of the reproductive system (these glands include the anterior pituitary, the adrenal cortex, and the gonads—the testes in males and the ovaries in females). Much of the development of the reproductive system occurs during puberty and is marked by the development of sex-specific characteristics in both male and female adolescents. Puberty is initiated by gonadotropin-releasing hormone (GnRH), a hormone produced and secreted by the hypothalamus. GnRH stimulates the anterior pituitary to secrete gonadotropins—hormones that regulate the function of the gonads. The levels of GnRH are regulated through a negative feedback loop; high levels of reproductive hormones inhibit the release of GnRH. Throughout life, gonadotropins regulate reproductive function and, in the case of women, the onset and cessation of reproductive capacity. The gonadotropins include two glycoprotein hormones: follicle-stimulating hormone (FSH) stimulates the production and maturation of sex cells, or gametes, including ova in women and sperm in men. FSH also promotes follicular growth; these follicles then release estrogens in the female ovaries. Luteinizing hormone (LH) triggers ovulation in women, as well as the production of estrogens and progesterone by the ovaries. LH stimulates production of testosterone by the male testes. Prolactin As its name implies, prolactin (PRL) promotes lactation (milk production) in women. During pregnancy, it contributes to development of the mammary glands, and after birth, it stimulates the mammary glands to produce breast milk. However, the effects of prolactin depend heavily upon the permissive effects of estrogens, progesterone, and other hormones. And as noted earlier, the let-down of milk occurs in response to stimulation from oxytocin. In a non-pregnant woman, prolactin secretion is inhibited by prolactin-inhibiting hormone (PIH), which is actually the neurotransmitter dopamine, and is released from neurons in the hypothalamus. Only during pregnancy do prolactin levels rise in response to prolactin-releasing hormone (PRH) from the hypothalamus. Intermediate Pituitary: Melanocyte-Stimulating Hormone The cells in the zone between the pituitary lobes secrete a hormone known as melanocyte-stimulating hormone (MSH) that is formed by cleavage of the pro-opiomelanocortin (POMC) precursor protein. Local production of MSH in the skin is responsible for melanin production in response to UV light exposure. The role of MSH made by the pituitary is more complicated. For instance, people with lighter skin generally have the same amount of MSH as people with darker skin. Nevertheless, this hormone is capable of darkening of the skin by inducing melanin production in the skin’s melanocytes. Women also show increased MSH production during pregnancy; in combination with estrogens, it can lead to darker skin pigmentation, especially the skin of the areolas and labia minora. Figure 17.11 is a summary of the pituitary hormones and their principal effects. Figure 17.11 Major Pituitary Hormones Major pituitary hormones and their target organs. INTERACTIVE LINK Visit this link to watch an animation showing the role of the hypothalamus and the pituitary gland. Which hormone is released by the pituitary to stimulate the thyroid gland? The Thyroid Gland - Describe the location and anatomy of the thyroid gland - Discuss the synthesis of triiodothyronine and thyroxine - Explain the role of thyroid hormones in the regulation of basal metabolism - Identify the hormone produced by the parafollicular cells of the thyroid A butterfly-shaped organ, the thyroid gland is located anterior to the trachea, just inferior to the larynx (Figure 17.12). The medial region, called the isthmus, is flanked by wing-shaped left and right lobes. Each of the thyroid lobes are embedded with parathyroid glands, primarily on their posterior surfaces. The tissue of the thyroid gland is composed mostly of thyroid follicles. The follicles are made up of a central cavity filled with a sticky fluid called colloid. Surrounded by a wall of epithelial follicle cells, the colloid is the center of thyroid hormone production, and that production is dependent on the hormones’ essential and unique component: iodine. Figure 17.12 Thyroid Gland The thyroid gland is located in the neck where it wraps around the trachea. (a) Anterior view of the thyroid gland. (b) Posterior view of the thyroid gland. (c) The glandular tissue is composed primarily of thyroid follicles. The larger parafollicular cells often appear within the matrix of follicle cells. LM × 1332. (Micrograph provided by the Regents of University of Michigan Medical School © 2012) Synthesis and Release of Thyroid Hormones Hormones are produced in the colloid when atoms of the mineral iodine attach to a glycoprotein, called thyroglobulin, that is secreted into the colloid by the follicle cells. The following steps outline the hormones’ assembly: - Binding of TSH to its receptors in the follicle cells of the thyroid gland causes the cells to actively transport iodide ions (I–) across their cell membrane, from the bloodstream into the cytosol. As a result, the concentration of iodide ions “trapped” in the follicular cells is many times higher than the concentration in the bloodstream. - Iodide ions then move to the lumen of the follicle cells that border the colloid. There, the ions undergo oxidation (their negatively charged electrons are removed). The oxidation of two iodide ions (2 I–) results in iodine (I2), which passes through the follicle cell membrane into the colloid. - In the colloid, peroxidase enzymes link the iodine to the tyrosine amino acids in thyroglobulin to produce two intermediaries: a tyrosine attached to one iodine and a tyrosine attached to two iodines. When one of each of these intermediaries is linked by covalent bonds, the resulting compound is triiodothyronine (T3), a thyroid hormone with three iodines. Much more commonly, two copies of the second intermediary bond, forming tetraiodothyronine, also known as thyroxine (T4), a thyroid hormone with four iodines. These hormones remain in the colloid center of the thyroid follicles until TSH stimulates endocytosis of colloid back into the follicle cells. There, lysosomal enzymes break apart the thyroglobulin colloid, releasing free T3 and T4, which diffuse across the follicle cell membrane and enter the bloodstream. In the bloodstream, less than one percent of the circulating T3 and T4 remains unbound. This free T3 and T4 can cross the lipid bilayer of cell membranes and be taken up by cells. The remaining 99 percent of circulating T3 and T4 is bound to specialized transport proteins called thyroxine-binding globulins (TBGs), to albumin, or to other plasma proteins. This “packaging” prevents their free diffusion into body cells. When blood levels of T3 and T4 begin to decline, bound T3 and T4 are released from these plasma proteins and readily cross the membrane of target cells. T3 is more potent than T4, and many cells convert T4 to T3through the removal of an iodine atom. Regulation of TH Synthesis The release of T3 and T4 from the thyroid gland is regulated by thyroid-stimulating hormone (TSH). As shown in Figure 17.13, low blood levels of T3 and T4 stimulate the release of thyrotropin-releasing hormone (TRH) from the hypothalamus, which triggers secretion of TSH from the anterior pituitary. In turn, TSH stimulates the thyroid gland to secrete T3 and T4. The levels of TRH, TSH, T3, and T4 are regulated by a negative feedback system in which increasing levels of T3 and T4 decrease the production and secretion of TSH. Figure 17.13 Classic Negative Feedback Loop A classic negative feedback loop controls the regulation of thyroid hormone levels. Functions of Thyroid Hormones The thyroid hormones, T3 and T4, are often referred to as metabolic hormones because their levels influence the body’s basal metabolic rate, the amount of energy used by the body at rest. When T3 and T4 bind to intracellular receptors located on the mitochondria, they cause an increase in nutrient breakdown and the use of oxygen to produce ATP. In addition, T3 and T4 initiate the transcription of genes involved in glucose oxidation. Although these mechanisms prompt cells to produce more ATP, the process is inefficient, and an abnormally increased level of heat is released as a byproduct of these reactions. This so-called calorigenic effect (calor- = “heat”) raises body temperature. Adequate levels of thyroid hormones are also required for protein synthesis and for fetal and childhood tissue development and growth. They are especially critical for normal development of the nervous system both in utero and in early childhood, and they continue to support neurological function in adults. As noted earlier, these thyroid hormones have a complex interrelationship with reproductive hormones, and deficiencies can influence libido, fertility, and other aspects of reproductive function. Finally, thyroid hormones increase the body’s sensitivity to catecholamines (epinephrine and norepinephrine) from the adrenal medulla by upregulation of receptors in the blood vessels. When levels of T3 and T4 hormones are excessive, this effect accelerates the heart rate, strengthens the heartbeat, and increases blood pressure. Because thyroid hormones regulate metabolism, heat production, protein synthesis, and many other body functions, thyroid disorders can have severe and widespread consequences. DISORDERS OF THE... Endocrine System: Iodine Deficiency, Hypothyroidism, and Hyperthyroidism As discussed above, dietary iodine is required for the synthesis of T3 and T4. But for much of the world’s population, foods do not provide adequate levels of this mineral, because the amount varies according to the level in the soil in which the food was grown, as well as the irrigation and fertilizers used. Marine fish and shrimp tend to have high levels because they concentrate iodine from seawater, but many people in landlocked regions lack access to seafood. Thus, the primary source of dietary iodine in many countries is iodized salt. Fortification of salt with iodine began in the United States in 1924, and international efforts to iodize salt in the world’s poorest nations continue today. Dietary iodine deficiency can result in the impaired ability to synthesize T3 and T4, leading to a variety of severe disorders. When T3 and T4 cannot be produced, TSH is secreted in increasing amounts. As a result of this hyperstimulation, thyroglobulin accumulates in the thyroid gland follicles, increasing their deposits of colloid. The accumulation of colloid increases the overall size of the thyroid gland, a condition called a goiter (Figure 17.14). A goiter is only a visible indication of the deficiency. Other iodine deficiency disorders include impaired growth and development, decreased fertility, and prenatal and infant death. Moreover, iodine deficiency is the primary cause of preventable mental retardation worldwide. Neonatal hypothyroidism (cretinism) is characterized by cognitive deficits, short stature, and sometimes deafness and muteness in children and adults born to mothers who were iodine-deficient during pregnancy. Figure 17.14 Goiter (credit: “Almazi”/Wikimedia Commons) In areas of the world with access to iodized salt, dietary deficiency is rare. Instead, inflammation of the thyroid gland is the more common cause of low blood levels of thyroid hormones. Called hypothyroidism, the condition is characterized by a low metabolic rate, weight gain, cold extremities, constipation, reduced libido, menstrual irregularities, and reduced mental activity. In contrast, hyperthyroidism—an abnormally elevated blood level of thyroid hormones—is often caused by a pituitary or thyroid tumor. In Graves’ disease, the hyperthyroid state results from an autoimmune reaction in which antibodies overstimulate the follicle cells of the thyroid gland. Hyperthyroidism can lead to an increased metabolic rate, excessive body heat and sweating, diarrhea, weight loss, tremors, and increased heart rate. The person’s eyes may bulge (called exophthalmos) as antibodies produce inflammation in the soft tissues of the orbits. The person may also develop a goiter. Calcitonin The thyroid gland also secretes a hormone called calcitonin that is produced by the parafollicular cells (also called C cells) that stud the tissue between distinct follicles. Calcitonin is released in response to a rise in blood calcium levels. It appears to have a function in decreasing blood calcium concentrations by: - Inhibiting the activity of osteoclasts, bone cells that release calcium into the circulation by degrading bone matrix - Increasing osteoblastic activity - Decreasing calcium absorption in the intestines - Increasing calcium loss in the urine However, these functions are usually not significant in maintaining calcium homeostasis, so the importance of calcitonin is not entirely understood. Pharmaceutical preparations of calcitonin are sometimes prescribed to reduce osteoclast activity in people with osteoporosis and to reduce the degradation of cartilage in people with osteoarthritis. The hormones secreted by thyroid are summarized in Table 17.4. Thyroid Hormones \| Associated hormones \| Chemical class \| Effect \| \|---\|---\|---\| \| Thyroxine (T4), triiodothyronine (T3) \| Amine \| Stimulate basal metabolic rate \| \| Calcitonin \| Peptide \| Reduces blood Ca2+ levels \| Table 17.4 Of course, calcium is critical for many other biological processes. It is a second messenger in many signaling pathways, and is essential for muscle contraction, nerve impulse transmission, and blood clotting. Given these roles, it is not surprising that blood calcium levels are tightly regulated by the endocrine system. The organs involved in the regulation are the parathyroid glands. The Parathyroid Glands - Describe the location and structure of the parathyroid glands - Describe the hormonal control of blood calcium levels - Discuss the physiological response of parathyroid dysfunction The parathyroid glands are tiny, round structures usually found embedded in the posterior surface of the thyroid gland (Figure 17.15). A thick connective tissue capsule separates the glands from the thyroid tissue. Most people have four parathyroid glands, but occasionally there are more in tissues of the neck or chest. The function of one type of parathyroid cells, the oxyphil cells, is not clear. The primary functional cells of the parathyroid glands are the chief cells. These epithelial cells produce and secrete the parathyroid hormone (PTH), the major hormone involved in the regulation of blood calcium levels. Figure 17.15 Parathyroid Glands The small parathyroid glands are embedded in the posterior surface of the thyroid gland. LM × 760. (Micrograph provided by the Regents of University of Michigan Medical School © 2012) INTERACTIVE LINK View the University of Michigan WebScope to explore the tissue sample in greater detail. The parathyroid glands produce and secrete PTH, a peptide hormone, in response to low blood calcium levels (Figure 17.16). PTH secretion causes the release of calcium from the bones by stimulating osteoclasts, which secrete enzymes that degrade bone and release calcium into the interstitial fluid. PTH also inhibits osteoblasts, the cells involved in bone deposition, thereby sparing blood calcium. PTH causes increased reabsorption of calcium (and magnesium) in the kidney tubules from the urine filtrate. In addition, PTH initiates the production of the steroid hormone calcitriol (also known as 1,25-dihydroxyvitamin D), which is the active form of vitamin D3, in the kidneys. Calcitriol then stimulates increased absorption of dietary calcium by the intestines. A negative feedback loop regulates the levels of PTH, with rising blood calcium levels inhibiting further release of PTH. Figure 17.16 Parathyroid Hormone in Maintaining Blood Calcium Homeostasis Parathyroid hormone increases blood calcium levels when they drop too low. Conversely, calcitonin, which is released from the thyroid gland, decreases blood calcium levels when they become too high. These two mechanisms constantly maintain blood calcium concentration at homeostasis. Abnormally high activity of the parathyroid gland can cause hyperparathyroidism, a disorder caused by an overproduction of PTH that results in excessive calcium reabsorption from bone. Hyperparathyroidism can significantly decrease bone density, leading to spontaneous fractures or deformities. As blood calcium levels rise, cell membrane permeability to sodium is decreased, and the responsiveness of the nervous system is reduced. At the same time, calcium deposits may collect in the body’s tissues and organs, impairing their functioning. In contrast, abnormally low blood calcium levels may be caused by parathyroid hormone deficiency, called hypoparathyroidism, which may develop following injury or surgery involving the thyroid gland. Low blood calcium increases membrane permeability to sodium, resulting in muscle twitching, cramping, spasms, or convulsions. Severe deficits can paralyze muscles, including those involved in breathing, and can be fatal. When blood calcium levels are high, calcitonin is produced and secreted by the parafollicular cells of the thyroid gland. As discussed earlier, calcitonin inhibits the activity of osteoclasts, reduces the absorption of dietary calcium in the intestine, and signals the kidneys to reabsorb less calcium, resulting in larger amounts of calcium excreted in the urine. The Adrenal Glands - Describe the location and structure of the adrenal glands - Identify the hormones produced by the adrenal cortex and adrenal medulla, and summarize their target cells and effects The adrenal glands are wedges of glandular and neuroendocrine tissue adhering to the top of the kidneys by a fibrous capsule (Figure 17.17). The adrenal glands have a rich blood supply and experience one of the highest rates of blood flow in the body. They are served by several arteries branching off the aorta, including the suprarenal and renal arteries. Blood flows to each adrenal gland at the adrenal cortex and then drains into the adrenal medulla. Adrenal hormones are released into the circulation via the left and right suprarenal veins. Figure 17.17 Adrenal Glands Both adrenal glands sit atop the kidneys and are composed of an outer cortex and an inner medulla, all surrounded by a connective tissue capsule. The cortex can be subdivided into additional zones, all of which produce different types of hormones. LM × 204. (Micrograph provided by the Regents of University of Michigan Medical School © 2012) INTERACTIVE LINK View the University of Michigan WebScope to explore the tissue sample in greater detail. The adrenal gland consists of an outer cortex of glandular tissue and an inner medulla of nervous tissue. The cortex itself is divided into three zones: the zona glomerulosa, the zona fasciculata, and the zona reticularis. Each region secretes its own set of hormones. The adrenal cortex, as a component of the hypothalamic-pituitary-adrenal (HPA) axis, secretes steroid hormones important for the regulation of the long-term stress response, blood pressure and blood volume, nutrient uptake and storage, fluid and electrolyte balance, and inflammation. The HPA axis involves the stimulation of hormone release of adrenocorticotropic hormone (ACTH) from the pituitary by the hypothalamus. ACTH then stimulates the adrenal cortex to produce the hormone cortisol. This pathway will be discussed in more detail below. The adrenal medulla is neuroendocrine tissue composed of postganglionic sympathetic nervous system (SNS) neurons. It is really an extension of the autonomic nervous system, which regulates homeostasis in the body. The sympathomedullary (SAM) pathway involves the stimulation of the medulla by impulses from the hypothalamus via neurons from the thoracic spinal cord. The medulla is stimulated to secrete the amine hormones epinephrine and norepinephrine. One of the major functions of the adrenal gland is to respond to stress. Stress can be either physical or psychological or both. Physical stresses include exposing the body to injury, walking outside in cold and wet conditions without a coat on, or malnutrition. Psychological stresses include the perception of a physical threat, a fight with a loved one, or just a bad day at school. The body responds in different ways to short-term stress and long-term stress following a pattern known as the general adaptation syndrome (GAS). Stage one of GAS is called the alarm reaction. This is short-term stress, the fight-or-flight response, mediated by the hormones epinephrine and norepinephrine from the adrenal medulla via the SAM pathway. Their function is to prepare the body for extreme physical exertion. Once this stress is relieved, the body quickly returns to normal. The section on the adrenal medulla covers this response in more detail. If the stress is not soon relieved, the body adapts to the stress in the second stage called the stage of resistance. If a person is starving for example, the body may send signals to the gastrointestinal tract to maximize the absorption of nutrients from food. If the stress continues for a longer term however, the body responds with symptoms quite different than the fight-or-flight response. During the stage of exhaustion, individuals may begin to suffer depression, the suppression of their immune response, severe fatigue, or even a fatal heart attack. These symptoms are mediated by the hormones of the adrenal cortex, especially cortisol, released as a result of signals from the HPA axis. Adrenal hormones also have several non–stress-related functions, including the increase of blood sodium and glucose levels, which will be described in detail below. Adrenal Cortex The adrenal cortex consists of multiple layers of lipid-storing cells that occur in three structurally distinct regions. Each of these regions produces different hormones. INTERACTIVE LINK Visit this link to view an animation describing the location and function of the adrenal glands. Which hormone produced by the adrenal glands is responsible for the mobilization of energy stores? Hormones of the Zona Glomerulosa The most superficial region of the adrenal cortex is the zona glomerulosa, which produces a group of hormones collectively referred to as mineralocorticoids because of their effect on body minerals, especially sodium and potassium. These hormones are essential for fluid and electrolyte balance. Aldosterone is the major mineralocorticoid. It is important in the regulation of the concentration of sodium and potassium ions in urine, sweat, and saliva. For example, it is released in response to elevated blood K+, low blood Na+, low blood pressure, or low blood volume. In response, aldosterone increases the excretion of K+ and the retention of Na+, which in turn increases blood volume and blood pressure. Its secretion is prompted when CRH from the hypothalamus triggers ACTH release from the anterior pituitary. Aldosterone is also a key component of the renin-angiotensin-aldosterone system (RAAS) in which specialized cells of the kidneys secrete the enzyme renin in response to low blood volume or low blood pressure. Renin then catalyzes the conversion of the blood protein angiotensinogen, produced by the liver, to the hormone angiotensin I. Angiotensin I is converted in the lungs to angiotensin II by angiotensin-converting enzyme (ACE). Angiotensin II has three major functions: - Initiating vasoconstriction of the arterioles, decreasing blood flow - Stimulating kidney tubules to reabsorb NaCl and water, increasing blood volume - Signaling the adrenal cortex to secrete aldosterone, the effects of which further contribute to fluid retention, restoring blood pressure and blood volume For individuals with hypertension, or high blood pressure, drugs are available that block the production of angiotensin II. These drugs, known as ACE inhibitors, block the ACE enzyme from converting angiotensin I to angiotensin II, thus mitigating the latter’s ability to increase blood pressure. Hormones of the Zona Fasciculata The intermediate region of the adrenal cortex is the zona fasciculata, named as such because the cells form small fascicles (bundles) separated by tiny blood vessels. The cells of the zona fasciculata produce hormones called glucocorticoids because of their role in glucose metabolism. The most important of these is cortisol, some of which the liver converts to cortisone. A glucocorticoid produced in much smaller amounts is corticosterone. In response to long-term stressors, the hypothalamus secretes CRH, which in turn triggers the release of ACTH by the anterior pituitary. ACTH triggers the release of the glucocorticoids. Their overall effect is to inhibit tissue building while stimulating the breakdown of stored nutrients to maintain adequate fuel supplies. In conditions of long-term stress, for example, cortisol promotes the catabolism of glycogen to glucose, the catabolism of stored triglycerides into fatty acids and glycerol, and the catabolism of muscle proteins into amino acids. These raw materials can then be used to synthesize additional glucose and ketones for use as body fuels. The hippocampus, which is part of the temporal lobe of the cerebral cortices and important in memory formation, is highly sensitive to stress levels because of its many glucocorticoid receptors. You are probably familiar with prescription and over-the-counter medications containing glucocorticoids, such as cortisone injections into inflamed joints, prednisone tablets and steroid-based inhalers used to manage severe asthma, and hydrocortisone creams applied to relieve itchy skin rashes. These drugs reflect another role of cortisol—the downregulation of the immune system, which inhibits the inflammatory response. Hormones of the Zona Reticularis The deepest region of the adrenal cortex is the zona reticularis, which produces small amounts of a class of steroid sex hormones called androgens. During puberty and most of adulthood, androgens are produced in the gonads. The androgens produced in the zona reticularis supplement the gonadal androgens. They are produced in response to ACTH from the anterior pituitary and are converted in the tissues to testosterone or estrogens. In adult women, they may contribute to the sex drive, but their function in adult men is not well understood. In post-menopausal women, as the functions of the ovaries decline, the main source of estrogens becomes the androgens produced by the zona reticularis. Adrenal Medulla As noted earlier, the adrenal cortex releases glucocorticoids in response to long-term stress such as severe illness. In contrast, the adrenal medulla releases its hormones in response to acute, short-term stress mediated by the sympathetic nervous system (SNS). The medullary tissue is composed of unique postganglionic SNS neurons called chromaffin cells, which are large and irregularly shaped, and produce the neurotransmitters epinephrine (also called adrenaline) and norepinephrine (or noradrenaline). Epinephrine is produced in greater quantities—approximately a 4 to 1 ratio with norepinephrine—and is the more powerful hormone. Because the chromaffin cells release epinephrine and norepinephrine into the systemic circulation, where they travel widely and exert effects on distant cells, they are considered hormones. Derived from the amino acid tyrosine, they are chemically classified as catecholamines. The secretion of medullary epinephrine and norepinephrine is controlled by a neural pathway that originates from the hypothalamus in response to danger or stress (the SAM pathway). Both epinephrine and norepinephrine signal the liver and skeletal muscle cells to convert glycogen into glucose, resulting in increased blood glucose levels. These hormones increase the heart rate, pulse, and blood pressure to prepare the body to fight the perceived threat or flee from it. In addition, the pathway dilates the airways, raising blood oxygen levels. It also prompts vasodilation, further increasing the oxygenation of important organs such as the lungs, brain, heart, and skeletal muscle. At the same time, it triggers vasoconstriction to blood vessels serving less essential organs such as the gastrointestinal tract, kidneys, and skin, and downregulates some components of the immune system. Other effects include a dry mouth, loss of appetite, pupil dilation, and a loss of peripheral vision. The major hormones of the adrenal glands are summarized in Table 17.5. Hormones of the Adrenal Glands \| Adrenal gland \| Associated hormones \| Chemical class \| Effect \| \|---\|---\|---\|---\| \| Adrenal cortex \| Aldosterone \| Steroid \| Increases blood Na+ levels \| \| Adrenal cortex \| Cortisol, corticosterone, cortisone \| Steroid \| Increase blood glucose levels \| \| Adrenal medulla \| Epinephrine, norepinephrine \| Amine \| Stimulate fight-or-flight response \| Table 17.5 Disorders Involving the Adrenal Glands Several disorders are caused by the dysregulation of the hormones produced by the adrenal glands. For example, Cushing’s disease is a disorder characterized by high blood glucose levels and the accumulation of lipid deposits on the face and neck. It is caused by hypersecretion of cortisol. The most common source of Cushing’s disease is a pituitary tumor that secretes cortisol or ACTH in abnormally high amounts. Other common signs of Cushing’s disease include the development of a moon-shaped face, a buffalo hump on the back of the neck, rapid weight gain, and hair loss. Chronically elevated glucose levels are also associated with an elevated risk of developing type 2 diabetes. In addition to hyperglycemia, chronically elevated glucocorticoids compromise immunity, resistance to infection, and memory, and can result in rapid weight gain and hair loss. In contrast, the hyposecretion of corticosteroids can result in Addison’s disease, a rare disorder that causes low blood glucose levels and low blood sodium levels. The signs and symptoms of Addison’s disease are vague and are typical of other disorders as well, making diagnosis difficult. They may include general weakness, abdominal pain, weight loss, nausea, vomiting, sweating, and cravings for salty food. The Pineal Gland - Describe the location and structure of the pineal gland - Discuss the function of melatonin Recall that the hypothalamus, part of the diencephalon of the brain, sits inferior and somewhat anterior to the thalamus. Inferior but somewhat posterior to the thalamus is the pineal gland, a tiny endocrine gland whose functions are not entirely clear. The pinealocyte cells that make up the pineal gland are known to produce and secrete the amine hormone melatonin, which is derived from serotonin. The secretion of melatonin varies according to the level of light received from the environment. When photons of light stimulate the retinas of the eyes, a nerve impulse is sent to a region of the hypothalamus called the suprachiasmatic nucleus (SCN), which is important in regulating biological rhythms. From the SCN, the nerve signal is carried to the spinal cord and eventually to the pineal gland, where the production of melatonin is inhibited. As a result, blood levels of melatonin fall, promoting wakefulness. In contrast, as light levels decline—such as during the evening—melatonin production increases, boosting blood levels and causing drowsiness. INTERACTIVE LINK Visit this link to view an animation describing the function of the hormone melatonin. What should you avoid doing in the middle of your sleep cycle that would lower melatonin? The secretion of melatonin may influence the body’s circadian rhythms, the dark-light fluctuations that affect not only sleepiness and wakefulness, but also appetite and body temperature. Interestingly, children have higher melatonin levels than adults, which may prevent the release of gonadotropins from the anterior pituitary, thereby inhibiting the onset of puberty. Finally, an antioxidant role of melatonin is the subject of current research. Jet lag occurs when a person travels across several time zones and feels sleepy during the day or wakeful at night. Traveling across multiple time zones significantly disturbs the light-dark cycle regulated by melatonin. It can take up to several days for melatonin synthesis to adjust to the light-dark patterns in the new environment, resulting in jet lag. Some air travelers take melatonin supplements to induce sleep. Gonadal and Placental Hormones - Identify the most important hormones produced by the testes and ovaries - Name the hormones produced by the placenta and state their functions This section briefly discusses the hormonal role of the gonads—the male testes and female ovaries—which produce the sex cells (sperm and ova) and secrete the gonadal hormones. The roles of the gonadotropins released from the anterior pituitary (FSH and LH) were discussed earlier. The primary hormone produced by the male testes is testosterone, a steroid hormone important in the development of the male reproductive system, the maturation of sperm cells, and the development of male secondary sex characteristics such as a deepened voice, body hair, and increased muscle mass. Interestingly, testosterone is also produced in the female ovaries, but at a much reduced level. In addition, the testes produce the peptide hormone inhibin, which inhibits the secretion of FSH from the anterior pituitary gland. FSH stimulates spermatogenesis. The primary hormones produced by the ovaries are estrogens, which include estradiol, estriol, and estrone. Estrogens play an important role in a larger number of physiological processes, including the development of the female reproductive system, regulation of the menstrual cycle, the development of female secondary sex characteristics such as increased adipose tissue and the development of breast tissue, and the maintenance of pregnancy. Another significant ovarian hormone is progesterone, which contributes to regulation of the menstrual cycle and is important in preparing the body for pregnancy as well as maintaining pregnancy. In addition, the granulosa cells of the ovarian follicles produce inhibin, which—as in males—inhibits the secretion of FSH.During the initial stages of pregnancy, an organ called the placenta develops within the uterus. The placenta supplies oxygen and nutrients to the fetus, excretes waste products, and produces and secretes estrogens and progesterone. The placenta produces human chorionic gonadotropin (hCG) as well. The hCG hormone promotes progesterone synthesis and reduces the mother’s immune function to protect the fetus from immune rejection. It also secretes human placental lactogen (hPL), which plays a role in preparing the breasts for lactation, and relaxin, which is thought to help soften and widen the pubic symphysis in preparation for childbirth. The hormones controlling reproduction are summarized in Table 17.6. Reproductive Hormones \| Gonad \| Associated hormones \| Chemical class \| Effect \| \|---\|---\|---\|---\| \| Testes \| Testosterone \| Steroid \| Stimulates development of male secondary sex characteristics and sperm production \| \| Testes \| Inhibin \| Protein \| Inhibits FSH release from pituitary \| \| Ovaries \| Estrogens and progesterone \| Steroid \| Stimulate development of female secondary sex characteristics and prepare the body for childbirth \| \| Placenta \| Human chorionic gonadotropin \| Protein \| Promotes progesterone synthesis during pregnancy and inhibits immune response against fetus \| Table 17.6 EVERYDAY CONNECTION Anabolic Steroids The endocrine system can be exploited for illegal or unethical purposes. A prominent example of this is the use of steroid drugs by professional athletes. Commonly used for performance enhancement, anabolic steroids are synthetic versions of the male sex hormone, testosterone. By boosting natural levels of this hormone, athletes experience increased muscle mass. Synthetic versions of human growth hormone are also used to build muscle mass. The use of performance-enhancing drugs is banned by all major collegiate and professional sports organizations in the United States because they impart an unfair advantage to athletes who take them. In addition, the drugs can cause significant and dangerous side effects. For example, anabolic steroid use can increase cholesterol levels, raise blood pressure, and damage the liver. Altered testosterone levels (both too low or too high) have been implicated in causing structural damage to the heart, and increasing the risk for cardiac arrhythmias, heart attacks, congestive heart failure, and sudden death. Paradoxically, steroids can have a feminizing effect in males, including shriveled testicles and enlarged breast tissue. In females, their use can cause masculinizing effects such as an enlarged clitoris and growth of facial hair. In both sexes, their use can promote increased aggression (commonly known as “roid-rage”), depression, sleep disturbances, severe acne, and infertility. The Endocrine Pancreas - Describe the location and structure of the pancreas, and the morphology and function of the pancreatic islets - Compare and contrast the functions of insulin and glucagon The pancreas is a long, slender organ, most of which is located posterior to the bottom half of the stomach (Figure 17.18). Although it is primarily an exocrine gland, secreting a variety of digestive enzymes, the pancreas has an endocrine function. Its pancreatic islets—clusters of cells formerly known as the islets of Langerhans—secrete the hormones glucagon, insulin, somatostatin, and pancreatic polypeptide (PP). Figure 17.18 Pancreas The pancreatic exocrine function involves the acinar cells secreting digestive enzymes that are transported into the small intestine by the pancreatic duct. Its endocrine function involves the secretion of insulin (produced by beta cells) and glucagon (produced by alpha cells) within the pancreatic islets. These two hormones regulate the rate of glucose metabolism in the body. The micrograph reveals pancreatic islets. LM × 760. (Micrograph provided by the Regents of University of Michigan Medical School © 2012) INTERACTIVE LINK View the University of Michigan WebScope to explore the tissue sample in greater detail. Cells and Secretions of the Pancreatic Islets The pancreatic islets each contain four varieties of cells: - The alpha cell produces the hormone glucagon and makes up approximately 20 percent of each islet. Glucagon plays an important role in blood glucose regulation; low blood glucose levels stimulate its release. - The beta cell produces the hormone insulin and makes up approximately 75 percent of each islet. Elevated blood glucose levels stimulate the release of insulin. - The delta cell accounts for four percent of the islet cells and secretes the peptide hormone somatostatin. Recall that somatostatin is also released by the hypothalamus (as GHIH), and the stomach and intestines also secrete it. An inhibiting hormone, pancreatic somatostatin inhibits the release of both glucagon and insulin. - The PP cell accounts for about one percent of islet cells and secretes the pancreatic polypeptide hormone. It is thought to play a role in appetite, as well as in the regulation of pancreatic exocrine and endocrine secretions. Pancreatic polypeptide released following a meal may reduce further food consumption; however, it is also released in response to fasting. Regulation of Blood Glucose Levels by Insulin and Glucagon Glucose is required for cellular respiration and is the preferred fuel for all body cells. The body derives glucose from the breakdown of the carbohydrate-containing foods and drinks we consume. Glucose not immediately taken up by cells for fuel can be stored by the liver and muscles as glycogen, or converted to triglycerides and stored in the adipose tissue. Hormones regulate both the storage and the utilization of glucose as required. Receptors located in the pancreas sense blood glucose levels, and subsequently the pancreatic cells secrete glucagon or insulin to maintain normal levels. Glucagon Receptors in the pancreas can sense the decline in blood glucose levels, such as during periods of fasting or during prolonged labor or exercise (Figure 17.19). In response, the alpha cells of the pancreas secrete the hormone glucagon, which has several effects: - It stimulates the liver to convert its stores of glycogen back into glucose. This response is known as glycogenolysis. The glucose is then released into the circulation for use by body cells. - It stimulates the liver to take up amino acids from the blood and convert them into glucose. This response is known as gluconeogenesis. - It stimulates lipolysis, the breakdown of stored triglycerides into free fatty acids and glycerol. Some of the free glycerol released into the bloodstream travels to the liver, which converts it into glucose. This is also a form of gluconeogenesis. Taken together, these actions increase blood glucose levels. The activity of glucagon is regulated through a negative feedback mechanism; rising blood glucose levels inhibit further glucagon production and secretion. Figure 17.19 Homeostatic Regulation of Blood Glucose Levels Blood glucose concentration is tightly maintained between 70 mg/dL and 110 mg/dL. If blood glucose concentration rises above this range, insulin is released, which stimulates body cells to remove glucose from the blood. If blood glucose concentration drops below this range, glucagon is released, which stimulates body cells to release glucose into the blood. Insulin The primary function of insulin is to facilitate the uptake of glucose into body cells. Red blood cells, as well as cells of the brain, liver, kidneys, and the lining of the small intestine, do not have insulin receptors on their cell membranes and do not require insulin for glucose uptake. Although all other body cells do require insulin if they are to take glucose from the bloodstream, skeletal muscle cells and adipose cells are the primary targets of insulin. The presence of food in the intestine triggers the release of gastrointestinal tract hormones such as glucose-dependent insulinotropic peptide (previously known as gastric inhibitory peptide). This is in turn the initial trigger for insulin production and secretion by the beta cells of the pancreas. Once nutrient absorption occurs, the resulting surge in blood glucose levels further stimulates insulin secretion. Precisely how insulin facilitates glucose uptake is not entirely clear. However, insulin appears to activate a tyrosine kinase receptor, triggering the phosphorylation of many substrates within the cell. These multiple biochemical reactions converge to support the movement of intracellular vesicles containing facilitative glucose transporters to the cell membrane. In the absence of insulin, these transport proteins are normally recycled slowly between the cell membrane and cell interior. Insulin triggers the rapid movement of a pool of glucose transporter vesicles to the cell membrane, where they fuse and expose the glucose transporters to the extracellular fluid. The transporters then move glucose by facilitated diffusion into the cell interior. INTERACTIVE LINK Visit this link to view an animation describing the location and function of the pancreas. What goes wrong in the function of insulin in type 2 diabetes? Insulin also reduces blood glucose levels by stimulating glycolysis, the metabolism of glucose for generation of ATP. Moreover, it stimulates the liver to convert excess glucose into glycogen for storage, and it inhibits enzymes involved in glycogenolysis and gluconeogenesis. Finally, insulin promotes triglyceride and protein synthesis. The secretion of insulin is regulated through a negative feedback mechanism. As blood glucose levels decrease, further insulin release is inhibited. The pancreatic hormones are summarized in Table 17.7. Hormones of the Pancreas \| Associated hormones \| Chemical class \| Effect \| \|---\|---\|---\| \| Insulin (beta cells) \| Protein \| Reduces blood glucose levels \| \| Glucagon (alpha cells) \| Protein \| Increases blood glucose levels \| \| Somatostatin (delta cells) \| Protein \| Inhibits insulin and glucagon release \| \| Pancreatic polypeptide (PP cells) \| Protein \| Role in appetite \| Table 17.7 DISORDERS OF THE... Endocrine System: Diabetes Mellitus Dysfunction of insulin production and secretion, as well as the target cells’ responsiveness to insulin, can lead to a condition called diabetes mellitus. An increasingly common disease, diabetes mellitus has been diagnosed in more than 18 million adults in the United States, and more than 200,000 children. It is estimated that up to 7 million more adults have the condition but have not been diagnosed. In addition, approximately 79 million people in the US are estimated to have pre-diabetes, a condition in which blood glucose levels are abnormally high, but not yet high enough to be classified as diabetes. There are two main forms of diabetes mellitus. Type 1 diabetes is an autoimmune disease affecting the beta cells of the pancreas. Certain genes are recognized to increase susceptibility. The beta cells of people with type 1 diabetes do not produce insulin; thus, synthetic insulin must be administered by injection or infusion. This form of diabetes accounts for less than five percent of all diabetes cases. Type 2 diabetes accounts for approximately 95 percent of all cases. It is acquired, and lifestyle factors such as poor diet, inactivity, and the presence of pre-diabetes greatly increase a person’s risk. About 80 to 90 percent of people with type 2 diabetes are overweight or obese. In type 2 diabetes, cells become resistant to the effects of insulin. In response, the pancreas increases its insulin secretion, but over time, the beta cells become exhausted. In many cases, type 2 diabetes can be reversed by moderate weight loss, regular physical activity, and consumption of a healthy diet; however, if blood glucose levels cannot be controlled, the diabetic will eventually require insulin. Two of the early manifestations of diabetes are excessive urination and excessive thirst. They demonstrate how the out-of-control levels of glucose in the blood affect kidney function. The kidneys are responsible for filtering glucose from the blood. Excessive blood glucose draws water into the urine, and as a result the person eliminates an abnormally large quantity of sweet urine. The use of body water to dilute the urine leaves the body dehydrated, and so the person is unusually and continually thirsty. The person may also experience persistent hunger because the body cells are unable to access the glucose in the bloodstream. Over time, persistently high levels of glucose in the blood injure tissues throughout the body, especially those of the blood vessels and nerves. Inflammation and injury of the lining of arteries lead to atherosclerosis and an increased risk of heart attack and stroke. Damage to the microscopic blood vessels of the kidney impairs kidney function and can lead to kidney failure. Damage to blood vessels that serve the eyes can lead to blindness. Blood vessel damage also reduces circulation to the limbs, whereas nerve damage leads to a loss of sensation, called neuropathy, particularly in the hands and feet. Together, these changes increase the risk of injury, infection, and tissue death (necrosis), contributing to a high rate of toe, foot, and lower leg amputations in people with diabetes. Uncontrolled diabetes can also lead to a dangerous form of metabolic acidosis called ketoacidosis. Deprived of glucose, cells increasingly rely on fat stores for fuel. However, in a glucose-deficient state, the liver is forced to use an alternative lipid metabolism pathway that results in the increased production of ketone bodies (or ketones), which are acidic. The build-up of ketones in the blood causes ketoacidosis, which—if left untreated—may lead to a life-threatening “diabetic coma.” Together, these complications make diabetes the seventh leading cause of death in the United States. Diabetes is diagnosed when lab tests reveal that blood glucose levels are higher than normal, a condition called hyperglycemia. The treatment of diabetes depends on the type, the severity of the condition, and the ability of the patient to make lifestyle changes. As noted earlier, moderate weight loss, regular physical activity, and consumption of a healthful diet can reduce blood glucose levels. Some patients with type 2 diabetes may be unable to control their disease with these lifestyle changes, and will require medication. Historically, the first-line treatment of type 2 diabetes was insulin. Research advances have resulted in alternative options, including medications that enhance pancreatic function. INTERACTIVE LINK Visit this link to view an animation describing the role of insulin and the pancreas in diabetes. Organs with Secondary Endocrine Functions - Identify the organs with a secondary endocrine function, the hormone they produce, and its effects In your study of anatomy and physiology, you have already encountered a few of the many organs of the body that have secondary endocrine functions. Here, you will learn about the hormone-producing activities of the heart, gastrointestinal tract, kidneys, skeleton, adipose tissue, skin, and thymus. Heart When the body experiences an increase in blood volume or pressure, the cells of the heart’s atrial wall stretch. In response, specialized cells in the wall of the atria produce and secrete the peptide hormone atrial natriuretic peptide (ANP). ANP signals the kidneys to reduce sodium reabsorption, thereby decreasing the amount of water reabsorbed from the urine filtrate and reducing blood volume. Other actions of ANP include the inhibition of renin secretion, thus inhibition of the renin-angiotensin-aldosterone system (RAAS) and vasodilation. Therefore, ANP aids in decreasing blood pressure, blood volume, and blood sodium levels. Gastrointestinal Tract The endocrine cells of the GI tract are located in the mucosa of the stomach and small intestine. Some of these hormones are secreted in response to eating a meal and aid in digestion. An example of a hormone secreted by the stomach cells is gastrin, a peptide hormone secreted in response to stomach distention that stimulates the release of hydrochloric acid. Secretin is a peptide hormone secreted by the small intestine as acidic chyme (partially digested food and fluid) moves from the stomach. It stimulates the release of bicarbonate from the pancreas, which buffers the acidic chyme, and inhibits the further secretion of hydrochloric acid by the stomach. Cholecystokinin (CCK) is another peptide hormone released from the small intestine. It promotes the secretion of pancreatic enzymes and the release of bile from the gallbladder, both of which facilitate digestion. Other hormones produced by the intestinal cells aid in glucose metabolism, such as by stimulating the pancreatic beta cells to secrete insulin, reducing glucagon secretion from the alpha cells, or enhancing cellular sensitivity to insulin. Kidneys The kidneys participate in several complex endocrine pathways and produce certain hormones. A decline in blood flow to the kidneys stimulates them to release the enzyme renin, triggering the renin-angiotensin-aldosterone (RAAS) system, and stimulating the reabsorption of sodium and water. The reabsorption increases blood flow and blood pressure. The kidneys also play a role in regulating blood calcium levels through the production of calcitriol from vitamin D3, which is released in response to the secretion of parathyroid hormone (PTH). In addition, the kidneys produce the hormone erythropoietin (EPO) in response to low oxygen levels. EPO stimulates the production of red blood cells (erythrocytes) in the bone marrow, thereby increasing oxygen delivery to tissues. You may have heard of EPO as a performance-enhancing drug (in a synthetic form). Skeleton Although bone has long been recognized as a target for hormones, only recently have researchers recognized that the skeleton itself produces at least two hormones. Fibroblast growth factor 23 (FGF23) is produced by bone cells in response to increased blood levels of vitamin D3 or phosphate. It triggers the kidneys to inhibit the formation of calcitriol from vitamin D3 and to increase phosphorus excretion. Osteocalcin, produced by osteoblasts, stimulates the pancreatic beta cells to increase insulin production. It also acts on peripheral tissues to increase their sensitivity to insulin and their utilization of glucose. Adipose Tissue Adipose tissue produces and secretes several hormones involved in lipid metabolism and storage. One important example is leptin, a protein manufactured by adipose cells that circulates in amounts directly proportional to levels of body fat. Leptin is released in response to food consumption and acts by binding to brain neurons involved in energy intake and expenditure. Binding of leptin produces a feeling of satiety after a meal, thereby reducing appetite. It also appears that the binding of leptin to brain receptors triggers the sympathetic nervous system to regulate bone metabolism, increasing deposition of cortical bone. Adiponectin—another hormone synthesized by adipose cells—appears to reduce cellular insulin resistance and to protect blood vessels from inflammation and atherosclerosis. Its levels are lower in people who are obese, and rise following weight loss. Skin The skin functions as an endocrine organ in the production of the inactive form of vitamin D3, cholecalciferol. When cholesterol present in the epidermis is exposed to ultraviolet radiation, it is converted to cholecalciferol, which then enters the blood. In the liver, cholecalciferol is converted to an intermediate that travels to the kidneys and is further converted to calcitriol, the active form of vitamin D3. Vitamin D is important in a variety of physiological processes, including intestinal calcium absorption and immune system function. In some studies, low levels of vitamin D have been associated with increased risks of cancer, severe asthma, and multiple sclerosis. Vitamin D deficiency in children causes rickets, and in adults, osteomalacia—both of which are characterized by bone deterioration. Thymus The thymus is an organ of the immune system that is larger and more active during infancy and early childhood, and begins to atrophy as we age. Its endocrine function is the production of a group of hormones called thymosins that contribute to the development and differentiation of T lymphocytes, which are immune cells. Although the role of thymosins is not yet well understood, it is clear that they contribute to the immune response. Thymosins have been found in tissues other than the thymus and have a wide variety of functions, so the thymosins cannot be strictly categorized as thymic hormones. Liver The liver is responsible for secreting at least four important hormones or hormone precursors: insulin-like growth factor (somatomedin), angiotensinogen, thrombopoetin, and hepcidin. Insulin-like growth factor-1 is the immediate stimulus for growth in the body, especially of the bones. Angiotensinogen is the precursor to angiotensin, mentioned earlier, which increases blood pressure. Thrombopoetin stimulates the production of the blood’s platelets. Hepcidins block the release of iron from cells in the body, helping to regulate iron homeostasis in our body fluids. The major hormones of these other organs are summarized in Table 17.8. Organs with Secondary Endocrine Functions and Their Major Hormones \| Organ \| Major hormones \| Effects \| \|---\|---\|---\| \| Heart \| Atrial natriuretic peptide (ANP) \| Reduces blood volume, blood pressure, and Na+concentration \| \| Gastrointestinal tract \| Gastrin, secretin, and cholecystokinin \| Aid digestion of food and buffering of stomach acids \| \| Gastrointestinal tract \| Glucose-dependent insulinotropic peptide (GIP) and glucagon-like peptide 1 (GLP-1) \| Stimulate beta cells of the pancreas to release insulin \| \| Kidneys \| Renin \| Stimulates release of aldosterone \| \| Kidneys \| Calcitriol \| Aids in the absorption of Ca2+ \| \| Kidneys \| Erythropoietin \| Triggers the formation of red blood cells in the bone marrow \| \| Skeleton \| FGF23 \| Inhibits production of calcitriol and increases phosphate excretion \| \| Skeleton \| Osteocalcin \| Increases insulin production \| \| Adipose tissue \| Leptin \| Promotes satiety signals in the brain \| \| Adipose tissue \| Adiponectin \| Reduces insulin resistance \| \| Skin \| Cholecalciferol \| Modified to form vitamin D \| \| Thymus (and other organs) \| Thymosins \| Among other things, aids in the development of T lymphocytes of the immune system \| \| Liver \| Insulin-like growth factor-1 \| Stimulates bodily growth \| \| Liver \| Angiotensinogen \| Raises blood pressure \| \| Liver \| Thrombopoetin \| Causes increase in platelets \| \| Liver \| Hepcidin \| Blocks release of iron into body fluids \| Table 17.8 Development and Aging of the Endocrine System - Describe the embryonic origins of the endocrine system - Discuss the effects of aging on the endocrine system The endocrine system arises from all three embryonic germ layers. The endocrine glands that produce the steroid hormones, such as the gonads and adrenal cortex, arise from the mesoderm. In contrast, endocrine glands that arise from the endoderm and ectoderm produce the amine, peptide, and protein hormones. The pituitary gland arises from two distinct areas of the ectoderm: the anterior pituitary gland arises from the oral ectoderm, whereas the posterior pituitary gland arises from the neural ectoderm at the base of the hypothalamus. The pineal gland also arises from the ectoderm. The two structures of the adrenal glands arise from two different germ layers: the adrenal cortex from the mesoderm and the adrenal medulla from ectoderm neural cells. The endoderm gives rise to the thyroid and parathyroid glands, as well as the pancreas and the thymus. As the body ages, changes occur that affect the endocrine system, sometimes altering the production, secretion, and catabolism of hormones. For example, the structure of the anterior pituitary gland changes as vascularization decreases and the connective tissue content increases with increasing age. This restructuring affects the gland’s hormone production. For example, the amount of human growth hormone that is produced declines with age, resulting in the reduced muscle mass commonly observed in the elderly. The adrenal glands also undergo changes as the body ages; as fibrous tissue increases, the production of cortisol and aldosterone decreases. Interestingly, the production and secretion of epinephrine and norepinephrine remain normal throughout the aging process. A well-known example of the aging process affecting an endocrine gland is menopause and the decline of ovarian function. With increasing age, the ovaries decrease in both size and weight and become progressively less sensitive to gonadotropins. This gradually causes a decrease in estrogen and progesterone levels, leading to menopause and the inability to reproduce. Low levels of estrogens and progesterone are also associated with some disease states, such as osteoporosis, atherosclerosis, and hyperlipidemia, or abnormal blood lipid levels. Testosterone levels also decline with age, a condition called andropause (or viropause); however, this decline is much less dramatic than the decline of estrogens in women, and much more gradual, rarely affecting sperm production until very old age. Although this means that males maintain their ability to father children for decades longer than females, the quantity, quality, and motility of their sperm is often reduced. As the body ages, the thyroid gland produces less of the thyroid hormones, causing a gradual decrease in the basal metabolic rate. The lower metabolic rate reduces the production of body heat and increases levels of body fat. Parathyroid hormones, on the other hand, increase with age. This may be because of reduced dietary calcium levels, causing a compensatory increase in parathyroid hormone. However, increased parathyroid hormone levels combined with decreased levels of calcitonin (and estrogens in women) can lead to osteoporosis as PTH stimulates demineralization of bones to increase blood calcium levels. Notice that osteoporosis is common in both elderly males and females. Increasing age also affects glucose metabolism, as blood glucose levels spike more rapidly and take longer to return to normal in the elderly. In addition, increasing glucose intolerance may occur because of a gradual decline in cellular insulin sensitivity. Almost 27 percent of Americans aged 65 and older have diabetes. Key Terms - acromegaly - disorder in adults caused when abnormally high levels of GH trigger growth of bones in the face, hands, and feet - adenylyl cyclase - membrane-bound enzyme that converts ATP to cyclic AMP, creating cAMP, as a result of G-protein activation - adrenal cortex - outer region of the adrenal glands consisting of multiple layers of epithelial cells and capillary networks that produces mineralocorticoids and glucocorticoids - adrenal glands - endocrine glands located at the top of each kidney that are important for the regulation of the stress response, blood pressure and blood volume, water homeostasis, and electrolyte levels - adrenal medulla - inner layer of the adrenal glands that plays an important role in the stress response by producing epinephrine and norepinephrine - adrenocorticotropic hormone (ACTH) - anterior pituitary hormone that stimulates the adrenal cortex to secrete corticosteroid hormones (also called corticotropin) - alarm reaction - the short-term stress, or the fight-or-flight response, of stage one of the general adaptation syndrome mediated by the hormones epinephrine and norepinephrine - aldosterone - hormone produced and secreted by the adrenal cortex that stimulates sodium and fluid retention and increases blood volume and blood pressure - alpha cell - pancreatic islet cell type that produces the hormone glucagon - angiotensin-converting enzyme - the enzyme that converts angiotensin I to angiotensin II - antidiuretic hormone (ADH) - hypothalamic hormone that is stored by the posterior pituitary and that signals the kidneys to reabsorb water - atrial natriuretic peptide (ANP) - peptide hormone produced by the walls of the atria in response to high blood pressure, blood volume, or blood sodium that reduces the reabsorption of sodium and water in the kidneys and promotes vasodilation - autocrine - chemical signal that elicits a response in the same cell that secreted it - beta cell - pancreatic islet cell type that produces the hormone insulin - calcitonin - peptide hormone produced and secreted by the parafollicular cells (C cells) of the thyroid gland that functions to decrease blood calcium levels - chromaffin - neuroendocrine cells of the adrenal medulla - colloid - viscous fluid in the central cavity of thyroid follicles, containing the glycoprotein thyroglobulin - cortisol - glucocorticoid important in gluconeogenesis, the catabolism of glycogen, and downregulation of the immune system - cyclic adenosine monophosphate (cAMP) - second messenger that, in response to adenylyl cyclase activation, triggers a phosphorylation cascade - delta cell - minor cell type in the pancreas that secretes the hormone somatostatin - diabetes mellitus - condition caused by destruction or dysfunction of the beta cells of the pancreas or cellular resistance to insulin that results in abnormally high blood glucose levels - diacylglycerol (DAG) - molecule that, like cAMP, activates protein kinases, thereby initiating a phosphorylation cascade - downregulation - decrease in the number of hormone receptors, typically in response to chronically excessive levels of a hormone - endocrine gland - tissue or organ that secretes hormones into the blood and lymph without ducts such that they may be transported to organs distant from the site of secretion - endocrine system - cells, tissues, and organs that secrete hormones as a primary or secondary function and play an integral role in normal bodily processes - epinephrine - primary and most potent catecholamine hormone secreted by the adrenal medulla in response to short-term stress; also called adrenaline - erythropoietin (EPO) - protein hormone secreted in response to low oxygen levels that triggers the bone marrow to produce red blood cells - estrogens - class of predominantly female sex hormones important for the development and growth of the female reproductive tract, secondary sex characteristics, the female reproductive cycle, and the maintenance of pregnancy - exocrine system - cells, tissues, and organs that secrete substances directly to target tissues via glandular ducts - first messenger - hormone that binds to a cell membrane hormone receptor and triggers activation of a second messenger system - follicle-stimulating hormone (FSH) - anterior pituitary hormone that stimulates the production and maturation of sex cells - G protein - protein associated with a cell membrane hormone receptor that initiates the next step in a second messenger system upon activation by hormone–receptor binding - general adaptation syndrome (GAS) - the human body’s three-stage response pattern to short- and long-term stress - gigantism - disorder in children caused when abnormally high levels of GH prompt excessive growth - glucagon - pancreatic hormone that stimulates the catabolism of glycogen to glucose, thereby increasing blood glucose levels - glucocorticoids - hormones produced by the zona fasciculata of the adrenal cortex that influence glucose metabolism - goiter - enlargement of the thyroid gland either as a result of iodine deficiency or hyperthyroidism - gonadotropins - hormones that regulate the function of the gonads - growth hormone (GH) - anterior pituitary hormone that promotes tissue building and influences nutrient metabolism (also called somatotropin) - hormone - secretion of an endocrine organ that travels via the bloodstream or lymphatics to induce a response in target cells or tissues in another part of the body - hormone receptor - protein within a cell or on the cell membrane that binds a hormone, initiating the target cell response - hyperglycemia - abnormally high blood glucose levels - hyperparathyroidism - disorder caused by overproduction of PTH that results in abnormally elevated blood calcium - hyperthyroidism - clinically abnormal, elevated level of thyroid hormone in the blood; characterized by an increased metabolic rate, excess body heat, sweating, diarrhea, weight loss, and increased heart rate - hypoparathyroidism - disorder caused by underproduction of PTH that results in abnormally low blood calcium - hypophyseal portal system - network of blood vessels that enables hypothalamic hormones to travel into the anterior lobe of the pituitary without entering the systemic circulation - hypothalamus - region of the diencephalon inferior to the thalamus that functions in neural and endocrine signaling - hypothyroidism - clinically abnormal, low level of thyroid hormone in the blood; characterized by low metabolic rate, weight gain, cold extremities, constipation, and reduced mental activity - infundibulum - stalk containing vasculature and neural tissue that connects the pituitary gland to the hypothalamus (also called the pituitary stalk) - inhibin - hormone secreted by the male and female gonads that inhibits FSH production by the anterior pituitary - inositol triphosphate (IP3) - molecule that initiates the release of calcium ions from intracellular stores - insulin - pancreatic hormone that enhances the cellular uptake and utilization of glucose, thereby decreasing blood glucose levels - insulin-like growth factors (IGF) - protein that enhances cellular proliferation, inhibits apoptosis, and stimulates the cellular uptake of amino acids for protein synthesis - leptin - protein hormone secreted by adipose tissues in response to food consumption that promotes satiety - luteinizing hormone (LH) - anterior pituitary hormone that triggers ovulation and the production of ovarian hormones in females, and the production of testosterone in males - melatonin - amino acid–derived hormone that is secreted in response to low light and causes drowsiness - mineralocorticoids - hormones produced by the zona glomerulosa cells of the adrenal cortex that influence fluid and electrolyte balance - neonatal hypothyroidism - condition characterized by cognitive deficits, short stature, and other signs and symptoms in people born to women who were iodine-deficient during pregnancy - norepinephrine - secondary catecholamine hormone secreted by the adrenal medulla in response to short-term stress; also called noradrenaline - osmoreceptor - hypothalamic sensory receptor that is stimulated by changes in solute concentration (osmotic pressure) in the blood - oxytocin - hypothalamic hormone stored in the posterior pituitary gland and important in stimulating uterine contractions in labor, milk ejection during breastfeeding, and feelings of attachment (also produced in males) - pancreas - organ with both exocrine and endocrine functions located posterior to the stomach that is important for digestion and the regulation of blood glucose - pancreatic islets - specialized clusters of pancreatic cells that have endocrine functions; also called islets of Langerhans - paracrine - chemical signal that elicits a response in neighboring cells; also called paracrine factor - parathyroid glands - small, round glands embedded in the posterior thyroid gland that produce parathyroid hormone (PTH) - parathyroid hormone (PTH) - peptide hormone produced and secreted by the parathyroid glands in response to low blood calcium levels - phosphodiesterase (PDE) - cytosolic enzyme that deactivates and degrades cAMP - phosphorylation cascade - signaling event in which multiple protein kinases phosphorylate the next protein substrate by transferring a phosphate group from ATP to the protein - pineal gland - endocrine gland that secretes melatonin, which is important in regulating the sleep-wake cycle - pinealocyte - cell of the pineal gland that produces and secretes the hormone melatonin - pituitary dwarfism - disorder in children caused when abnormally low levels of GH result in growth retardation - pituitary gland - bean-sized organ suspended from the hypothalamus that produces, stores, and secretes hormones in response to hypothalamic stimulation (also called hypophysis) - PP cell - minor cell type in the pancreas that secretes the hormone pancreatic polypeptide - progesterone - predominantly female sex hormone important in regulating the female reproductive cycle and the maintenance of pregnancy - prolactin (PRL) - anterior pituitary hormone that promotes development of the mammary glands and the production of breast milk - protein kinase - enzyme that initiates a phosphorylation cascade upon activation - second messenger - molecule that initiates a signaling cascade in response to hormone binding on a cell membrane receptor and activation of a G protein - stage of exhaustion - stage three of the general adaptation syndrome; the body’s long-term response to stress mediated by the hormones of the adrenal cortex - stage of resistance - stage two of the general adaptation syndrome; the body’s continued response to stress after stage one diminishes - testosterone - steroid hormone secreted by the male testes and important in the maturation of sperm cells, growth and development of the male reproductive system, and the development of male secondary sex characteristics - thymosins - hormones produced and secreted by the thymus that play an important role in the development and differentiation of T cells - thymus - organ that is involved in the development and maturation of T-cells and is particularly active during infancy and childhood - thyroid gland - large endocrine gland responsible for the synthesis of thyroid hormones - thyroid-stimulating hormone (TSH) - anterior pituitary hormone that triggers secretion of thyroid hormones by the thyroid gland (also called thyrotropin) - thyroxine - (also, tetraiodothyronine, T4) amino acid–derived thyroid hormone that is more abundant but less potent than T3 and often converted to T3 by target cells - triiodothyronine - (also, T3) amino acid–derived thyroid hormone that is less abundant but more potent than T4 - upregulation - increase in the number of hormone receptors, typically in response to chronically reduced levels of a hormone - zona fasciculata - intermediate region of the adrenal cortex that produce hormones called glucocorticoids - zona glomerulosa - most superficial region of the adrenal cortex, which produces the hormones collectively referred to as mineralocorticoids - zona reticularis - deepest region of the adrenal cortex, which produces the steroid sex hormones called androgens Chapter Review 17.1 An Overview of the Endocrine System The endocrine system consists of cells, tissues, and organs that secrete hormones critical to homeostasis. The body coordinates its functions through two major types of communication: neural and endocrine. Neural communication includes both electrical and chemical signaling between neurons and target cells. Endocrine communication involves chemical signaling via the release of hormones into the extracellular fluid. From there, hormones diffuse into the bloodstream and may travel to distant body regions, where they elicit a response in target cells. Endocrine glands are ductless glands that secrete hormones. Many organs of the body with other primary functions—such as the heart, stomach, and kidneys—also have hormone-secreting cells. 17.2 Hormones Hormones are derived from amino acids or lipids. Amine hormones originate from the amino acids tryptophan or tyrosine. Larger amino acid hormones include peptides and protein hormones. Steroid hormones are derived from cholesterol. Steroid hormones and thyroid hormone are lipid soluble. All other amino acid–derived hormones are water soluble. Hydrophobic hormones are able to diffuse through the membrane and interact with an intracellular receptor. In contrast, hydrophilic hormones must interact with cell membrane receptors. These are typically associated with a G protein, which becomes activated when the hormone binds the receptor. This initiates a signaling cascade that involves a second messenger, such as cyclic adenosine monophosphate (cAMP). Second messenger systems greatly amplify the hormone signal, creating a broader, more efficient, and faster response. Hormones are released upon stimulation that is of either chemical or neural origin. Regulation of hormone release is primarily achieved through negative feedback. Various stimuli may cause the release of hormones, but there are three major types. Humoral stimuli are changes in ion or nutrient levels in the blood. Hormonal stimuli are changes in hormone levels that initiate or inhibit the secretion of another hormone. Finally, a neural stimulus occurs when a nerve impulse prompts the secretion or inhibition of a hormone. 17.3 The Pituitary Gland and Hypothalamus The hypothalamus–pituitary complex is located in the diencephalon of the brain. The hypothalamus and the pituitary gland are connected by a structure called the infundibulum, which contains vasculature and nerve axons. The pituitary gland is divided into two distinct structures with different embryonic origins. The posterior lobe houses the axon terminals of hypothalamic neurons. It stores and releases into the bloodstream two hypothalamic hormones: oxytocin and antidiuretic hormone (ADH). The anterior lobe is connected to the hypothalamus by vasculature in the infundibulum and produces and secretes six hormones. Their secretion is regulated, however, by releasing and inhibiting hormones from the hypothalamus. The six anterior pituitary hormones are: growth hormone (GH), thyroid-stimulating hormone (TSH), adrenocorticotropic hormone (ACTH), follicle-stimulating hormone (FSH), luteinizing hormone (LH), and prolactin (PRL). 17.4 The Thyroid Gland The thyroid gland is a butterfly-shaped organ located in the neck anterior to the trachea. Its hormones regulate basal metabolism, oxygen use, nutrient metabolism, the production of ATP, and calcium homeostasis. They also contribute to protein synthesis and the normal growth and development of body tissues, including maturation of the nervous system, and they increase the body’s sensitivity to catecholamines. The thyroid hormones triiodothyronine (T3) and thyroxine (T4) are produced and secreted by the thyroid gland in response to thyroid-stimulating hormone (TSH) from the anterior pituitary. Synthesis of the amino acid–derived T3 and T4 hormones requires iodine. Insufficient amounts of iodine in the diet can lead to goiter, cretinism, and many other disorders. 17.5 The Parathyroid Glands Calcium is required for a variety of important physiologic processes, including neuromuscular functioning; thus, blood calcium levels are closely regulated. The parathyroid glands are small structures located on the posterior thyroid gland that produce parathyroid hormone (PTH), which regulates blood calcium levels. Low blood calcium levels cause the production and secretion of PTH. In contrast, elevated blood calcium levels inhibit secretion of PTH and trigger secretion of the thyroid hormone calcitonin. Underproduction of PTH can result in hypoparathyroidism. In contrast, overproduction of PTH can result in hyperparathyroidism. 17.6 The Adrenal Glands The adrenal glands, located superior to each kidney, consist of two regions: the adrenal cortex and adrenal medulla. The adrenal cortex—the outer layer of the gland—produces mineralocorticoids, glucocorticoids, and androgens. The adrenal medulla at the core of the gland produces epinephrine and norepinephrine. The adrenal glands mediate a short-term stress response and a long-term stress response. A perceived threat results in the secretion of epinephrine and norepinephrine from the adrenal medulla, which mediate the fight-or-flight response. The long-term stress response is mediated by the secretion of CRH from the hypothalamus, which triggers ACTH, which in turn stimulates the secretion of corticosteroids from the adrenal cortex. The mineralocorticoids, chiefly aldosterone, cause sodium and fluid retention, which increases blood volume and blood pressure. 17.7 The Pineal Gland The pineal gland is an endocrine structure of the diencephalon of the brain, and is located inferior and posterior to the thalamus. It is made up of pinealocytes. These cells produce and secrete the hormone melatonin in response to low light levels. High blood levels of melatonin induce drowsiness. Jet lag, caused by traveling across several time zones, occurs because melatonin synthesis takes several days to readjust to the light-dark patterns in the new environment. 17.8 Gonadal and Placental Hormones The male and female reproductive system is regulated by follicle-stimulating hormone (FSH) and luteinizing hormone (LH) produced by the anterior lobe of the pituitary gland in response to gonadotropin-releasing hormone (GnRH) from the hypothalamus. In males, FSH stimulates sperm maturation, which is inhibited by the hormone inhibin. The steroid hormone testosterone, a type of androgen, is released in response to LH and is responsible for the maturation and maintenance of the male reproductive system, as well as the development of male secondary sex characteristics. In females, FSH promotes egg maturation and LH signals the secretion of the female sex hormones, the estrogens and progesterone. Both of these hormones are important in the development and maintenance of the female reproductive system, as well as maintaining pregnancy. The placenta develops during early pregnancy, and secretes several hormones important for maintaining the pregnancy. 17.9 The Endocrine Pancreas The pancreas has both exocrine and endocrine functions. The pancreatic islet cell types include alpha cells, which produce glucagon; beta cells, which produce insulin; delta cells, which produce somatostatin; and PP cells, which produce pancreatic polypeptide. Insulin and glucagon are involved in the regulation of glucose metabolism. Insulin is produced by the beta cells in response to high blood glucose levels. It enhances glucose uptake and utilization by target cells, as well as the storage of excess glucose for later use. Dysfunction of the production of insulin or target cell resistance to the effects of insulin causes diabetes mellitus, a disorder characterized by high blood glucose levels. The hormone glucagon is produced and secreted by the alpha cells of the pancreas in response to low blood glucose levels. Glucagon stimulates mechanisms that increase blood glucose levels, such as the catabolism of glycogen into glucose. 17.10 Organs with Secondary Endocrine Functions Some organs have a secondary endocrine function. For example, the walls of the atria of the heart produce the hormone atrial natriuretic peptide (ANP), the gastrointestinal tract produces the hormones gastrin, secretin, and cholecystokinin, which aid in digestion, and the kidneys produce erythropoietin (EPO), which stimulates the formation of red blood cells. Even bone, adipose tissue, and the skin have secondary endocrine functions. 17.11 Development and Aging of the Endocrine System The endocrine system originates from all three germ layers of the embryo, including the endoderm, ectoderm, and mesoderm. In general, different hormone classes arise from distinct germ layers. Aging affects the endocrine glands, potentially affecting hormone production and secretion, and can cause disease. The production of hormones, such as human growth hormone, cortisol, aldosterone, sex hormones, and the thyroid hormones, decreases with age. Interactive Link Questions Visit this link to watch an animation of the events that occur when a hormone binds to a cell membrane receptor. What is the secondary messenger made by adenylyl cyclase during the activation of liver cells by epinephrine? 2.Visit this link to watch an animation showing the role of the hypothalamus and the pituitary gland. Which hormone is released by the pituitary to stimulate the thyroid gland? 3.Visit this link to view an animation describing the location and function of the adrenal glands. Which hormone produced by the adrenal glands is responsible for mobilization of energy stores? 4.Visit this link to view an animation describing the function of the hormone melatonin. What should you avoid doing in the middle of your sleep cycle that would lower melatonin? 5.Visit this link to view an animation describing the location and function of the pancreas. What goes wrong in the function of insulin in type 2 diabetes? Review Questions Endocrine glands ________. - secrete hormones that travel through a duct to the target organs - release neurotransmitters into the synaptic cleft - secrete chemical messengers that travel in the bloodstream - include sebaceous glands and sweat glands Chemical signaling that affects neighboring cells is called ________. - autocrine - paracrine - endocrine - neuron A newly developed pesticide has been observed to bind to an intracellular hormone receptor. If ingested, residue from this pesticide could disrupt levels of ________. - melatonin - thyroid hormone - growth hormone - insulin A small molecule binds to a G protein, preventing its activation. What direct effect will this have on signaling that involves cAMP? - The hormone will not be able to bind to the hormone receptor. - Adenylyl cyclase will not be activated. - Excessive quantities of cAMP will be produced. - The phosphorylation cascade will be initiated. A student is in a car accident, and although not hurt, immediately experiences pupil dilation, increased heart rate, and rapid breathing. What type of endocrine system stimulus did the student receive? - humoral - hormonal - neural - positive feedback The hypothalamus is functionally and anatomically connected to the posterior pituitary lobe by a bridge of ________. - blood vessels - nerve axons - cartilage - bone Which of the following is an anterior pituitary hormone? - ADH - oxytocin - TSH - cortisol How many hormones are produced by the posterior pituitary? - 0 - 1 - 2 - 6 Which of the following hormones contributes to the regulation of the body’s fluid and electrolyte balance? - adrenocorticotropic hormone - antidiuretic hormone - luteinizing hormone - all of the above Which of the following statements about the thyroid gland is true? - It is located anterior to the trachea and inferior to the larynx. - The parathyroid glands are embedded within it. - It manufactures three hormones. - all of the above The secretion of thyroid hormones is controlled by ________. - TSH from the hypothalamus - TSH from the anterior pituitary - thyroxine from the anterior pituitary - thyroglobulin from the thyroid’s parafollicular cells The development of a goiter indicates that ________. - the anterior pituitary is abnormally enlarged - there is hypertrophy of the thyroid’s follicle cells - there is an excessive accumulation of colloid in the thyroid follicles - the anterior pituitary is secreting excessive growth hormone Iodide ions cross from the bloodstream into follicle cells via ________. - simple diffusion - facilitated diffusion - active transport - osmosis When blood calcium levels are low, PTH stimulates ________. - urinary excretion of calcium by the kidneys - a reduction in calcium absorption from the intestines - the activity of osteoblasts - the activity of osteoclasts Which of the following can result from hyperparathyroidism? - increased bone deposition - fractures - convulsions - all of the above The adrenal glands are attached superiorly to which organ? - thyroid - liver - kidneys - hypothalamus What secretory cell type is found in the adrenal medulla? - chromaffin cells - neuroglial cells - follicle cells - oxyphil cells Cushing’s disease is a disorder caused by ________. - abnormally low levels of cortisol - abnormally high levels of cortisol - abnormally low levels of aldosterone - abnormally high levels of aldosterone Which of the following responses s not part of the fight-or-flight response? - pupil dilation - increased oxygen supply to the lungs - suppressed digestion - reduced mental activity What cells secrete melatonin? - melanocytes - pinealocytes - suprachiasmatic nucleus cells - retinal cells The production of melatonin is inhibited by ________. - declining levels of light - exposure to bright light - the secretion of serotonin - the activity of pinealocytes The gonads produce what class of hormones? - amine hormones - peptide hormones - steroid hormones - catecholamines The production of FSH by the anterior pituitary is reduced by which hormone? - estrogens - progesterone - relaxin - inhibin The function of the placental hormone human placental lactogen (hPL) is to ________. - prepare the breasts for lactation - nourish the placenta - regulate the menstrual cycle - all of the above If an autoimmune disorder targets the alpha cells, production of which hormone would be directly affected? - somatostatin - pancreatic polypeptide - insulin - glucagon Which of the following statements about insulin is true? - Insulin acts as a transport protein, carrying glucose across the cell membrane. - Insulin facilitates the movement of intracellular glucose transporters to the cell membrane. - Insulin stimulates the breakdown of stored glycogen into glucose. - Insulin stimulates the kidneys to reabsorb glucose into the bloodstream. The walls of the atria produce which hormone? - cholecystokinin - atrial natriuretic peptide - renin - calcitriol The end result of the RAAS is to ________. - reduce blood volume - increase blood glucose - reduce blood pressure - increase blood pressure Athletes may take synthetic EPO to boost their ________. - blood calcium levels - secretion of growth hormone - blood oxygen levels - muscle mass Hormones produced by the thymus play a role in the ________. - development of T cells - preparation of the body for childbirth - regulation of appetite - release of hydrochloric acid in the stomach The anterior pituitary gland develops from which embryonic germ layer? - oral ectoderm - neural ectoderm - mesoderm - endoderm In the elderly, decreased thyroid function causes ________. - increased tolerance for cold - decreased basal metabolic rate - decreased body fat - osteoporosis Critical Thinking Questions Describe several main differences in the communication methods used by the endocrine system and the nervous system. 39.Compare and contrast endocrine and exocrine glands. 40.True or false: Neurotransmitters are a special class of paracrines. Explain your answer. 41.Compare and contrast the signaling events involved with the second messengers cAMP and IP3. 42.Describe the mechanism of hormone response resulting from the binding of a hormone with an intracellular receptor. 43.Compare and contrast the anatomical relationship of the anterior and posterior lobes of the pituitary gland to the hypothalamus. 44.Name the target tissues for prolactin. 45.Explain why maternal iodine deficiency might lead to neurological impairment in the fetus. 46.Define hyperthyroidism and explain why one of its symptoms is weight loss. 47.Describe the role of negative feedback in the function of the parathyroid gland. 48.Explain why someone with a parathyroid gland tumor might develop kidney stones. 49.What are the three regions of the adrenal cortex and what hormones do they produce? 50.If innervation to the adrenal medulla were disrupted, what would be the physiological outcome? 51.Compare and contrast the short-term and long-term stress response. 52.Seasonal affective disorder (SAD) is a mood disorder characterized by, among other symptoms, increased appetite, sluggishness, and increased sleepiness. It occurs most commonly during the winter months, especially in regions with long winter nights. Propose a role for melatonin in SAD and a possible non-drug therapy. 53.Retinitis pigmentosa (RP) is a disease that causes deterioration of the retinas of the eyes. Describe the impact RP would have on melatonin levels. 54.Compare and contrast the role of estrogens and progesterone. 55.Describe the role of placental secretion of relaxin in preparation for childbirth. 56.What would be the physiological consequence of a disease that destroyed the beta cells of the pancreas? 57.Why is foot care extremely important for people with diabetes mellitus? 58.Summarize the role of GI tract hormones following a meal. 59.Compare and contrast the thymus gland in infancy and adulthood. 60.Distinguish between the effects of menopause and andropause on fertility.	oercommons	2025-03-18T00:37:02.036361	null	{ "license": "Creative Commons - Attribution - https://creativecommons.org/licenses/by/4.0/", "url": "https://oercommons.org/courseware/lesson/56380/overview", "title": "Anatomy and Physiology, Regulation, Integration, and Control", "author": null }
https://oercommons.org/courseware/lesson/56376/overview	Anatomy of the Nervous System Introduction Figure 13.1 Human Nervous System The ability to balance like an acrobat combines functions throughout the nervous system. The central and peripheral divisions coordinate control of the body using the senses of balance, body position, and touch on the soles of the feet. (credit: Rhett Sutphin) CHAPTER OBJECTIVES After studying this chapter, you will be able to: - Relate the developmental processes of the embryonic nervous system to the adult structures - Name the major regions of the adult nervous system - Locate regions of the cerebral cortex on the basis of anatomical landmarks common to all human brains - Describe the regions of the spinal cord in cross-section - List the cranial nerves in order of anatomical location and provide the central and peripheral connections - List the spinal nerves by vertebral region and by which nerve plexus each supplies The nervous system is responsible for controlling much of the body, both through somatic (voluntary) and autonomic (involuntary) functions. The structures of the nervous system must be described in detail to understand how many of these functions are possible. There is a physiological concept known as localization of function that states that certain structures are specifically responsible for prescribed functions. It is an underlying concept in all of anatomy and physiology, but the nervous system illustrates the concept very well. Fresh, unstained nervous tissue can be described as gray or white matter, and within those two types of tissue it can be very hard to see any detail. However, as specific regions and structures have been described, they were related to specific functions. Understanding these structures and the functions they perform requires a detailed description of the anatomy of the nervous system, delving deep into what the central and peripheral structures are. The place to start this study of the nervous system is the beginning of the individual human life, within the womb. The embryonic development of the nervous system allows for a simple framework on which progressively more complicated structures can be built. With this framework in place, a thorough investigation of the nervous system is possible. The Embryologic Perspective - Describe the growth and differentiation of the neural tube - Relate the different stages of development to the adult structures of the central nervous system - Explain the expansion of the ventricular system of the adult brain from the central canal of the neural tube - Describe the connections of the diencephalon and cerebellum on the basis of patterns of embryonic development The brain is a complex organ composed of gray parts and white matter, which can be hard to distinguish. Starting from an embryologic perspective allows you to understand more easily how the parts relate to each other. The embryonic nervous system begins as a very simple structure—essentially just a straight line, which then gets increasingly complex. Looking at the development of the nervous system with a couple of early snapshots makes it easier to understand the whole complex system. Many structures that appear to be adjacent in the adult brain are not connected, and the connections that exist may seem arbitrary. But there is an underlying order to the system that comes from how different parts develop. By following the developmental pattern, it is possible to learn what the major regions of the nervous system are. The Neural Tube To begin, a sperm cell and an egg cell fuse to become a fertilized egg. The fertilized egg cell, or zygote, starts dividing to generate the cells that make up an entire organism. Sixteen days after fertilization, the developing embryo’s cells belong to one of three germ layers that give rise to the different tissues in the body. The endoderm, or inner tissue, is responsible for generating the lining tissues of various spaces within the body, such as the mucosae of the digestive and respiratory systems. The mesoderm, or middle tissue, gives rise to most of the muscle and connective tissues. Finally the ectoderm, or outer tissue, develops into the integumentary system (the skin) and the nervous system. It is probably not difficult to see that the outer tissue of the embryo becomes the outer covering of the body. But how is it responsible for the nervous system? As the embryo develops, a portion of the ectoderm differentiates into a specialized region of neuroectoderm, which is the precursor for the tissue of the nervous system. Molecular signals induce cells in this region to differentiate into the neuroepithelium, forming a neural plate. The cells then begin to change shape, causing the tissue to buckle and fold inward (Figure 13.2). A neural groove forms, visible as a line along the dorsal surface of the embryo. The ridge-like edge on either side of the neural groove is referred as the neural fold. As the neural folds come together and converge, the underlying structure forms into a tube just beneath the ectoderm called the neural tube. Cells from the neural folds then separate from the ectoderm to form a cluster of cells referred to as the neural crest, which runs lateral to the neural tube. The neural crest migrates away from the nascent, or embryonic, central nervous system (CNS) that will form along the neural groove and develops into several parts of the peripheral nervous system (PNS), including the enteric nervous tissue. Many tissues that are not part of the nervous system also arise from the neural crest, such as craniofacial cartilage and bone, and melanocytes. Figure 13.2 Early Embryonic Development of Nervous System The neuroectoderm begins to fold inward to form the neural groove. As the two sides of the neural groove converge, they form the neural tube, which lies beneath the ectoderm. The anterior end of the neural tube will develop into the brain, and the posterior portion will become the spinal cord. The neural crest develops into peripheral structures. At this point, the early nervous system is a simple, hollow tube. It runs from the anterior end of the embryo to the posterior end. Beginning at 25 days, the anterior end develops into the brain, and the posterior portion becomes the spinal cord. This is the most basic arrangement of tissue in the nervous system, and it gives rise to the more complex structures by the fourth week of development. Primary Vesicles As the anterior end of the neural tube starts to develop into the brain, it undergoes a couple of enlargements; the result is the production of sac-like vesicles. Similar to a child’s balloon animal, the long, straight neural tube begins to take on a new shape. Three vesicles form at the first stage, which are called primary vesicles. These vesicles are given names that are based on Greek words, the main root word being enkephalon, which means “brain” (en- = “inside”; kephalon = “head”). The prefix to each generally corresponds to its position along the length of the developing nervous system. The prosencephalon (pros- = “in front”) is the forward-most vesicle, and the term can be loosely translated to mean forebrain. The mesencephalon (mes- = “middle”) is the next vesicle, which can be called the midbrain. The third vesicle at this stage is the rhombencephalon. The first part of this word is also the root of the word rhombus, which is a geometrical figure with four sides of equal length (a square is a rhombus with 90° angles). Whereas prosencephalon and mesencephalon translate into the English words forebrain and midbrain, there is not a word for “four-sided-figure-brain.” However, the third vesicle can be called the hindbrain. One way of thinking about how the brain is arranged is to use these three regions—forebrain, midbrain, and hindbrain—which are based on the primary vesicle stage of development (Figure 13.3a). Secondary Vesicles The brain continues to develop, and the vesicles differentiate further (see Figure 13.3b). The three primary vesicles become five secondary vesicles. The prosencephalon enlarges into two new vesicles called the telencephalon and the diencephalon. The telecephalon will become the cerebrum. The diencephalon gives rise to several adult structures; two that will be important are the thalamus and the hypothalamus. In the embryonic diencephalon, a structure known as the eye cup develops, which will eventually become the retina, the nervous tissue of the eye called the retina. This is a rare example of nervous tissue developing as part of the CNS structures in the embryo, but becoming a peripheral structure in the fully formed nervous system. The mesencephalon does not differentiate into any finer divisions. The midbrain is an established region of the brain at the primary vesicle stage of development and remains that way. The rest of the brain develops around it and constitutes a large percentage of the mass of the brain. Dividing the brain into forebrain, midbrain, and hindbrain is useful in considering its developmental pattern, but the midbrain is a small proportion of the entire brain, relatively speaking. The rhombencephalon develops into the metencephalon and myelencephalon. The metencephalon corresponds to the adult structure known as the pons and also gives rise to the cerebellum. The cerebellum (from the Latin meaning “little brain”) accounts for about 10 percent of the mass of the brain and is an important structure in itself. The most significant connection between the cerebellum and the rest of the brain is at the pons, because the pons and cerebellum develop out of the same vesicle. The myelencephalon corresponds to the adult structure known as the medulla oblongata. The structures that come from the mesencephalon and rhombencephalon, except for the cerebellum, are collectively considered the brain stem, which specifically includes the midbrain, pons, and medulla. Figure 13.3 Primary and Secondary Vesicle Stages of Development The embryonic brain develops complexity through enlargements of the neural tube called vesicles; (a) The primary vesicle stage has three regions, and (b) the secondary vesicle stage has five regions. INTERACTIVE LINK Watch this animation to examine the development of the brain, starting with the neural tube. As the anterior end of the neural tube develops, it enlarges into the primary vesicles that establish the forebrain, midbrain, and hindbrain. Those structures continue to develop throughout the rest of embryonic development and into adolescence. They are the basis of the structure of the fully developed adult brain. How would you describe the difference in the relative sizes of the three regions of the brain when comparing the early (25th embryonic day) brain and the adult brain? Spinal Cord Development While the brain is developing from the anterior neural tube, the spinal cord is developing from the posterior neural tube. However, its structure does not differ from the basic layout of the neural tube. It is a long, straight cord with a small, hollow space down the center. The neural tube is defined in terms of its anterior versus posterior portions, but it also has a dorsal–ventral dimension. As the neural tube separates from the rest of the ectoderm, the side closest to the surface is dorsal, and the deeper side is ventral. As the spinal cord develops, the cells making up the wall of the neural tube proliferate and differentiate into the neurons and glia of the spinal cord. The dorsal tissues will be associated with sensory functions, and the ventral tissues will be associated with motor functions. Relating Embryonic Development to the Adult Brain Embryonic development can help in understanding the structure of the adult brain because it establishes a framework on which more complex structures can be built. First, the neural tube establishes the anterior–posterior dimension of the nervous system, which is called the neuraxis. The embryonic nervous system in mammals can be said to have a standard arrangement. Humans (and other primates, to some degree) make this complicated by standing up and walking on two legs. The anterior–posterior dimension of the neuraxis overlays the superior–inferior dimension of the body. However, there is a major curve between the brain stem and forebrain, which is called the cephalic flexure. Because of this, the neuraxis starts in an inferior position—the end of the spinal cord—and ends in an anterior position, the front of the cerebrum. If this is confusing, just imagine a four-legged animal standing up on two legs. Without the flexure in the brain stem, and at the top of the neck, that animal would be looking straight up instead of straight in front (Figure 13.4). Figure 13.4 Human Neuraxis The mammalian nervous system is arranged with the neural tube running along an anterior to posterior axis, from nose to tail for a four-legged animal like a dog. Humans, as two-legged animals, have a bend in the neuraxis between the brain stem and the diencephalon, along with a bend in the neck, so that the eyes and the face are oriented forward. In summary, the primary vesicles help to establish the basic regions of the nervous system: forebrain, midbrain, and hindbrain. These divisions are useful in certain situations, but they are not equivalent regions. The midbrain is small compared with the hindbrain and particularly the forebrain. The secondary vesicles go on to establish the major regions of the adult nervous system that will be followed in this text. The telencephalon is the cerebrum, which is the major portion of the human brain. The diencephalon continues to be referred to by this Greek name, because there is no better term for it (dia- = “through”). The diencephalon is between the cerebrum and the rest of the nervous system and can be described as the region through which all projections have to pass between the cerebrum and everything else. The brain stem includes the midbrain, pons, and medulla, which correspond to the mesencephalon, metencephalon, and myelencephalon. The cerebellum, being a large portion of the brain, is considered a separate region. Table 13.1 connects the different stages of development to the adult structures of the CNS. One other benefit of considering embryonic development is that certain connections are more obvious because of how these adult structures are related. The retina, which began as part of the diencephalon, is primarily connected to the diencephalon. The eyes are just inferior to the anterior-most part of the cerebrum, but the optic nerve extends back to the thalamus as the optic tract, with branches into a region of the hypothalamus. There is also a connection of the optic tract to the midbrain, but the mesencephalon is adjacent to the diencephalon, so that is not difficult to imagine. The cerebellum originates out of the metencephalon, and its largest white matter connection is to the pons, also from the metencephalon. There are connections between the cerebellum and both the medulla and midbrain, which are adjacent structures in the secondary vesicle stage of development. In the adult brain, the cerebellum seems close to the cerebrum, but there is no direct connection between them. Another aspect of the adult CNS structures that relates to embryonic development is the ventricles—open spaces within the CNS where cerebrospinal fluid circulates. They are the remnant of the hollow center of the neural tube. The four ventricles and the tubular spaces associated with them can be linked back to the hollow center of the embryonic brain (see Table 13.1). Stages of Embryonic Development \| Neural tube \| Primary vesicle stage \| Secondary vesicle stage \| Adult structures \| Ventricles \| \|---\|---\|---\|---\|---\| \| Anterior neural tube \| Prosencephalon \| Telencephalon \| Cerebrum \| Lateral ventricles \| \| Anterior neural tube \| Prosencephalon \| Diencephalon \| Diencephalon \| Third ventricle \| \| Anterior neural tube \| Mesencephalon \| Mesencephalon \| Midbrain \| Cerebral aqueduct \| \| Anterior neural tube \| Rhombencephalon \| Metencephalon \| Pons cerebellum \| Fourth ventricle \| \| Anterior neural tube \| Rhombencephalon \| Myelencephalon \| Medulla \| Fourth ventricle \| \| Posterior neural tube \| Spinal cord \| Central canal \| Table 13.1 DISORDERS OF THE... Nervous System Early formation of the nervous system depends on the formation of the neural tube. A groove forms along the dorsal surface of the embryo, which becomes deeper until its edges meet and close off to form the tube. If this fails to happen, especially in the posterior region where the spinal cord forms, a developmental defect called spina bifida occurs. The closing of the neural tube is important for more than just the proper formation of the nervous system. The surrounding tissues are dependent on the correct development of the tube. The connective tissues surrounding the CNS can be involved as well. There are three classes of this disorder: occulta, meningocele, and myelomeningocele (Figure 13.5). The first type, spina bifida occulta, is the mildest because the vertebral bones do not fully surround the spinal cord, but the spinal cord itself is not affected. No functional differences may be noticed, which is what the word occulta means; it is hidden spina bifida. The other two types both involve the formation of a cyst—a fluid-filled sac of the connective tissues that cover the spinal cord called the meninges. “Meningocele” means that the meninges protrude through the spinal column but nerves may not be involved and few symptoms are present, though complications may arise later in life. “Myelomeningocele” means that the meninges protrude and spinal nerves are involved, and therefore severe neurological symptoms can be present. Often surgery to close the opening or to remove the cyst is necessary. The earlier that surgery can be performed, the better the chances of controlling or limiting further damage or infection at the opening. For many children with meningocele, surgery will alleviate the pain, although they may experience some functional loss. Because the myelomeningocele form of spina bifida involves more extensive damage to the nervous tissue, neurological damage may persist, but symptoms can often be handled. Complications of the spinal cord may present later in life, but overall life expectancy is not reduced. Figure 13.5 Spinal Bifida (a) Spina bifida is a birth defect of the spinal cord caused when the neural tube does not completely close, but the rest of development continues. The result is the emergence of meninges and neural tissue through the vertebral column. (b) Fetal myelomeningocele is evident in this ultrasound taken at 21 weeks. INTERACTIVE LINK Watch this video to learn about the white matter in the cerebrum that develops during childhood and adolescence. This is a composite of MRI images taken of the brains of people from 5 years of age through 20 years of age, demonstrating how the cerebrum changes. As the color changes to blue, the ratio of gray matter to white matter changes. The caption for the video describes it as “less gray matter,” which is another way of saying “more white matter.” If the brain does not finish developing until approximately 20 years of age, can teenagers be held responsible for behaving badly? The Central Nervous System - Name the major regions of the adult brain - Describe the connections between the cerebrum and brain stem through the diencephalon, and from those regions into the spinal cord - Recognize the complex connections within the subcortical structures of the basal nuclei - Explain the arrangement of gray and white matter in the spinal cord The brain and the spinal cord are the central nervous system, and they represent the main organs of the nervous system. The spinal cord is a single structure, whereas the adult brain is described in terms of four major regions: the cerebrum, the diencephalon, the brain stem, and the cerebellum. A person’s conscious experiences are based on neural activity in the brain. The regulation of homeostasis is governed by a specialized region in the brain. The coordination of reflexes depends on the integration of sensory and motor pathways in the spinal cord. The Cerebrum The iconic gray mantle of the human brain, which appears to make up most of the mass of the brain, is the cerebrum (Figure 13.6). The wrinkled portion is the cerebral cortex, and the rest of the structure is beneath that outer covering. There is a large separation between the two sides of the cerebrum called the longitudinal fissure. It separates the cerebrum into two distinct halves, a right and left cerebral hemisphere. Deep within the cerebrum, the white matter of the corpus callosum provides the major pathway for communication between the two hemispheres of the cerebral cortex. Figure 13.6 The Cerebrum The cerebrum is a large component of the CNS in humans, and the most obvious aspect of it is the folded surface called the cerebral cortex. Many of the higher neurological functions, such as memory, emotion, and consciousness, are the result of cerebral function. The complexity of the cerebrum is different across vertebrate species. The cerebrum of the most primitive vertebrates is not much more than the connection for the sense of smell. In mammals, the cerebrum comprises the outer gray matter that is the cortex (from the Latin word meaning “bark of a tree”) and several deep nuclei that belong to three important functional groups. The basal nuclei are responsible for cognitive processing, the most important function being that associated with planning movements. The basal forebrain contains nuclei that are important in learning and memory. The limbic cortex is the region of the cerebral cortex that is part of the limbic system, a collection of structures involved in emotion, memory, and behavior. Cerebral Cortex The cerebrum is covered by a continuous layer of gray matter that wraps around either side of the forebrain—the cerebral cortex. This thin, extensive region of wrinkled gray matter is responsible for the higher functions of the nervous system. A gyrus(plural = gyri) is the ridge of one of those wrinkles, and a sulcus (plural = sulci) is the groove between two gyri. The pattern of these folds of tissue indicates specific regions of the cerebral cortex. The head is limited by the size of the birth canal, and the brain must fit inside the cranial cavity of the skull. Extensive folding in the cerebral cortex enables more gray matter to fit into this limited space. If the gray matter of the cortex were peeled off of the cerebrum and laid out flat, its surface area would be roughly equal to one square meter. The folding of the cortex maximizes the amount of gray matter in the cranial cavity. During embryonic development, as the telencephalon expands within the skull, the brain goes through a regular course of growth that results in everyone’s brain having a similar pattern of folds. The surface of the brain can be mapped on the basis of the locations of large gyri and sulci. Using these landmarks, the cortex can be separated into four major regions, or lobes (Figure 13.7). The lateral sulcus that separates the temporal lobe from the other regions is one such landmark. Superior to the lateral sulcus are the parietal lobe and frontal lobe, which are separated from each other by the central sulcus. The posterior region of the cortex is the occipital lobe, which has no obvious anatomical border between it and the parietal or temporal lobes on the lateral surface of the brain. From the medial surface, an obvious landmark separating the parietal and occipital lobes is called the parieto-occipital sulcus. The fact that there is no obvious anatomical border between these lobes is consistent with the functions of these regions being interrelated. Figure 13.7 Lobes of the Cerebral Cortex The cerebral cortex is divided into four lobes. Extensive folding increases the surface area available for cerebral functions. Different regions of the cerebral cortex can be associated with particular functions, a concept known as localization of function. In the early 1900s, a German neuroscientist named Korbinian Brodmann performed an extensive study of the microscopic anatomy—the cytoarchitecture—of the cerebral cortex and divided the cortex into 52 separate regions on the basis of the histology of the cortex. His work resulted in a system of classification known as Brodmann’s areas, which is still used today to describe the anatomical distinctions within the cortex (Figure 13.8). The results from Brodmann’s work on the anatomy align very well with the functional differences within the cortex. Areas 17 and 18 in the occipital lobe are responsible for primary visual perception. That visual information is complex, so it is processed in the temporal and parietal lobes as well. The temporal lobe is associated with primary auditory sensation, known as Brodmann’s areas 41 and 42 in the superior temporal lobe. Because regions of the temporal lobe are part of the limbic system, memory is an important function associated with that lobe. Memory is essentially a sensory function; memories are recalled sensations such as the smell of Mom’s baking or the sound of a barking dog. Even memories of movement are really the memory of sensory feedback from those movements, such as stretching muscles or the movement of the skin around a joint. Structures in the temporal lobe are responsible for establishing long-term memory, but the ultimate location of those memories is usually in the region in which the sensory perception was processed. The main sensation associated with the parietal lobe is somatosensation, meaning the general sensations associated with the body. Posterior to the central sulcus is the postcentral gyrus, the primary somatosensory cortex, which is identified as Brodmann’s areas 1, 2, and 3. All of the tactile senses are processed in this area, including touch, pressure, tickle, pain, itch, and vibration, as well as more general senses of the body such as proprioception and kinesthesia, which are the senses of body position and movement, respectively. Anterior to the central sulcus is the frontal lobe, which is primarily associated with motor functions. The precentral gyrus is the primary motor cortex. Cells from this region of the cerebral cortex are the upper motor neurons that instruct cells in the spinal cord to move skeletal muscles. Anterior to this region are a few areas that are associated with planned movements. The premotor area is responsible for thinking of a movement to be made. The frontal eye fields are important in eliciting eye movements and in attending to visual stimuli. Broca’s area is responsible for the production of language, or controlling movements responsible for speech; in the vast majority of people, it is located only on the left side. Anterior to these regions is the prefrontal lobe, which serves cognitive functions that can be the basis of personality, short-term memory, and consciousness. The prefrontal lobotomy is an outdated mode of treatment for personality disorders (psychiatric conditions) that profoundly affected the personality of the patient. Figure 13.8 Brodmann's Areas of the Cerebral Cortex Brodmann mapping of functionally distinct regions of the cortex was based on its cytoarchitecture at a microscopic level. Subcortical structures Beneath the cerebral cortex are sets of nuclei known as subcortical nuclei that augment cortical processes. The nuclei of the basal forebrain serve as the primary location for acetylcholine production, which modulates the overall activity of the cortex, possibly leading to greater attention to sensory stimuli. Alzheimer’s disease is associated with a loss of neurons in the basal forebrain. The hippocampus and amygdala are medial-lobe structures that, along with the adjacent cortex, are involved in long-term memory formation and emotional responses. The basal nuclei are a set of nuclei in the cerebrum responsible for comparing cortical processing with the general state of activity in the nervous system to influence the likelihood of movement taking place. For example, while a student is sitting in a classroom listening to a lecture, the basal nuclei will keep the urge to jump up and scream from actually happening. (The basal nuclei are also referred to as the basal ganglia, although that is potentially confusing because the term ganglia is typically used for peripheral structures.) The major structures of the basal nuclei that control movement are the caudate, putamen, and globus pallidus, which are located deep in the cerebrum. The caudate is a long nucleus that follows the basic C-shape of the cerebrum from the frontal lobe, through the parietal and occipital lobes, into the temporal lobe. The putamen is mostly deep in the anterior regions of the frontal and parietal lobes. Together, the caudate and putamen are called the striatum. The globus pallidus is a layered nucleus that lies just medial to the putamen; they are called the lenticular nuclei because they look like curved pieces fitting together like lenses. The globus pallidus has two subdivisions, the external and internal segments, which are lateral and medial, respectively. These nuclei are depicted in a frontal section of the brain in Figure 13.9. Figure 13.9 Frontal Section of Cerebral Cortex and Basal Nuclei The major components of the basal nuclei, shown in a frontal section of the brain, are the caudate (just lateral to the lateral ventricle), the putamen (inferior to the caudate and separated by the large white-matter structure called the internal capsule), and the globus pallidus (medial to the putamen). The basal nuclei in the cerebrum are connected with a few more nuclei in the brain stem that together act as a functional group that forms a motor pathway. Two streams of information processing take place in the basal nuclei. All input to the basal nuclei is from the cortex into the striatum (Figure 13.10). The direct pathway is the projection of axons from the striatum to the globus pallidus internal segment (GPi) and the substantia nigra pars reticulata (SNr). The GPi/SNr then projects to the thalamus, which projects back to the cortex. The indirect pathway is the projection of axons from the striatum to the globus pallidus external segment (GPe), then to the subthalamic nucleus (STN), and finally to GPi/SNr. The two streams both target the GPi/SNr, but one has a direct projection and the other goes through a few intervening nuclei. The direct pathway causes the disinhibitionof the thalamus (inhibition of one cell on a target cell that then inhibits the first cell), whereas the indirect pathway causes, or reinforces, the normal inhibition of the thalamus. The thalamus then can either excite the cortex (as a result of the direct pathway) or fail to excite the cortex (as a result of the indirect pathway). Figure 13.10 Connections of Basal Nuclei Input to the basal nuclei is from the cerebral cortex, which is an excitatory connection releasing glutamate as a neurotransmitter. This input is to the striatum, or the caudate and putamen. In the direct pathway, the striatum projects to the internal segment of the globus pallidus and the substantia nigra pars reticulata (GPi/SNr). This is an inhibitory pathway, in which GABA is released at the synapse, and the target cells are hyperpolarized and less likely to fire. The output from the basal nuclei is to the thalamus, which is an inhibitory projection using GABA. The switch between the two pathways is the substantia nigra pars compacta, which projects to the striatum and releases the neurotransmitter dopamine. Dopamine receptors are either excitatory (D1-type receptors) or inhibitory (D2-type receptors). The direct pathway is activated by dopamine, and the indirect pathway is inhibited by dopamine. When the substantia nigra pars compacta is firing, it signals to the basal nuclei that the body is in an active state, and movement will be more likely. When the substantia nigra pars compacta is silent, the body is in a passive state, and movement is inhibited. To illustrate this situation, while a student is sitting listening to a lecture, the substantia nigra pars compacta would be silent and the student less likely to get up and walk around. Likewise, while the professor is lecturing, and walking around at the front of the classroom, the professor’s substantia nigra pars compacta would be active, in keeping with his or her activity level. INTERACTIVE LINK Watch this video to learn about the basal nuclei (also known as the basal ganglia), which have two pathways that process information within the cerebrum. As shown in this video, the direct pathway is the shorter pathway through the system that results in increased activity in the cerebral cortex and increased motor activity. The direct pathway is described as resulting in “disinhibition” of the thalamus. What does disinhibition mean? What are the two neurons doing individually to cause this? INTERACTIVE LINK Watch this video to learn about the basal nuclei (also known as the basal ganglia), which have two pathways that process information within the cerebrum. As shown in this video, the indirect pathway is the longer pathway through the system that results in decreased activity in the cerebral cortex, and therefore less motor activity. The indirect pathway has an extra couple of connections in it, including disinhibition of the subthalamic nucleus. What is the end result on the thalamus, and therefore on movement initiated by the cerebral cortex? EVERYDAY CONNECTION The Myth of Left Brain/Right Brain There is a persistent myth that people are “right-brained” or “left-brained,” which is an oversimplification of an important concept about the cerebral hemispheres. There is some lateralization of function, in which the left side of the brain is devoted to language function and the right side is devoted to spatial and nonverbal reasoning. Whereas these functions are predominantly associated with those sides of the brain, there is no monopoly by either side on these functions. Many pervasive functions, such as language, are distributed globally around the cerebrum. Some of the support for this misconception has come from studies of split brains. A drastic way to deal with a rare and devastating neurological condition (intractable epilepsy) is to separate the two hemispheres of the brain. After sectioning the corpus callosum, a split-brained patient will have trouble producing verbal responses on the basis of sensory information processed on the right side of the cerebrum, leading to the idea that the left side is responsible for language function. However, there are well-documented cases of language functions lost from damage to the right side of the brain. The deficits seen in damage to the left side of the brain are classified as aphasia, a loss of speech function; damage on the right side can affect the use of language. Right-side damage can result in a loss of ability to understand figurative aspects of speech, such as jokes, irony, or metaphors. Nonverbal aspects of speech can be affected by damage to the right side, such as facial expression or body language, and right-side damage can lead to a “flat affect” in speech, or a loss of emotional expression in speech—sounding like a robot when talking. The Diencephalon The diencephalon is the one region of the adult brain that retains its name from embryologic development. The etymology of the word diencephalon translates to “through brain.” It is the connection between the cerebrum and the rest of the nervous system, with one exception. The rest of the brain, the spinal cord, and the PNS all send information to the cerebrum through the diencephalon. Output from the cerebrum passes through the diencephalon. The single exception is the system associated with olfaction, or the sense of smell, which connects directly with the cerebrum. In the earliest vertebrate species, the cerebrum was not much more than olfactory bulbs that received peripheral information about the chemical environment (to call it smell in these organisms is imprecise because they lived in the ocean). The diencephalon is deep beneath the cerebrum and constitutes the walls of the third ventricle. The diencephalon can be described as any region of the brain with “thalamus” in its name. The two major regions of the diencephalon are the thalamus itself and the hypothalamus (Figure 13.11). There are other structures, such as the epithalamus, which contains the pineal gland, or the subthalamus, which includes the subthalamic nucleus that is part of the basal nuclei. Thalamus The thalamus is a collection of nuclei that relay information between the cerebral cortex and the periphery, spinal cord, or brain stem. All sensory information, except for the sense of smell, passes through the thalamus before processing by the cortex. Axons from the peripheral sensory organs, or intermediate nuclei, synapse in the thalamus, and thalamic neurons project directly to the cerebrum. It is a requisite synapse in any sensory pathway, except for olfaction. The thalamus does not just pass the information on, it also processes that information. For example, the portion of the thalamus that receives visual information will influence what visual stimuli are important, or what receives attention. The cerebrum also sends information down to the thalamus, which usually communicates motor commands. This involves interactions with the cerebellum and other nuclei in the brain stem. The cerebrum interacts with the basal nuclei, which involves connections with the thalamus. The primary output of the basal nuclei is to the thalamus, which relays that output to the cerebral cortex. The cortex also sends information to the thalamus that will then influence the effects of the basal nuclei. Hypothalamus Inferior and slightly anterior to the thalamus is the hypothalamus, the other major region of the diencephalon. The hypothalamus is a collection of nuclei that are largely involved in regulating homeostasis. The hypothalamus is the executive region in charge of the autonomic nervous system and the endocrine system through its regulation of the anterior pituitary gland. Other parts of the hypothalamus are involved in memory and emotion as part of the limbic system. Figure 13.11 The Diencephalon The diencephalon is composed primarily of the thalamus and hypothalamus, which together define the walls of the third ventricle. The thalami are two elongated, ovoid structures on either side of the midline that make contact in the middle. The hypothalamus is inferior and anterior to the thalamus, culminating in a sharp angle to which the pituitary gland is attached. Brain Stem The midbrain and hindbrain (composed of the pons and the medulla) are collectively referred to as the brain stem (Figure 13.12). The structure emerges from the ventral surface of the forebrain as a tapering cone that connects the brain to the spinal cord. Attached to the brain stem, but considered a separate region of the adult brain, is the cerebellum. The midbrain coordinates sensory representations of the visual, auditory, and somatosensory perceptual spaces. The pons is the main connection with the cerebellum. The pons and the medulla regulate several crucial functions, including the cardiovascular and respiratory systems and rates. The cranial nerves connect through the brain stem and provide the brain with the sensory input and motor output associated with the head and neck, including most of the special senses. The major ascending and descending pathways between the spinal cord and brain, specifically the cerebrum, pass through the brain stem. Figure 13.12 The Brain Stem The brain stem comprises three regions: the midbrain, the pons, and the medulla. Midbrain One of the original regions of the embryonic brain, the midbrain is a small region between the thalamus and pons. It is separated into the tectum and tegmentum, from the Latin words for roof and floor, respectively. The cerebral aqueduct passes through the center of the midbrain, such that these regions are the roof and floor of that canal. The tectum is composed of four bumps known as the colliculi (singular = colliculus), which means “little hill” in Latin. The inferior colliculus is the inferior pair of these enlargements and is part of the auditory brain stem pathway. Neurons of the inferior colliculus project to the thalamus, which then sends auditory information to the cerebrum for the conscious perception of sound. The superior colliculus is the superior pair and combines sensory information about visual space, auditory space, and somatosensory space. Activity in the superior colliculus is related to orienting the eyes to a sound or touch stimulus. If you are walking along the sidewalk on campus and you hear chirping, the superior colliculus coordinates that information with your awareness of the visual location of the tree right above you. That is the correlation of auditory and visual maps. If you suddenly feel something wet fall on your head, your superior colliculus integrates that with the auditory and visual maps and you know that the chirping bird just relieved itself on you. You want to look up to see the culprit, but do not. The tegmentum is continuous with the gray matter of the rest of the brain stem. Throughout the midbrain, pons, and medulla, the tegmentum contains the nuclei that receive and send information through the cranial nerves, as well as regions that regulate important functions such as those of the cardiovascular and respiratory systems. Pons The word pons comes from the Latin word for bridge. It is visible on the anterior surface of the brain stem as the thick bundle of white matter attached to the cerebellum. The pons is the main connection between the cerebellum and the brain stem. The bridge-like white matter is only the anterior surface of the pons; the gray matter beneath that is a continuation of the tegmentum from the midbrain. Gray matter in the tegmentum region of the pons contains neurons receiving descending input from the forebrain that is sent to the cerebellum. Medulla The medulla is the region known as the myelencephalon in the embryonic brain. The initial portion of the name, “myel,” refers to the significant white matter found in this region—especially on its exterior, which is continuous with the white matter of the spinal cord. The tegmentum of the midbrain and pons continues into the medulla because this gray matter is responsible for processing cranial nerve information. A diffuse region of gray matter throughout the brain stem, known as the reticular formation, is related to sleep and wakefulness, such as general brain activity and attention. The Cerebellum The cerebellum, as the name suggests, is the “little brain.” It is covered in gyri and sulci like the cerebrum, and looks like a miniature version of that part of the brain (Figure 13.13). The cerebellum is largely responsible for comparing information from the cerebrum with sensory feedback from the periphery through the spinal cord. It accounts for approximately 10 percent of the mass of the brain. Figure 13.13 The Cerebellum The cerebellum is situated on the posterior surface of the brain stem. Descending input from the cerebellum enters through the large white matter structure of the pons. Ascending input from the periphery and spinal cord enters through the fibers of the inferior olive. Output goes to the midbrain, which sends a descending signal to the spinal cord. Descending fibers from the cerebrum have branches that connect to neurons in the pons. Those neurons project into the cerebellum, providing a copy of motor commands sent to the spinal cord. Sensory information from the periphery, which enters through spinal or cranial nerves, is copied to a nucleus in the medulla known as the inferior olive. Fibers from this nucleus enter the cerebellum and are compared with the descending commands from the cerebrum. If the primary motor cortex of the frontal lobe sends a command down to the spinal cord to initiate walking, a copy of that instruction is sent to the cerebellum. Sensory feedback from the muscles and joints, proprioceptive information about the movements of walking, and sensations of balance are sent to the cerebellum through the inferior olive and the cerebellum compares them. If walking is not coordinated, perhaps because the ground is uneven or a strong wind is blowing, then the cerebellum sends out a corrective command to compensate for the difference between the original cortical command and the sensory feedback. The output of the cerebellum is into the midbrain, which then sends a descending input to the spinal cord to correct the messages going to skeletal muscles. The Spinal Cord The description of the CNS is concentrated on the structures of the brain, but the spinal cord is another major organ of the system. Whereas the brain develops out of expansions of the neural tube into primary and then secondary vesicles, the spinal cord maintains the tube structure and is only specialized into certain regions. As the spinal cord continues to develop in the newborn, anatomical features mark its surface. The anterior midline is marked by the anterior median fissure, and the posterior midline is marked by the posterior median sulcus. Axons enter the posterior side through the dorsal (posterior) nerve root, which marks the posterolateral sulcus on either side. The axons emerging from the anterior side do so through the ventral (anterior) nerve root. Note that it is common to see the terms dorsal (dorsal = “back”) and ventral (ventral = “belly”) used interchangeably with posterior and anterior, particularly in reference to nerves and the structures of the spinal cord. You should learn to be comfortable with both. On the whole, the posterior regions are responsible for sensory functions and the anterior regions are associated with motor functions. This comes from the initial development of the spinal cord, which is divided into the basal plate and the alar plate. The basal plate is closest to the ventral midline of the neural tube, which will become the anterior face of the spinal cord and gives rise to motor neurons. The alar plate is on the dorsal side of the neural tube and gives rise to neurons that will receive sensory input from the periphery. The length of the spinal cord is divided into regions that correspond to the regions of the vertebral column. The name of a spinal cord region corresponds to the level at which spinal nerves pass through the intervertebral foramina. Immediately adjacent to the brain stem is the cervical region, followed by the thoracic, then the lumbar, and finally the sacral region. The spinal cord is not the full length of the vertebral column because the spinal cord does not grow significantly longer after the first or second year, but the skeleton continues to grow. The nerves that emerge from the spinal cord pass through the intervertebral formina at the respective levels. As the vertebral column grows, these nerves grow with it and result in a long bundle of nerves that resembles a horse’s tail and is named the cauda equina. The sacral spinal cord is at the level of the upper lumbar vertebral bones. The spinal nerves extend from their various levels to the proper level of the vertebral column. Gray Horns In cross-section, the gray matter of the spinal cord has the appearance of an ink-blot test, with the spread of the gray matter on one side replicated on the other—a shape reminiscent of a bulbous capital “H.” As shown in Figure 13.14, the gray matter is subdivided into regions that are referred to as horns. The posterior horn is responsible for sensory processing. The anterior horn sends out motor signals to the skeletal muscles. The lateral horn, which is only found in the thoracic, upper lumbar, and sacral regions, is the central component of the sympathetic division of the autonomic nervous system. Some of the largest neurons of the spinal cord are the multipolar motor neurons in the anterior horn. The fibers that cause contraction of skeletal muscles are the axons of these neurons. The motor neuron that causes contraction of the big toe, for example, is located in the sacral spinal cord. The axon that has to reach all the way to the belly of that muscle may be a meter in length. The neuronal cell body that maintains that long fiber must be quite large, possibly several hundred micrometers in diameter, making it one of the largest cells in the body. Figure 13.14 Cross-section of Spinal Cord The cross-section of a thoracic spinal cord segment shows the posterior, anterior, and lateral horns of gray matter, as well as the posterior, anterior, and lateral columns of white matter. LM × 40. (Micrograph provided by the Regents of University of Michigan Medical School © 2012) White Columns Just as the gray matter is separated into horns, the white matter of the spinal cord is separated into columns. Ascending tractsof nervous system fibers in these columns carry sensory information up to the brain, whereas descending tracts carry motor commands from the brain. Looking at the spinal cord longitudinally, the columns extend along its length as continuous bands of white matter. Between the two posterior horns of gray matter are the posterior columns. Between the two anterior horns, and bounded by the axons of motor neurons emerging from that gray matter area, are the anterior columns. The white matter on either side of the spinal cord, between the posterior horn and the axons of the anterior horn neurons, are the lateral columns. The posterior columns are composed of axons of ascending tracts. The anterior and lateral columns are composed of many different groups of axons of both ascending and descending tracts—the latter carrying motor commands down from the brain to the spinal cord to control output to the periphery. INTERACTIVE LINK Watch this video to learn about the gray matter of the spinal cord that receives input from fibers of the dorsal (posterior) root and sends information out through the fibers of the ventral (anterior) root. As discussed in this video, these connections represent the interactions of the CNS with peripheral structures for both sensory and motor functions. The cervical and lumbar spinal cords have enlargements as a result of larger populations of neurons. What are these enlargements responsible for? DISORDERS OF THE... Basal Nuclei Parkinson’s disease is a disorder of the basal nuclei, specifically of the substantia nigra, that demonstrates the effects of the direct and indirect pathways. Parkinson’s disease is the result of neurons in the substantia nigra pars compacta dying. These neurons release dopamine into the striatum. Without that modulatory influence, the basal nuclei are stuck in the indirect pathway, without the direct pathway being activated. The direct pathway is responsible for increasing cortical movement commands. The increased activity of the indirect pathway results in the hypokinetic disorder of Parkinson’s disease. Parkinson’s disease is neurodegenerative, meaning that neurons die that cannot be replaced, so there is no cure for the disorder. Treatments for Parkinson’s disease are aimed at increasing dopamine levels in the striatum. Currently, the most common way of doing that is by providing the amino acid L-DOPA, which is a precursor to the neurotransmitter dopamine and can cross the blood-brain barrier. With levels of the precursor elevated, the remaining cells of the substantia nigra pars compacta can make more neurotransmitter and have a greater effect. Unfortunately, the patient will become less responsive to L-DOPA treatment as time progresses, and it can cause increased dopamine levels elsewhere in the brain, which are associated with psychosis or schizophrenia. INTERACTIVE LINK Visit this site for a thorough explanation of Parkinson’s disease. INTERACTIVE LINK Compared with the nearest evolutionary relative, the chimpanzee, the human has a brain that is huge. At a point in the past, a common ancestor gave rise to the two species of humans and chimpanzees. That evolutionary history is long and is still an area of intense study. But something happened to increase the size of the human brain relative to the chimpanzee. Read this article in which the author explores the current understanding of why this happened. According to one hypothesis about the expansion of brain size, what tissue might have been sacrificed so energy was available to grow our larger brain? Based on what you know about that tissue and nervous tissue, why would there be a trade-off between them in terms of energy use? Circulation and the Central Nervous System - Describe the vessels that supply the CNS with blood - Name the components of the ventricular system and the regions of the brain in which each is located - Explain the production of cerebrospinal fluid and its flow through the ventricles - Explain how a disruption in circulation would result in a stroke The CNS is crucial to the operation of the body, and any compromise in the brain and spinal cord can lead to severe difficulties. The CNS has a privileged blood supply, as suggested by the blood-brain barrier. The function of the tissue in the CNS is crucial to the survival of the organism, so the contents of the blood cannot simply pass into the central nervous tissue. To protect this region from the toxins and pathogens that may be traveling through the blood stream, there is strict control over what can move out of the general systems and into the brain and spinal cord. Because of this privilege, the CNS needs specialized structures for the maintenance of circulation. This begins with a unique arrangement of blood vessels carrying fresh blood into the CNS. Beyond the supply of blood, the CNS filters that blood into cerebrospinal fluid (CSF), which is then circulated through the cavities of the brain and spinal cord called ventricles. Blood Supply to the Brain A lack of oxygen to the CNS can be devastating, and the cardiovascular system has specific regulatory reflexes to ensure that the blood supply is not interrupted. There are multiple routes for blood to get into the CNS, with specializations to protect that blood supply and to maximize the ability of the brain to get an uninterrupted perfusion. Arterial Supply The major artery carrying recently oxygenated blood away from the heart is the aorta. The very first branches off the aorta supply the heart with nutrients and oxygen. The next branches give rise to the common carotid arteries, which further branch into the internal carotid arteries. The external carotid arteries supply blood to the tissues on the surface of the cranium. The bases of the common carotids contain stretch receptors that immediately respond to the drop in blood pressure upon standing. The orthostatic reflex is a reaction to this change in body position, so that blood pressure is maintained against the increasing effect of gravity (orthostatic means “standing up”). Heart rate increases—a reflex of the sympathetic division of the autonomic nervous system—and this raises blood pressure. The internal carotid artery enters the cranium through the carotid canal in the temporal bone. A second set of vessels that supply the CNS are the vertebral arteries, which are protected as they pass through the neck region by the transverse foramina of the cervical vertebrae. The vertebral arteries enter the cranium through the foramen magnum of the occipital bone. Branches off the left and right vertebral arteries merge into the anterior spinal artery supplying the anterior aspect of the spinal cord, found along the anterior median fissure. The two vertebral arteries then merge into the basilar artery, which gives rise to branches to the brain stem and cerebellum. The left and right internal carotid arteries and branches of the basilar artery all become the circle of Willis, a confluence of arteries that can maintain perfusion of the brain even if narrowing or a blockage limits flow through one part (Figure 13.15). Figure 13.15 Circle of Willis The blood supply to the brain enters through the internal carotid arteries and the vertebral arteries, eventually giving rise to the circle of Willis. INTERACTIVE LINK Watch this animation to see how blood flows to the brain and passes through the circle of Willis before being distributed through the cerebrum. The circle of Willis is a specialized arrangement of arteries that ensure constant perfusion of the cerebrum even in the event of a blockage of one of the arteries in the circle. The animation shows the normal direction of flow through the circle of Willis to the middle cerebral artery. Where would the blood come from if there were a blockage just posterior to the middle cerebral artery on the left? Venous Return After passing through the CNS, blood returns to the circulation through a series of dural sinuses and veins (Figure 13.16). The superior sagittal sinus runs in the groove of the longitudinal fissure, where it absorbs CSF from the meninges. The superior sagittal sinus drains to the confluence of sinuses, along with the occipital sinuses and straight sinus, to then drain into the transverse sinuses. The transverse sinuses connect to the sigmoid sinuses, which then connect to the jugular veins. From there, the blood continues toward the heart to be pumped to the lungs for reoxygenation. Figure 13.16 Dural Sinuses and Veins Blood drains from the brain through a series of sinuses that connect to the jugular veins. Protective Coverings of the Brain and Spinal Cord The outer surface of the CNS is covered by a series of membranes composed of connective tissue called the meninges, which protect the brain. The dura mater is a thick fibrous layer and a strong protective sheath over the entire brain and spinal cord. It is anchored to the inner surface of the cranium and vertebral cavity. The arachnoid mater is a membrane of thin fibrous tissue that forms a loose sac around the CNS. Beneath the arachnoid is a thin, filamentous mesh called the arachnoid trabeculae, which looks like a spider web, giving this layer its name. Directly adjacent to the surface of the CNS is the pia mater, a thin fibrous membrane that follows the convolutions of gyri and sulci in the cerebral cortex and fits into other grooves and indentations (Figure 13.17). Figure 13.17 Meningeal Layers of Superior Sagittal Sinus The layers of the meninges in the longitudinal fissure of the superior sagittal sinus are shown, with the dura mater adjacent to the inner surface of the cranium, the pia mater adjacent to the surface of the brain, and the arachnoid and subarachnoid space between them. An arachnoid villus is shown emerging into the dural sinus to allow CSF to filter back into the blood for drainage. Dura Mater Like a thick cap covering the brain, the dura mater is a tough outer covering. The name comes from the Latin for “tough mother” to represent its physically protective role. It encloses the entire CNS and the major blood vessels that enter the cranium and vertebral cavity. It is directly attached to the inner surface of the bones of the cranium and to the very end of the vertebral cavity. There are infoldings of the dura that fit into large crevasses of the brain. Two infoldings go through the midline separations of the cerebrum and cerebellum; one forms a shelf-like tent between the occipital lobes of the cerebrum and the cerebellum, and the other surrounds the pituitary gland. The dura also surrounds and supports the venous sinuses. Arachnoid Mater The middle layer of the meninges is the arachnoid, named for the spider-web–like trabeculae between it and the pia mater. The arachnoid defines a sac-like enclosure around the CNS. The trabeculae are found in the subarachnoid space, which is filled with circulating CSF. The arachnoid emerges into the dural sinuses as the arachnoid granulations, where the CSF is filtered back into the blood for drainage from the nervous system. The subarachnoid space is filled with circulating CSF, which also provides a liquid cushion to the brain and spinal cord. Similar to clinical blood work, a sample of CSF can be withdrawn to find chemical evidence of neuropathology or metabolic traces of the biochemical functions of nervous tissue. Pia Mater The outer surface of the CNS is covered in the thin fibrous membrane of the pia mater. It is thought to have a continuous layer of cells providing a fluid-impermeable membrane. The name pia mater comes from the Latin for “tender mother,” suggesting the thin membrane is a gentle covering for the brain. The pia extends into every convolution of the CNS, lining the inside of the sulci in the cerebral and cerebellar cortices. At the end of the spinal cord, a thin filament extends from the inferior end of CNS at the upper lumbar region of the vertebral column to the sacral end of the vertebral column. Because the spinal cord does not extend through the lower lumbar region of the vertebral column, a needle can be inserted through the dura and arachnoid layers to withdraw CSF. This procedure is called a lumbar puncture and avoids the risk of damaging the central tissue of the spinal cord. Blood vessels that are nourishing the central nervous tissue are between the pia mater and the nervous tissue. DISORDERS OF THE... Meninges Meningitis is an inflammation of the meninges, the three layers of fibrous membrane that surround the CNS. Meningitis can be caused by infection by bacteria or viruses. The particular pathogens are not special to meningitis; it is just an inflammation of that specific set of tissues from what might be a broader infection. Bacterial meningitis can be caused by Streptococcus, Staphylococcus, or the tuberculosis pathogen, among many others. Viral meningitis is usually the result of common enteroviruses (such as those that cause intestinal disorders), but may be the result of the herpes virus or West Nile virus. Bacterial meningitis tends to be more severe. The symptoms associated with meningitis can be fever, chills, nausea, vomiting, light sensitivity, soreness of the neck, or severe headache. More important are the neurological symptoms, such as changes in mental state (confusion, memory deficits, and other dementia-type symptoms). A serious risk of meningitis can be damage to peripheral structures because of the nerves that pass through the meninges. Hearing loss is a common result of meningitis. The primary test for meningitis is a lumbar puncture. A needle inserted into the lumbar region of the spinal column through the dura mater and arachnoid membrane into the subarachnoid space can be used to withdraw the fluid for chemical testing. Fatality occurs in 5 to 40 percent of children and 20 to 50 percent of adults with bacterial meningitis. Treatment of bacterial meningitis is through antibiotics, but viral meningitis cannot be treated with antibiotics because viruses do not respond to that type of drug. Fortunately, the viral forms are milder. INTERACTIVE LINK Watch this video that describes the procedure known as the lumbar puncture, a medical procedure used to sample the CSF. Because of the anatomy of the CNS, it is a relative safe location to insert a needle. Why is the lumbar puncture performed in the lower lumbar area of the vertebral column? The Ventricular System Cerebrospinal fluid (CSF) circulates throughout and around the CNS. In other tissues, water and small molecules are filtered through capillaries as the major contributor to the interstitial fluid. In the brain, CSF is produced in special structures to perfuse through the nervous tissue of the CNS and is continuous with the interstitial fluid. Specifically, CSF circulates to remove metabolic wastes from the interstitial fluids of nervous tissues and return them to the blood stream. The ventricles are the open spaces within the brain where CSF circulates. In some of these spaces, CSF is produced by filtering of the blood that is performed by a specialized membrane known as a choroid plexus. The CSF circulates through all of the ventricles to eventually emerge into the subarachnoid space where it will be reabsorbed into the blood. The Ventricles There are four ventricles within the brain, all of which developed from the original hollow space within the neural tube, the central canal. The first two are named the lateral ventricles and are deep within the cerebrum. These ventricles are connected to the third ventricle by two openings called the interventricular foramina. The third ventricle is the space between the left and right sides of the diencephalon, which opens into the cerebral aqueduct that passes through the midbrain. The aqueduct opens into the fourth ventricle, which is the space between the cerebellum and the pons and upper medulla (Figure 13.18). Figure 13.18 Cerebrospinal Fluid Circulation The choroid plexus in the four ventricles produce CSF, which is circulated through the ventricular system and then enters the subarachnoid space through the median and lateral apertures. The CSF is then reabsorbed into the blood at the arachnoid granulations, where the arachnoid membrane emerges into the dural sinuses. As the telencephalon enlarges and grows into the cranial cavity, it is limited by the space within the skull. The telencephalon is the most anterior region of what was the neural tube, but cannot grow past the limit of the frontal bone of the skull. Because the cerebrum fits into this space, it takes on a C-shaped formation, through the frontal, parietal, occipital, and finally temporal regions. The space within the telencephalon is stretched into this same C-shape. The two ventricles are in the left and right sides, and were at one time referred to as the first and second ventricles. The interventricular foramina connect the frontal region of the lateral ventricles with the third ventricle. The third ventricle is the space bounded by the medial walls of the hypothalamus and thalamus. The two thalami touch in the center in most brains as the massa intermedia, which is surrounded by the third ventricle. The cerebral aqueduct opens just inferior to the epithalamus and passes through the midbrain. The tectum and tegmentum of the midbrain are the roof and floor of the cerebral aqueduct, respectively. The aqueduct opens up into the fourth ventricle. The floor of the fourth ventricle is the dorsal surface of the pons and upper medulla (that gray matter making a continuation of the tegmentum of the midbrain). The fourth ventricle then narrows into the central canal of the spinal cord. The ventricular system opens up to the subarachnoid space from the fourth ventricle. The single median aperture and the pair of lateral apertures connect to the subarachnoid space so that CSF can flow through the ventricles and around the outside of the CNS. Cerebrospinal fluid is produced within the ventricles by a type of specialized membrane called a choroid plexus. Ependymal cells (one of the types of glial cells described in the introduction to the nervous system) surround blood capillaries and filter the blood to make CSF. The fluid is a clear solution with a limited amount of the constituents of blood. It is essentially water, small molecules, and electrolytes. Oxygen and carbon dioxide are dissolved into the CSF, as they are in blood, and can diffuse between the fluid and the nervous tissue. Cerebrospinal Fluid Circulation The choroid plexuses are found in all four ventricles. Observed in dissection, they appear as soft, fuzzy structures that may still be pink, depending on how well the circulatory system is cleared in preparation of the tissue. The CSF is produced from components extracted from the blood, so its flow out of the ventricles is tied to the pulse of cardiovascular circulation. From the lateral ventricles, the CSF flows into the third ventricle, where more CSF is produced, and then through the cerebral aqueduct into the fourth ventricle where even more CSF is produced. A very small amount of CSF is filtered at any one of the plexuses, for a total of about 500 milliliters daily, but it is continuously made and pulses through the ventricular system, keeping the fluid moving. From the fourth ventricle, CSF can continue down the central canal of the spinal cord, but this is essentially a cul-de-sac, so more of the fluid leaves the ventricular system and moves into the subarachnoid space through the median and lateral apertures. Within the subarachnoid space, the CSF flows around all of the CNS, providing two important functions. As with elsewhere in its circulation, the CSF picks up metabolic wastes from the nervous tissue and moves it out of the CNS. It also acts as a liquid cushion for the brain and spinal cord. By surrounding the entire system in the subarachnoid space, it provides a thin buffer around the organs within the strong, protective dura mater. The arachnoid granulations are outpocketings of the arachnoid membrane into the dural sinuses so that CSF can be reabsorbed into the blood, along with the metabolic wastes. From the dural sinuses, blood drains out of the head and neck through the jugular veins, along with the rest of the circulation for blood, to be reoxygenated by the lungs and wastes to be filtered out by the kidneys (Table 13.2). INTERACTIVE LINK Watch this animation that shows the flow of CSF through the brain and spinal cord, and how it originates from the ventricles and then spreads into the space within the meninges, where the fluids then move into the venous sinuses to return to the cardiovascular circulation. What are the structures that produce CSF and where are they found? How are the structures indicated in this animation? Components of CSF Circulation \| Lateral ventricles \| Third ventricle \| Cerebral aqueduct \| Fourth ventricle \| Central canal \| Subarachnoid space \| \| \|---\|---\|---\|---\|---\|---\|---\| \| Location in CNS \| Cerebrum \| Diencephalon \| Midbrain \| Between pons/upper medulla and cerebellum \| Spinal cord \| External to entire CNS \| \| Blood vessel structure \| Choroid plexus \| Choroid plexus \| None \| Choroid plexus \| None \| Arachnoid granulations \| Table 13.2 DISORDERS OF THE... Central Nervous System The supply of blood to the brain is crucial to its ability to perform many functions. Without a steady supply of oxygen, and to a lesser extent glucose, the nervous tissue in the brain cannot keep up its extensive electrical activity. These nutrients get into the brain through the blood, and if blood flow is interrupted, neurological function is compromised. The common name for a disruption of blood supply to the brain is a stroke. It is caused by a blockage to an artery in the brain. The blockage is from some type of embolus: a blood clot, a fat embolus, or an air bubble. When the blood cannot travel through the artery, the surrounding tissue that is deprived starves and dies. Strokes will often result in the loss of very specific functions. A stroke in the lateral medulla, for example, can cause a loss in the ability to swallow. Sometimes, seemingly unrelated functions will be lost because they are dependent on structures in the same region. Along with the swallowing in the previous example, a stroke in that region could affect sensory functions from the face or extremities because important white matter pathways also pass through the lateral medulla. Loss of blood flow to specific regions of the cortex can lead to the loss of specific higher functions, from the ability to recognize faces to the ability to move a particular region of the body. Severe or limited memory loss can be the result of a temporal lobe stroke. Related to strokes are transient ischemic attacks (TIAs), which can also be called “mini-strokes.” These are events in which a physical blockage may be temporary, cutting off the blood supply and oxygen to a region, but not to the extent that it causes cell death in that region. While the neurons in that area are recovering from the event, neurological function may be lost. Function can return if the area is able to recover from the event. Recovery from a stroke (or TIA) is strongly dependent on the speed of treatment. Often, the person who is present and notices something is wrong must then make a decision. The mnemonic FAST helps people remember what to look for when someone is dealing with sudden losses of neurological function. If someone complains of feeling “funny,” check these things quickly: Look at the person’s face. Does he or she have problems moving Face muscles and making regular facial expressions? Ask the person to raise his or her Arms above the head. Can the person lift one arm but not the other? Has the person’s Speech changed? Is he or she slurring words or having trouble saying things? If any of these things have happened, then it is Time to call for help. Sometimes, treatment with blood-thinning drugs can alleviate the problem, and recovery is possible. If the tissue is damaged, the amazing thing about the nervous system is that it is adaptable. With physical, occupational, and speech therapy, victims of strokes can recover, or more accurately relearn, functions. The Peripheral Nervous System - Describe the structures found in the PNS - Distinguish between somatic and autonomic structures, including the special peripheral structures of the enteric nervous system - Name the twelve cranial nerves and explain the functions associated with each - Describe the sensory and motor components of spinal nerves and the plexuses that they pass through The PNS is not as contained as the CNS because it is defined as everything that is not the CNS. Some peripheral structures are incorporated into the other organs of the body. In describing the anatomy of the PNS, it is necessary to describe the common structures, the nerves and the ganglia, as they are found in various parts of the body. Many of the neural structures that are incorporated into other organs are features of the digestive system; these structures are known as the enteric nervous systemand are a special subset of the PNS. Ganglia A ganglion is a group of neuron cell bodies in the periphery. Ganglia can be categorized, for the most part, as either sensory ganglia or autonomic ganglia, referring to their primary functions. The most common type of sensory ganglion is a dorsal (posterior) root ganglion. These ganglia are the cell bodies of neurons with axons that are sensory endings in the periphery, such as in the skin, and that extend into the CNS through the dorsal nerve root. The ganglion is an enlargement of the nerve root. Under microscopic inspection, it can be seen to include the cell bodies of the neurons, as well as bundles of fibers that are the posterior nerve root (Figure 13.19). The cells of the dorsal root ganglion are unipolar cells, classifying them by shape. Also, the small round nuclei of satellite cells can be seen surrounding—as if they were orbiting—the neuron cell bodies. Figure 13.19 Dorsal Root Ganglion The cell bodies of sensory neurons, which are unipolar neurons by shape, are seen in this photomicrograph. Also, the fibrous region is composed of the axons of these neurons that are passing through the ganglion to be part of the dorsal nerve root (tissue source: canine). LM × 40. (Micrograph provided by the Regents of University of Michigan Medical School © 2012) Figure 13.20 Spinal Cord and Root Ganglion The slide includes both a cross-section of the lumbar spinal cord and a section of the dorsal root ganglion (see also Figure 13.19) (tissue source: canine). LM × 1600. (Micrograph provided by the Regents of University of Michigan Medical School © 2012) INTERACTIVE LINK View the University of Michigan WebScope to explore the tissue sample in greater detail. If you zoom in on the dorsal root ganglion, you can see smaller satellite glial cells surrounding the large cell bodies of the sensory neurons. From what structure do satellite cells derive during embryologic development? Another type of sensory ganglion is a cranial nerve ganglion. This is analogous to the dorsal root ganglion, except that it is associated with a cranial nerve instead of a spinal nerve. The roots of cranial nerves are within the cranium, whereas the ganglia are outside the skull. For example, the trigeminal ganglion is superficial to the temporal bone whereas its associated nerve is attached to the mid-pons region of the brain stem. The neurons of cranial nerve ganglia are also unipolar in shape with associated satellite cells. The other major category of ganglia are those of the autonomic nervous system, which is divided into the sympathetic and parasympathetic nervous systems. The sympathetic chain ganglia constitute a row of ganglia along the vertebral column that receive central input from the lateral horn of the thoracic and upper lumbar spinal cord. Superior to the chain ganglia are three paravertebral ganglia in the cervical region. Three other autonomic ganglia that are related to the sympathetic chain are the prevertebral ganglia, which are located outside of the chain but have similar functions. They are referred to as prevertebral because they are anterior to the vertebral column. The neurons of these autonomic ganglia are multipolar in shape, with dendrites radiating out around the cell body where synapses from the spinal cord neurons are made. The neurons of the chain, paravertebral, and prevertebral ganglia then project to organs in the head and neck, thoracic, abdominal, and pelvic cavities to regulate the sympathetic aspect of homeostatic mechanisms. Another group of autonomic ganglia are the terminal ganglia that receive input from cranial nerves or sacral spinal nerves and are responsible for regulating the parasympathetic aspect of homeostatic mechanisms. These two sets of ganglia, sympathetic and parasympathetic, often project to the same organs—one input from the chain ganglia and one input from a terminal ganglion—to regulate the overall function of an organ. For example, the heart receives two inputs such as these; one increases heart rate, and the other decreases it. The terminal ganglia that receive input from cranial nerves are found in the head and neck, as well as the thoracic and upper abdominal cavities, whereas the terminal ganglia that receive sacral input are in the lower abdominal and pelvic cavities. Terminal ganglia below the head and neck are often incorporated into the wall of the target organ as a plexus. A plexus, in a general sense, is a network of fibers or vessels. This can apply to nervous tissue (as in this instance) or structures containing blood vessels (such as a choroid plexus). For example, the enteric plexus is the extensive network of axons and neurons in the wall of the small and large intestines. The enteric plexus is actually part of the enteric nervous system, along with the gastric plexuses and the esophageal plexus. Though the enteric nervous system receives input originating from central neurons of the autonomic nervous system, it does not require CNS input to function. In fact, it operates independently to regulate the digestive system. Nerves Bundles of axons in the PNS are referred to as nerves. These structures in the periphery are different than the central counterpart, called a tract. Nerves are composed of more than just nervous tissue. They have connective tissues invested in their structure, as well as blood vessels supplying the tissues with nourishment. The outer surface of a nerve is a surrounding layer of fibrous connective tissue called the epineurium. Within the nerve, axons are further bundled into fascicles, which are each surrounded by their own layer of fibrous connective tissue called perineurium. Finally, individual axons are surrounded by loose connective tissue called the endoneurium (Figure 13.21). These three layers are similar to the connective tissue sheaths for muscles. Nerves are associated with the region of the CNS to which they are connected, either as cranial nerves connected to the brain or spinal nerves connected to the spinal cord. Figure 13.21 Nerve Structure The structure of a nerve is organized by the layers of connective tissue on the outside, around each fascicle, and surrounding the individual nerve fibers (tissue source: simian). LM × 40. (Micrograph provided by the Regents of University of Michigan Medical School © 2012) Figure 13.22 Close-Up of Nerve Trunk Zoom in on this slide of a nerve trunk to examine the endoneurium, perineurium, and epineurium in greater detail (tissue source: simian). LM × 1600. (Micrograph provided by the Regents of University of Michigan Medical School © 2012) INTERACTIVE LINK View the University of Michigan WebScope to explore the tissue sample in greater detail. With what structures in a skeletal muscle are the endoneurium, perineurium, and epineurium comparable? Cranial Nerves The nerves attached to the brain are the cranial nerves, which are primarily responsible for the sensory and motor functions of the head and neck (one of these nerves targets organs in the thoracic and abdominal cavities as part of the parasympathetic nervous system). There are twelve cranial nerves, which are designated CNI through CNXII for “Cranial Nerve,” using Roman numerals for 1 through 12. They can be classified as sensory nerves, motor nerves, or a combination of both, meaning that the axons in these nerves originate out of sensory ganglia external to the cranium or motor nuclei within the brain stem. Sensory axons enter the brain to synapse in a nucleus. Motor axons connect to skeletal muscles of the head or neck. Three of the nerves are solely composed of sensory fibers; five are strictly motor; and the remaining four are mixed nerves. Learning the cranial nerves is a tradition in anatomy courses, and students have always used mnemonic devices to remember the nerve names. A traditional mnemonic is the rhyming couplet, “On Old Olympus’ Towering Tops/A Finn And German Viewed Some Hops,” in which the initial letter of each word corresponds to the initial letter in the name of each nerve. The names of the nerves have changed over the years to reflect current usage and more accurate naming. An exercise to help learn this sort of information is to generate a mnemonic using words that have personal significance. The names of the cranial nerves are listed in Table 13.3 along with a brief description of their function, their source (sensory ganglion or motor nucleus), and their target (sensory nucleus or skeletal muscle). They are listed here with a brief explanation of each nerve (Figure 13.23). The olfactory nerve and optic nerve are responsible for the sense of smell and vision, respectively. The oculomotor nerve is responsible for eye movements by controlling four of the extraocular muscles. It is also responsible for lifting the upper eyelid when the eyes point up, and for pupillary constriction. The trochlear nerve and the abducens nerve are both responsible for eye movement, but do so by controlling different extraocular muscles. The trigeminal nerve is responsible for cutaneous sensations of the face and controlling the muscles of mastication. The facial nerve is responsible for the muscles involved in facial expressions, as well as part of the sense of taste and the production of saliva. The vestibulocochlear nerve is responsible for the senses of hearing and balance. The glossopharyngeal nerve is responsible for controlling muscles in the oral cavity and upper throat, as well as part of the sense of taste and the production of saliva. The vagus nerve is responsible for contributing to homeostatic control of the organs of the thoracic and upper abdominal cavities. The spinal accessory nerveis responsible for controlling the muscles of the neck, along with cervical spinal nerves. The hypoglossal nerve is responsible for controlling the muscles of the lower throat and tongue. Figure 13.23 The Cranial Nerves The anatomical arrangement of the roots of the cranial nerves observed from an inferior view of the brain. Three of the cranial nerves also contain autonomic fibers, and a fourth is almost purely a component of the autonomic system. The oculomotor, facial, and glossopharyngeal nerves contain fibers that contact autonomic ganglia. The oculomotor fibers initiate pupillary constriction, whereas the facial and glossopharyngeal fibers both initiate salivation. The vagus nerve primarily targets autonomic ganglia in the thoracic and upper abdominal cavities. INTERACTIVE LINK Visit this site to read about a man who wakes with a headache and a loss of vision. His regular doctor sent him to an ophthalmologist to address the vision loss. The ophthalmologist recognizes a greater problem and immediately sends him to the emergency room. Once there, the patient undergoes a large battery of tests, but a definite cause cannot be found. A specialist recognizes the problem as meningitis, but the question is what caused it originally. How can that be cured? The loss of vision comes from swelling around the optic nerve, which probably presented as a bulge on the inside of the eye. Why is swelling related to meningitis going to push on the optic nerve? Another important aspect of the cranial nerves that lends itself to a mnemonic is the functional role each nerve plays. The nerves fall into one of three basic groups. They are sensory, motor, or both (see Table 13.3). The sentence, “Some Say Marry Money But My Brother Says Brains Beauty Matter More,” corresponds to the basic function of each nerve. The first, second, and eighth nerves are purely sensory: the olfactory (CNI), optic (CNII), and vestibulocochlear (CNVIII) nerves. The three eye-movement nerves are all motor: the oculomotor (CNIII), trochlear (CNIV), and abducens (CNVI). The spinal accessory (CNXI) and hypoglossal (CNXII) nerves are also strictly motor. The remainder of the nerves contain both sensory and motor fibers. They are the trigeminal (CNV), facial (CNVII), glossopharyngeal (CNIX), and vagus (CNX) nerves. The nerves that convey both are often related to each other. The trigeminal and facial nerves both concern the face; one concerns the sensations and the other concerns the muscle movements. The facial and glossopharyngeal nerves are both responsible for conveying gustatory, or taste, sensations as well as controlling salivary glands. The vagus nerve is involved in visceral responses to taste, namely the gag reflex. This is not an exhaustive list of what these combination nerves do, but there is a thread of relation between them. Cranial Nerves \| Mnemonic \| # \| Name \| Function (S/M/B) \| Central connection (nuclei) \| Peripheral connection (ganglion or muscle) \| \|---\|---\|---\|---\|---\|---\| \| On \| I \| Olfactory \| Smell (S) \| Olfactory bulb \| Olfactory epithelium \| \| Old \| II \| Optic \| Vision (S) \| Hypothalamus/thalamus/midbrain \| Retina (retinal ganglion cells) \| \| Olympus’ \| III \| Oculomotor \| Eye movements (M) \| Oculomotor nucleus \| Extraocular muscles (other 4), levator palpebrae superioris, ciliary ganglion (autonomic) \| \| Towering \| IV \| Trochlear \| Eye movements (M) \| Trochlear nucleus \| Superior oblique muscle \| \| Tops \| V \| Trigeminal \| Sensory/motor – face (B) \| Trigeminal nuclei in the midbrain, pons, and medulla \| Trigeminal \| \| A \| VI \| Abducens \| Eye movements (M) \| Abducens nucleus \| Lateral rectus muscle \| \| Finn \| VII \| Facial \| Motor – face, Taste (B) \| Facial nucleus, solitary nucleus, superior salivatory nucleus \| Facial muscles, Geniculate ganglion, Pterygopalatine ganglion (autonomic) \| \| And \| VIII \| Auditory (Vestibulocochlear) \| Hearing/balance (S) \| Cochlear nucleus, Vestibular nucleus/cerebellum \| Spiral ganglion (hearing), Vestibular ganglion (balance) \| \| German \| IX \| Glossopharyngeal \| Motor – throat Taste (B) \| Solitary nucleus, inferior salivatory nucleus, nucleus ambiguus \| Pharyngeal muscles, Geniculate ganglion, Otic ganglion (autonomic) \| \| Viewed \| X \| Vagus \| Motor/sensory – viscera (autonomic) (B) \| Medulla \| Terminal ganglia serving thoracic and upper abdominal organs (heart and small intestines) \| \| Some \| XI \| Spinal Accessory \| Motor – head and neck (M) \| Spinal accessory nucleus \| Neck muscles \| \| Hops \| XII \| Hypoglossal \| Motor – lower throat (M) \| Hypoglossal nucleus \| Muscles of the larynx and lower pharynx \| Table 13.3 Spinal Nerves The nerves connected to the spinal cord are the spinal nerves. The arrangement of these nerves is much more regular than that of the cranial nerves. All of the spinal nerves are combined sensory and motor axons that separate into two nerve roots. The sensory axons enter the spinal cord as the dorsal nerve root. The motor fibers, both somatic and autonomic, emerge as the ventral nerve root. The dorsal root ganglion for each nerve is an enlargement of the spinal nerve. There are 31 spinal nerves, named for the level of the spinal cord at which each one emerges. There are eight pairs of cervical nerves designated C1 to C8, twelve thoracic nerves designated T1 to T12, five pairs of lumbar nerves designated L1 to L5, five pairs of sacral nerves designated S1 to S5, and one pair of coccygeal nerves. The nerves are numbered from the superior to inferior positions, and each emerges from the vertebral column through the intervertebral foramen at its level. The first nerve, C1, emerges between the first cervical vertebra and the occipital bone. The second nerve, C2, emerges between the first and second cervical vertebrae. The same occurs for C3 to C7, but C8 emerges between the seventh cervical vertebra and the first thoracic vertebra. For the thoracic and lumbar nerves, each one emerges between the vertebra that has the same designation and the next vertebra in the column. The sacral nerves emerge from the sacral foramina along the length of that unique vertebra. Spinal nerves extend outward from the vertebral column to enervate the periphery. The nerves in the periphery are not straight continuations of the spinal nerves, but rather the reorganization of the axons in those nerves to follow different courses. Axons from different spinal nerves will come together into a systemic nerve. This occurs at four places along the length of the vertebral column, each identified as a nerve plexus, whereas the other spinal nerves directly correspond to nerves at their respective levels. In this instance, the word plexus is used to describe networks of nerve fibers with no associated cell bodies. Of the four nerve plexuses, two are found at the cervical level, one at the lumbar level, and one at the sacral level (Figure 13.24). The cervical plexus is composed of axons from spinal nerves C1 through C5 and branches into nerves in the posterior neck and head, as well as the phrenic nerve, which connects to the diaphragm at the base of the thoracic cavity. The other plexus from the cervical level is the brachial plexus. Spinal nerves C4 through T1 reorganize through this plexus to give rise to the nerves of the arms, as the name brachial suggests. A large nerve from this plexus is the radial nerve from which the axillary nerve branches to go to the armpit region. The radial nerve continues through the arm and is paralleled by the ulnar nerve and the median nerve. The lumbar plexus arises from all the lumbar spinal nerves and gives rise to nerves enervating the pelvic region and the anterior leg. The femoral nerve is one of the major nerves from this plexus, which gives rise to the saphenous nerve as a branch that extends through the anterior lower leg. The sacral plexus comes from the lower lumbar nerves L4 and L5 and the sacral nerves S1 to S4. The most significant systemic nerve to come from this plexus is the sciatic nerve, which is a combination of the tibial nerve and the fibular nerve. The sciatic nerve extends across the hip joint and is most commonly associated with the condition sciatica, which is the result of compression or irritation of the nerve or any of the spinal nerves giving rise to it. These plexuses are described as arising from spinal nerves and giving rise to certain systemic nerves, but they contain fibers that serve sensory functions or fibers that serve motor functions. This means that some fibers extend from cutaneous or other peripheral sensory surfaces and send action potentials into the CNS. Those are axons of sensory neurons in the dorsal root ganglia that enter the spinal cord through the dorsal nerve root. Other fibers are the axons of motor neurons of the anterior horn of the spinal cord, which emerge in the ventral nerve root and send action potentials to cause skeletal muscles to contract in their target regions. For example, the radial nerve contains fibers of cutaneous sensation in the arm, as well as motor fibers that move muscles in the arm. Spinal nerves of the thoracic region, T2 through T11, are not part of the plexuses but rather emerge and give rise to the intercostal nerves found between the ribs, which articulate with the vertebrae surrounding the spinal nerve. Figure 13.24 Nerve Plexuses of the Body There are four main nerve plexuses in the human body. The cervical plexus supplies nerves to the posterior head and neck, as well as to the diaphragm. The brachial plexus supplies nerves to the arm. The lumbar plexus supplies nerves to the anterior leg. The sacral plexus supplies nerves to the posterior leg. AGING AND THE... Nervous System Anosmia is the loss of the sense of smell. It is often the result of the olfactory nerve being severed, usually because of blunt force trauma to the head. The sensory neurons of the olfactory epithelium have a limited lifespan of approximately one to four months, and new ones are made on a regular basis. The new neurons extend their axons into the CNS by growing along the existing fibers of the olfactory nerve. The ability of these neurons to be replaced is lost with age. Age-related anosmia is not the result of impact trauma to the head, but rather a slow loss of the sensory neurons with no new neurons born to replace them. Smell is an important sense, especially for the enjoyment of food. There are only five tastes sensed by the tongue, and two of them are generally thought of as unpleasant tastes (sour and bitter). The rich sensory experience of food is the result of odor molecules associated with the food, both as food is moved into the mouth, and therefore passes under the nose, and when it is chewed and molecules are released to move up the pharynx into the posterior nasal cavity. Anosmia results in a loss of the enjoyment of food. As the replacement of olfactory neurons declines with age, anosmia can set in. Without the sense of smell, many sufferers complain of food tasting bland. Often, the only way to enjoy food is to add seasoning that can be sensed on the tongue, which usually means adding table salt. The problem with this solution, however, is that this increases sodium intake, which can lead to cardiovascular problems through water retention and the associated increase in blood pressure. Key Terms - abducens nerve - sixth cranial nerve; responsible for contraction of one of the extraocular muscles - alar plate - developmental region of the spinal cord that gives rise to the posterior horn of the gray matter - amygdala - nucleus deep in the temporal lobe of the cerebrum that is related to memory and emotional behavior - anterior column - white matter between the anterior horns of the spinal cord composed of many different groups of axons of both ascending and descending tracts - anterior horn - gray matter of the spinal cord containing multipolar motor neurons, sometimes referred to as the ventral horn - anterior median fissure - deep midline feature of the anterior spinal cord, marking the separation between the right and left sides of the cord - anterior spinal artery - blood vessel from the merged branches of the vertebral arteries that runs along the anterior surface of the spinal cord - arachnoid granulation - outpocket of the arachnoid membrane into the dural sinuses that allows for reabsorption of CSF into the blood - arachnoid mater - middle layer of the meninges named for the spider-web–like trabeculae that extend between it and the pia mater - arachnoid trabeculae - filaments between the arachnoid and pia mater within the subarachnoid space - ascending tract - central nervous system fibers carrying sensory information from the spinal cord or periphery to the brain - axillary nerve - systemic nerve of the arm that arises from the brachial plexus - basal forebrain - nuclei of the cerebrum related to modulation of sensory stimuli and attention through broad projections to the cerebral cortex, loss of which is related to Alzheimer’s disease - basal nuclei - nuclei of the cerebrum (with a few components in the upper brain stem and diencephalon) that are responsible for assessing cortical movement commands and comparing them with the general state of the individual through broad modulatory activity of dopamine neurons; largely related to motor functions, as evidenced through the symptoms of Parkinson’s and Huntington’s diseases - basal plate - developmental region of the spinal cord that gives rise to the lateral and anterior horns of gray matter - basilar artery - blood vessel from the merged vertebral arteries that runs along the dorsal surface of the brain stem - brachial plexus - nerve plexus associated with the lower cervical spinal nerves and first thoracic spinal nerve - brain stem - region of the adult brain that includes the midbrain, pons, and medulla oblongata and develops from the mesencephalon, metencephalon, and myelencephalon of the embryonic brain - Broca’s area - region of the frontal lobe associated with the motor commands necessary for speech production and located only in the cerebral hemisphere responsible for language production, which is the left side in approximately 95 percent of the population - Brodmann’s areas - mapping of regions of the cerebral cortex based on microscopic anatomy that relates specific areas to functional differences, as described by Brodmann in the early 1900s - carotid canal - opening in the temporal bone through which the internal carotid artery enters the cranium - cauda equina - bundle of spinal nerve roots that descend from the lower spinal cord below the first lumbar vertebra and lie within the vertebral cavity; has the appearance of a horse's tail - caudate - nucleus deep in the cerebrum that is part of the basal nuclei; along with the putamen, it is part of the striatum - central canal - hollow space within the spinal cord that is the remnant of the center of the neural tube - central sulcus - surface landmark of the cerebral cortex that marks the boundary between the frontal and parietal lobes - cephalic flexure - curve in midbrain of the embryo that positions the forebrain ventrally - cerebellum - region of the adult brain connected primarily to the pons that developed from the metencephalon (along with the pons) and is largely responsible for comparing information from the cerebrum with sensory feedback from the periphery through the spinal cord - cerebral aqueduct - connection of the ventricular system between the third and fourth ventricles located in the midbrain - cerebral cortex - outer gray matter covering the forebrain, marked by wrinkles and folds known as gyri and sulci - cerebral hemisphere - one half of the bilaterally symmetrical cerebrum - cerebrum - region of the adult brain that develops from the telencephalon and is responsible for higher neurological functions such as memory, emotion, and consciousness - cervical plexus - nerve plexus associated with the upper cervical spinal nerves - choroid plexus - specialized structures containing ependymal cells lining blood capillaries that filter blood to produce CSF in the four ventricles of the brain - circle of Willis - unique anatomical arrangement of blood vessels around the base of the brain that maintains perfusion of blood into the brain even if one component of the structure is blocked or narrowed - common carotid artery - blood vessel that branches off the aorta (or the brachiocephalic artery on the right) and supplies blood to the head and neck - corpus callosum - large white matter structure that connects the right and left cerebral hemispheres - cranial nerve - one of twelve nerves connected to the brain that are responsible for sensory or motor functions of the head and neck - cranial nerve ganglion - sensory ganglion of cranial nerves - descending tract - central nervous system fibers carrying motor commands from the brain to the spinal cord or periphery - diencephalon - region of the adult brain that retains its name from embryonic development and includes the thalamus and hypothalamus - direct pathway - connections within the basal nuclei from the striatum to the globus pallidus internal segment and substantia nigra pars reticulata that disinhibit the thalamus to increase cortical control of movement - disinhibition - disynaptic connection in which the first synapse inhibits the second cell, which then stops inhibiting the final target - dorsal (posterior) nerve root - axons entering the posterior horn of the spinal cord - dorsal (posterior) root ganglion - sensory ganglion attached to the posterior nerve root of a spinal nerve - dura mater - tough, fibrous, outer layer of the meninges that is attached to the inner surface of the cranium and vertebral column and surrounds the entire CNS - dural sinus - any of the venous structures surrounding the brain, enclosed within the dura mater, which drain blood from the CNS to the common venous return of the jugular veins - endoneurium - innermost layer of connective tissue that surrounds individual axons within a nerve - enteric nervous system - peripheral structures, namely ganglia and nerves, that are incorporated into the digestive system organs - enteric plexus - neuronal plexus in the wall of the intestines, which is part of the enteric nervous system - epineurium - outermost layer of connective tissue that surrounds an entire nerve - epithalamus - region of the diecephalon containing the pineal gland - esophageal plexus - neuronal plexus in the wall of the esophagus that is part of the enteric nervous system - extraocular muscles - six skeletal muscles that control eye movement within the orbit - facial nerve - seventh cranial nerve; responsible for contraction of the facial muscles and for part of the sense of taste, as well as causing saliva production - fascicle - small bundles of nerve or muscle fibers enclosed by connective tissue - femoral nerve - systemic nerve of the anterior leg that arises from the lumbar plexus - fibular nerve - systemic nerve of the posterior leg that begins as part of the sciatic nerve - foramen magnum - large opening in the occipital bone of the skull through which the spinal cord emerges and the vertebral arteries enter the cranium - forebrain - anterior region of the adult brain that develops from the prosencephalon and includes the cerebrum and diencephalon - fourth ventricle - the portion of the ventricular system that is in the region of the brain stem and opens into the subarachnoid space through the median and lateral apertures - frontal eye field - region of the frontal lobe associated with motor commands to orient the eyes toward an object of visual attention - frontal lobe - region of the cerebral cortex directly beneath the frontal bone of the cranium - gastric plexuses - neuronal networks in the wall of the stomach that are part of the enteric nervous system - globus pallidus - nuclei deep in the cerebrum that are part of the basal nuclei and can be divided into the internal and external segments - glossopharyngeal nerve - ninth cranial nerve; responsible for contraction of muscles in the tongue and throat and for part of the sense of taste, as well as causing saliva production - gyrus - ridge formed by convolutions on the surface of the cerebrum or cerebellum - hindbrain - posterior region of the adult brain that develops from the rhombencephalon and includes the pons, medulla oblongata, and cerebellum - hippocampus - gray matter deep in the temporal lobe that is very important for long-term memory formation - hypoglossal nerve - twelfth cranial nerve; responsible for contraction of muscles of the tongue - hypothalamus - major region of the diencephalon that is responsible for coordinating autonomic and endocrine control of homeostasis - indirect pathway - connections within the basal nuclei from the striatum through the globus pallidus external segment and subthalamic nucleus to the globus pallidus internal segment/substantia nigra pars compacta that result in inhibition of the thalamus to decrease cortical control of movement - inferior colliculus - half of the midbrain tectum that is part of the brain stem auditory pathway - inferior olive - nucleus in the medulla that is involved in processing information related to motor control - intercostal nerve - systemic nerve in the thoracic cavity that is found between two ribs - internal carotid artery - branch from the common carotid artery that enters the cranium and supplies blood to the brain - interventricular foramina - openings between the lateral ventricles and third ventricle allowing for the passage of CSF - jugular veins - blood vessels that return “used” blood from the head and neck - kinesthesia - general sensory perception of movement of the body - lateral apertures - pair of openings from the fourth ventricle to the subarachnoid space on either side and between the medulla and cerebellum - lateral column - white matter of the spinal cord between the posterior horn on one side and the axons from the anterior horn on the same side; composed of many different groups of axons, of both ascending and descending tracts, carrying motor commands to and from the brain - lateral horn - region of the spinal cord gray matter in the thoracic, upper lumbar, and sacral regions that is the central component of the sympathetic division of the autonomic nervous system - lateral sulcus - surface landmark of the cerebral cortex that marks the boundary between the temporal lobe and the frontal and parietal lobes - lateral ventricles - portions of the ventricular system that are in the region of the cerebrum - limbic cortex - collection of structures of the cerebral cortex that are involved in emotion, memory, and behavior and are part of the larger limbic system - limbic system - structures at the edge (limit) of the boundary between the forebrain and hindbrain that are most associated with emotional behavior and memory formation - longitudinal fissure - large separation along the midline between the two cerebral hemispheres - lumbar plexus - nerve plexus associated with the lumbar spinal nerves - lumbar puncture - procedure used to withdraw CSF from the lower lumbar region of the vertebral column that avoids the risk of damaging CNS tissue because the spinal cord ends at the upper lumbar vertebrae - median aperture - singular opening from the fourth ventricle into the subarachnoid space at the midline between the medulla and cerebellum - median nerve - systemic nerve of the arm, located between the ulnar and radial nerves - meninges - protective outer coverings of the CNS composed of connective tissue - mesencephalon - primary vesicle of the embryonic brain that does not significantly change through the rest of embryonic development and becomes the midbrain - metencephalon - secondary vesicle of the embryonic brain that develops into the pons and the cerebellum - midbrain - middle region of the adult brain that develops from the mesencephalon - myelencephalon - secondary vesicle of the embryonic brain that develops into the medulla - nerve plexus - network of nerves without neuronal cell bodies included - neural crest - tissue that detaches from the edges of the neural groove and migrates through the embryo to develop into peripheral structures of both nervous and non-nervous tissues - neural fold - elevated edge of the neural groove - neural groove - region of the neural plate that folds into the dorsal surface of the embryo and closes off to become the neural tube - neural plate - thickened layer of neuroepithelium that runs longitudinally along the dorsal surface of an embryo and gives rise to nervous system tissue - neural tube - precursor to structures of the central nervous system, formed by the invagination and separation of neuroepithelium - neuraxis - central axis to the nervous system, from the posterior to anterior ends of the neural tube; the inferior tip of the spinal cord to the anterior surface of the cerebrum - occipital lobe - region of the cerebral cortex directly beneath the occipital bone of the cranium - occipital sinuses - dural sinuses along the edge of the occipital lobes of the cerebrum - oculomotor nerve - third cranial nerve; responsible for contraction of four of the extraocular muscles, the muscle in the upper eyelid, and pupillary constriction - olfaction - special sense responsible for smell, which has a unique, direct connection to the cerebrum - olfactory nerve - first cranial nerve; responsible for the sense of smell - optic nerve - second cranial nerve; responsible for visual sensation - orthostatic reflex - sympathetic function that maintains blood pressure when standing to offset the increased effect of gravity - paravertebral ganglia - autonomic ganglia superior to the sympathetic chain ganglia - parietal lobe - region of the cerebral cortex directly beneath the parietal bone of the cranium - parieto-occipital sulcus - groove in the cerebral cortex representing the border between the parietal and occipital cortices - perineurium - layer of connective tissue surrounding fascicles within a nerve - phrenic nerve - systemic nerve from the cervical plexus that enervates the diaphragm - pia mater - thin, innermost membrane of the meninges that directly covers the surface of the CNS - plexus - network of nerves or nervous tissue - postcentral gyrus - primary motor cortex located in the frontal lobe of the cerebral cortex - posterior columns - white matter of the spinal cord that lies between the posterior horns of the gray matter, sometimes referred to as the dorsal column; composed of axons of ascending tracts that carry sensory information up to the brain - posterior horn - gray matter region of the spinal cord in which sensory input arrives, sometimes referred to as the dorsal horn - posterior median sulcus - midline feature of the posterior spinal cord, marking the separation between right and left sides of the cord - posterolateral sulcus - feature of the posterior spinal cord marking the entry of posterior nerve roots and the separation between the posterior and lateral columns of the white matter - precentral gyrus - ridge just posterior to the central sulcus, in the parietal lobe, where somatosensory processing initially takes place in the cerebrum - prefrontal lobe - specific region of the frontal lobe anterior to the more specific motor function areas, which can be related to the early planning of movements and intentions to the point of being personality-type functions - premotor area - region of the frontal lobe responsible for planning movements that will be executed through the primary motor cortex - prevertebral ganglia - autonomic ganglia that are anterior to the vertebral column and functionally related to the sympathetic chain ganglia - primary vesicle - initial enlargements of the anterior neural tube during embryonic development that develop into the forebrain, midbrain, and hindbrain - proprioception - general sensory perceptions providing information about location and movement of body parts; the “sense of the self” - prosencephalon - primary vesicle of the embryonic brain that develops into the forebrain, which includes the cerebrum and diencephalon - putamen - nucleus deep in the cerebrum that is part of the basal nuclei; along with the caudate, it is part of the striatum - radial nerve - systemic nerve of the arm, the distal component of which is located near the radial bone - reticular formation - diffuse region of gray matter throughout the brain stem that regulates sleep, wakefulness, and states of consciousness - rhombencephalon - primary vesicle of the embryonic brain that develops into the hindbrain, which includes the pons, cerebellum, and medulla - sacral plexus - nerve plexus associated with the lower lumbar and sacral spinal nerves - saphenous nerve - systemic nerve of the lower anterior leg that is a branch from the femoral nerve - sciatic nerve - systemic nerve from the sacral plexus that is a combination of the tibial and fibular nerves and extends across the hip joint and gluteal region into the upper posterior leg - sciatica - painful condition resulting from inflammation or compression of the sciatic nerve or any of the spinal nerves that contribute to it - secondary vesicle - five vesicles that develop from primary vesicles, continuing the process of differentiation of the embryonic brain - sigmoid sinuses - dural sinuses that drain directly into the jugular veins - somatosensation - general senses related to the body, usually thought of as the senses of touch, which would include pain, temperature, and proprioception - spinal accessory nerve - eleventh cranial nerve; responsible for contraction of neck muscles - spinal nerve - one of 31 nerves connected to the spinal cord - straight sinus - dural sinus that drains blood from the deep center of the brain to collect with the other sinuses - striatum - the caudate and putamen collectively, as part of the basal nuclei, which receive input from the cerebral cortex - subarachnoid space - space between the arachnoid mater and pia mater that contains CSF and the fibrous connections of the arachnoid trabeculae - subcortical nucleus - all the nuclei beneath the cerebral cortex, including the basal nuclei and the basal forebrain - substantia nigra pars compacta - nuclei within the basal nuclei that release dopamine to modulate the function of the striatum; part of the motor pathway - substantia nigra pars reticulata - nuclei within the basal nuclei that serve as an output center of the nuclei; part of the motor pathway - subthalamus - nucleus within the basal nuclei that is part of the indirect pathway - sulcus - groove formed by convolutions in the surface of the cerebral cortex - superior colliculus - half of the midbrain tectum that is responsible for aligning visual, auditory, and somatosensory spatial perceptions - superior sagittal sinus - dural sinus that runs along the top of the longitudinal fissure and drains blood from the majority of the outer cerebrum - sympathetic chain ganglia - autonomic ganglia in a chain along the anterolateral aspect of the vertebral column that are responsible for contributing to homeostatic mechanisms of the autonomic nervous system - systemic nerve - nerve in the periphery distal to a nerve plexus or spinal nerve - tectum - region of the midbrain, thought of as the roof of the cerebral aqueduct, which is subdivided into the inferior and superior colliculi - tegmentum - region of the midbrain, thought of as the floor of the cerebral aqueduct, which continues into the pons and medulla as the floor of the fourth ventricle - telencephalon - secondary vesicle of the embryonic brain that develops into the cerebrum - temporal lobe - region of the cerebral cortex directly beneath the temporal bone of the cranium - terminal ganglion - autonomic ganglia that are near or within the walls of organs that are responsible for contributing to homeostatic mechanisms of the autonomic nervous system - thalamus - major region of the diencephalon that is responsible for relaying information between the cerebrum and the hindbrain, spinal cord, and periphery - third ventricle - portion of the ventricular system that is in the region of the diencephalon - tibial nerve - systemic nerve of the posterior leg that begins as part of the sciatic nerve - transverse sinuses - dural sinuses that drain along either side of the occipital–cerebellar space - trigeminal ganglion - sensory ganglion that contributes sensory fibers to the trigeminal nerve - trigeminal nerve - fifth cranial nerve; responsible for cutaneous sensation of the face and contraction of the muscles of mastication - trochlear nerve - fourth cranial nerve; responsible for contraction of one of the extraocular muscles - ulnar nerve - systemic nerve of the arm located close to the ulna, a bone of the forearm - vagus nerve - tenth cranial nerve; responsible for the autonomic control of organs in the thoracic and upper abdominal cavities - ventral (anterior) nerve root - axons emerging from the anterior or lateral horns of the spinal cord - ventricles - remnants of the hollow center of the neural tube that are spaces for cerebrospinal fluid to circulate through the brain - vertebral arteries - arteries that ascend along either side of the vertebral column through the transverse foramina of the cervical vertebrae and enter the cranium through the foramen magnum - vestibulocochlear nerve - eighth cranial nerve; responsible for the sensations of hearing and balance Chapter Review 13.1 The Embryologic Perspective The development of the nervous system starts early in embryonic development. The outer layer of the embryo, the ectoderm, gives rise to the skin and the nervous system. A specialized region of this layer, the neuroectoderm, becomes a groove that folds in and becomes the neural tube beneath the dorsal surface of the embryo. The anterior end of the neural tube develops into the brain, and the posterior region becomes the spinal cord. Tissues at the edges of the neural groove, when it closes off, are called the neural crest and migrate through the embryo to give rise to PNS structures as well as some non-nervous tissues. The brain develops from this early tube structure and gives rise to specific regions of the adult brain. As the neural tube grows and differentiates, it enlarges into three vesicles that correspond to the forebrain, midbrain, and hindbrain regions of the adult brain. Later in development, two of these three vesicles differentiate further, resulting in five vesicles. Those five vesicles can be aligned with the four major regions of the adult brain. The cerebrum is formed directly from the telencephalon. The diencephalon is the only region that keeps its embryonic name. The mesencephalon, metencephalon, and myelencephalon become the brain stem. The cerebellum also develops from the metencephalon and is a separate region of the adult brain. The spinal cord develops out of the rest of the neural tube and retains the tube structure, with the nervous tissue thickening and the hollow center becoming a very small central canal through the cord. The rest of the hollow center of the neural tube corresponds to open spaces within the brain called the ventricles, where cerebrospinal fluid is found. 13.2 The Central Nervous System The adult brain is separated into four major regions: the cerebrum, the diencephalon, the brain stem, and the cerebellum. The cerebrum is the largest portion and contains the cerebral cortex and subcortical nuclei. It is divided into two halves by the longitudinal fissure. The cortex is separated into the frontal, parietal, temporal, and occipital lobes. The frontal lobe is responsible for motor functions, from planning movements through executing commands to be sent to the spinal cord and periphery. The most anterior portion of the frontal lobe is the prefrontal cortex, which is associated with aspects of personality through its influence on motor responses in decision-making. The other lobes are responsible for sensory functions. The parietal lobe is where somatosensation is processed. The occipital lobe is where visual processing begins, although the other parts of the brain can contribute to visual function. The temporal lobe contains the cortical area for auditory processing, but also has regions crucial for memory formation. Nuclei beneath the cerebral cortex, known as the subcortical nuclei, are responsible for augmenting cortical functions. The basal nuclei receive input from cortical areas and compare it with the general state of the individual through the activity of a dopamine-releasing nucleus. The output influences the activity of part of the thalamus that can then increase or decrease cortical activity that often results in changes to motor commands. The basal forebrain is responsible for modulating cortical activity in attention and memory. The limbic system includes deep cerebral nuclei that are responsible for emotion and memory. The diencephalon includes the thalamus and the hypothalamus, along with some other structures. The thalamus is a relay between the cerebrum and the rest of the nervous system. The hypothalamus coordinates homeostatic functions through the autonomic and endocrine systems. The brain stem is composed of the midbrain, pons, and medulla. It controls the head and neck region of the body through the cranial nerves. There are control centers in the brain stem that regulate the cardiovascular and respiratory systems. The cerebellum is connected to the brain stem, primarily at the pons, where it receives a copy of the descending input from the cerebrum to the spinal cord. It can compare this with sensory feedback input through the medulla and send output through the midbrain that can correct motor commands for coordination. 13.3 Circulation and the Central Nervous System The CNS has a privileged blood supply established by the blood-brain barrier. Establishing this barrier are anatomical structures that help to protect and isolate the CNS. The arterial blood to the brain comes from the internal carotid and vertebral arteries, which both contribute to the unique circle of Willis that provides constant perfusion of the brain even if one of the blood vessels is blocked or narrowed. That blood is eventually filtered to make a separate medium, the CSF, that circulates within the spaces of the brain and then into the surrounding space defined by the meninges, the protective covering of the brain and spinal cord. The blood that nourishes the brain and spinal cord is behind the glial-cell–enforced blood-brain barrier, which limits the exchange of material from blood vessels with the interstitial fluid of the nervous tissue. Thus, metabolic wastes are collected in cerebrospinal fluid that circulates through the CNS. This fluid is produced by filtering blood at the choroid plexuses in the four ventricles of the brain. It then circulates through the ventricles and into the subarachnoid space, between the pia mater and the arachnoid mater. From the arachnoid granulations, CSF is reabsorbed into the blood, removing the waste from the privileged central nervous tissue. The blood, now with the reabsorbed CSF, drains out of the cranium through the dural sinuses. The dura mater is the tough outer covering of the CNS, which is anchored to the inner surface of the cranial and vertebral cavities. It surrounds the venous space known as the dural sinuses, which connect to the jugular veins, where blood drains from the head and neck. 13.4 The Peripheral Nervous System The PNS is composed of the groups of neurons (ganglia) and bundles of axons (nerves) that are outside of the brain and spinal cord. Ganglia are of two types, sensory or autonomic. Sensory ganglia contain unipolar sensory neurons and are found on the dorsal root of all spinal nerves as well as associated with many of the cranial nerves. Autonomic ganglia are in the sympathetic chain, the associated paravertebral or prevertebral ganglia, or in terminal ganglia near or within the organs controlled by the autonomic nervous system. Nerves are classified as cranial nerves or spinal nerves on the basis of their connection to the brain or spinal cord, respectively. The twelve cranial nerves can be strictly sensory in function, strictly motor in function, or a combination of the two functions. Sensory fibers are axons of sensory ganglia that carry sensory information into the brain and target sensory nuclei. Motor fibers are axons of motor neurons in motor nuclei of the brain stem and target skeletal muscles of the head and neck. Spinal nerves are all mixed nerves with both sensory and motor fibers. Spinal nerves emerge from the spinal cord and reorganize through plexuses, which then give rise to systemic nerves. Thoracic spinal nerves are not part of any plexus, but give rise to the intercostal nerves directly. Interactive Link Questions Watch this animation to examine the development of the brain, starting with the neural tube. As the anterior end of the neural tube develops, it enlarges into the primary vesicles that establish the forebrain, midbrain, and hindbrain. Those structures continue to develop throughout the rest of embryonic development and into adolescence. They are the basis of the structure of the fully developed adult brain. How would you describe the difference in the relative sizes of the three regions of the brain when comparing the early (25th embryonic day) brain and the adult brain? 2.Watch this video to learn about the white matter in the cerebrum that develops during childhood and adolescence. This is a composite of MRI images taken of the brains of people from 5 years of age through 20 years of age, demonstrating how the cerebrum changes. As the color changes to blue, the ratio of gray matter to white matter changes. The caption for the video describes it as “less gray matter,” which is another way of saying “more white matter.” If the brain does not finish developing until approximately 20 years of age, can teenagers be held responsible for behaving badly? 3.Watch this video to learn about the basal nuclei (also known as the basal ganglia), which have two pathways that process information within the cerebrum. As shown in this video, the direct pathway is the shorter pathway through the system that results in increased activity in the cerebral cortex and increased motor activity. The direct pathway is described as resulting in “disinhibition” of the thalamus. What does disinhibition mean? What are the two neurons doing individually to cause this? 4.Watch this video to learn about the basal nuclei (also known as the basal ganglia), which have two pathways that process information within the cerebrum. As shown in this video, the indirect pathway is the longer pathway through the system that results in decreased activity in the cerebral cortex, and therefore less motor activity. The indirect pathway has an extra couple of connections in it, including disinhibition of the subthalamic nucleus. What is the end result on the thalamus, and therefore on movement initiated by the cerebral cortex? 5.Watch this video to learn about the gray matter of the spinal cord that receives input from fibers of the dorsal (posterior) root and sends information out through the fibers of the ventral (anterior) root. As discussed in this video, these connections represent the interactions of the CNS with peripheral structures for both sensory and motor functions. The cervical and lumbar spinal cords have enlargements as a result of larger populations of neurons. What are these enlargements responsible for? 6.Compared with the nearest evolutionary relative, the chimpanzee, the human has a brain that is huge. At a point in the past, a common ancestor gave rise to the two species of humans and chimpanzees. That evolutionary history is long and is still an area of intense study. But something happened to increase the size of the human brain relative to the chimpanzee. Read this article in which the author explores the current understanding of why this happened. According to one hypothesis about the expansion of brain size, what tissue might have been sacrificed so energy was available to grow our larger brain? Based on what you know about that tissue and nervous tissue, why would there be a trade-off between them in terms of energy use? 7.Watch this animation to see how blood flows to the brain and passes through the circle of Willis before being distributed through the cerebrum. The circle of Willis is a specialized arrangement of arteries that ensure constant perfusion of the cerebrum even in the event of a blockage of one of the arteries in the circle. The animation shows the normal direction of flow through the circle of Willis to the middle cerebral artery. Where would the blood come from if there were a blockage just posterior to the middle cerebral artery on the left? 8.Watch this video that describes the procedure known as the lumbar puncture, a medical procedure used to sample the CSF. Because of the anatomy of the CNS, it is a relative safe location to insert a needle. Why is the lumbar puncture performed in the lower lumbar area of the vertebral column? 9.Watch this animation that shows the flow of CSF through the brain and spinal cord, and how it originates from the ventricles and then spreads into the space within the meninges, where the fluids then move into the venous sinuses to return to the cardiovascular circulation. What are the structures that produce CSF and where are they found? How are the structures indicated in this animation? 10.Figure 13.20 If you zoom in on the DRG, you can see smaller satellite glial cells surrounding the large cell bodies of the sensory neurons. From what structure do satellite cells derive during embryologic development? 11.Figure 13.22 To what structures in a skeletal muscle are the endoneurium, perineurium, and epineurium comparable? 12.Visit this site to read about a man who wakes with a headache and a loss of vision. His regular doctor sent him to an ophthalmologist to address the vision loss. The ophthalmologist recognizes a greater problem and immediately sends him to the emergency room. Once there, the patient undergoes a large battery of tests, but a definite cause cannot be found. A specialist recognizes the problem as meningitis, but the question is what caused it originally. How can that be cured? The loss of vision comes from swelling around the optic nerve, which probably presented as a bulge on the inside of the eye. Why is swelling related to meningitis going to push on the optic nerve? Review Questions Aside from the nervous system, which other organ system develops out of the ectoderm? - digestive - respiratory - integumentary - urinary Which primary vesicle of the embryonic nervous system does not differentiate into more vesicles at the secondary stage? - prosencephalon - mesencephalon - diencephalon - rhombencephalon Which adult structure(s) arises from the diencephalon? - thalamus, hypothalamus, retina - midbrain, pons, medulla - pons and cerebellum - cerebrum Which non-nervous tissue develops from the neuroectoderm? - respiratory mucosa - vertebral bone - digestive lining - craniofacial bone Which structure is associated with the embryologic development of the peripheral nervous system? - neural crest - neuraxis - rhombencephalon - neural tube Which lobe of the cerebral cortex is responsible for generating motor commands? - temporal - parietal - occipital - frontal What region of the diencephalon coordinates homeostasis? - thalamus - epithalamus - hypothalamus - subthalamus What level of the brain stem is the major input to the cerebellum? - midbrain - pons - medulla - spinal cord What region of the spinal cord contains motor neurons that direct the movement of skeletal muscles? - anterior horn - posterior horn - lateral horn - alar plate Brodmann’s areas map different regions of the ________ to particular functions. - cerebellum - cerebral cortex - basal forebrain - corpus callosum What blood vessel enters the cranium to supply the brain with fresh, oxygenated blood? - common carotid artery - jugular vein - internal carotid artery - aorta Which layer of the meninges surrounds and supports the sinuses that form the route through which blood drains from the CNS? - dura mater - arachnoid mater - subarachnoid - pia mater What type of glial cell is responsible for filtering blood to produce CSF at the choroid plexus? - ependymal cell - astrocyte - oligodendrocyte - Schwann cell Which portion of the ventricular system is found within the diencephalon? - lateral ventricles - third ventricle - cerebral aqueduct - fourth ventricle What condition causes a stroke? - inflammation of meninges - lumbar puncture - infection of cerebral spinal fluid - disruption of blood to the brain What type of ganglion contains neurons that control homeostatic mechanisms of the body? - sensory ganglion - dorsal root ganglion - autonomic ganglion - cranial nerve ganglion Which ganglion is responsible for cutaneous sensations of the face? - otic ganglion - vestibular ganglion - geniculate ganglion - trigeminal ganglion What is the name for a bundle of axons within a nerve? - fascicle - tract - nerve root - epineurium Which cranial nerve does not control functions in the head and neck? - olfactory - trochlear - glossopharyngeal - vagus Which of these structures is not under direct control of the peripheral nervous system? - trigeminal ganglion - gastric plexus - sympathetic chain ganglia - cervical plexus Critical Thinking Questions Studying the embryonic development of the nervous system makes it easier to understand the complexity of the adult nervous system. Give one example of how development in the embryonic nervous system explains a more complex structure in the adult nervous system. 34.What happens in development that suggests that there is a special relationship between the skeletal structure of the head and the nervous system? 35.Damage to specific regions of the cerebral cortex, such as through a stroke, can result in specific losses of function. What functions would likely be lost by a stroke in the temporal lobe? 36.Why do the anatomical inputs to the cerebellum suggest that it can compare motor commands and sensory feedback? 37.Why can the circle of Willis maintain perfusion of the brain even if there is a blockage in one part of the structure? 38.Meningitis is an inflammation of the meninges that can have severe effects on neurological function. Why is infection of this structure potentially so dangerous? 39.Why are ganglia and nerves not surrounded by protective structures like the meninges of the CNS? 40.Testing for neurological function involves a series of tests of functions associated with the cranial nerves. What functions, and therefore which nerves, are being tested by asking a patient to follow the tip of a pen with their eyes?	oercommons	2025-03-18T00:37:02.175443	07/23/2019	{ "license": "Creative Commons - Attribution - https://creativecommons.org/licenses/by/4.0/", "url": "https://oercommons.org/courseware/lesson/56376/overview", "title": "Anatomy and Physiology, Regulation, Integration, and Control, Anatomy of the Nervous System", "author": null }
https://oercommons.org/courseware/lesson/56369/overview	Muscle Tissue Introduction Figure 10.1 Tennis Player Athletes rely on toned skeletal muscles to supply the force required for movement. (credit: Emmanuel Huybrechts/flickr) CHAPTER OBJECTIVES After studying this chapter, you will be able to: - Explain the organization of muscle tissue - Describe the function and structure of skeletal, cardiac muscle, and smooth muscle - Explain how muscles work with tendons to move the body - Describe how muscles contract and relax - Define the process of muscle metabolism - Explain how the nervous system controls muscle tension - Relate the connections between exercise and muscle performance - Explain the development and regeneration of muscle tissue When most people think of muscles, they think of the muscles that are visible just under the skin, particularly of the limbs. These are skeletal muscles, so-named because most of them move the skeleton. But there are two other types of muscle in the body, with distinctly different jobs. Cardiac muscle, found in the heart, is concerned with pumping blood through the circulatory system. Smooth muscle is concerned with various involuntary movements, such as having one’s hair stand on end when cold or frightened, or moving food through the digestive system. This chapter will examine the structure and function of these three types of muscles. Overview of Muscle Tissues - Describe the different types of muscle - Explain contractibility and extensibility Muscle is one of the four primary tissue types of the body, and the body contains three types of muscle tissue: skeletal muscle, cardiac muscle, and smooth muscle (Figure 10.2). All three muscle tissues have some properties in common; they all exhibit a quality called excitability as their plasma membranes can change their electrical states (from polarized to depolarized) and send an electrical wave called an action potential along the entire length of the membrane. While the nervous system can influence the excitability of cardiac and smooth muscle to some degree, skeletal muscle completely depends on signaling from the nervous system to work properly. On the other hand, both cardiac muscle and smooth muscle can respond to other stimuli, such as hormones and local stimuli. Figure 10.2 The Three Types of Muscle Tissue The body contains three types of muscle tissue: (a) skeletal muscle, (b) smooth muscle, and (c) cardiac muscle. From top, LM × 1600, LM × 1600, LM × 1600. (Micrographs provided by the Regents of University of Michigan Medical School © 2012) The muscles all begin the actual process of contracting (shortening) when a protein called actin is pulled by a protein called myosin. This occurs in striated muscle (skeletal and cardiac) after specific binding sites on the actin have been exposed in response to the interaction between calcium ions (Ca++) and proteins (troponin and tropomyosin) that “shield” the actin-binding sites. Ca++ also is required for the contraction of smooth muscle, although its role is different: here Ca++ activates enzymes, which in turn activate myosin heads. All muscles require adenosine triphosphate (ATP) to continue the process of contracting, and they all relax when the Ca++ is removed and the actin-binding sites are re-shielded. A muscle can return to its original length when relaxed due to a quality of muscle tissue called elasticity. It can recoil back to its original length due to elastic fibers. Muscle tissue also has the quality of extensibility; it can stretch or extend. Contractilityallows muscle tissue to pull on its attachment points and shorten with force. Differences among the three muscle types include the microscopic organization of their contractile proteins—actin and myosin. The actin and myosin proteins are arranged very regularly in the cytoplasm of individual muscle cells (referred to as fibers) in both skeletal muscle and cardiac muscle, which creates a pattern, or stripes, called striations. The striations are visible with a light microscope under high magnification (see Figure 10.2). Skeletal muscle fibers are multinucleated structures that compose the skeletal muscle. Cardiac muscle fibers each have one to two nuclei and are physically and electrically connected to each other so that the entire heart contracts as one unit (called a syncytium). Because the actin and myosin are not arranged in such regular fashion in smooth muscle, the cytoplasm of a smooth muscle fiber (which has only a single nucleus) has a uniform, nonstriated appearance (resulting in the name smooth muscle). However, the less organized appearance of smooth muscle should not be interpreted as less efficient. Smooth muscle in the walls of arteries is a critical component that regulates blood pressure necessary to push blood through the circulatory system; and smooth muscle in the skin, visceral organs, and internal passageways is essential for moving all materials through the body. Skeletal Muscle - Describe the layers of connective tissues packaging skeletal muscle - Explain how muscles work with tendons to move the body - Identify areas of the skeletal muscle fibers - Describe excitation-contraction coupling The best-known feature of skeletal muscle is its ability to contract and cause movement. Skeletal muscles act not only to produce movement but also to stop movement, such as resisting gravity to maintain posture. Small, constant adjustments of the skeletal muscles are needed to hold a body upright or balanced in any position. Muscles also prevent excess movement of the bones and joints, maintaining skeletal stability and preventing skeletal structure damage or deformation. Joints can become misaligned or dislocated entirely by pulling on the associated bones; muscles work to keep joints stable. Skeletal muscles are located throughout the body at the openings of internal tracts to control the movement of various substances. These muscles allow functions, such as swallowing, urination, and defecation, to be under voluntary control. Skeletal muscles also protect internal organs (particularly abdominal and pelvic organs) by acting as an external barrier or shield to external trauma and by supporting the weight of the organs. Skeletal muscles contribute to the maintenance of homeostasis in the body by generating heat. Muscle contraction requires energy, and when ATP is broken down, heat is produced. This heat is very noticeable during exercise, when sustained muscle movement causes body temperature to rise, and in cases of extreme cold, when shivering produces random skeletal muscle contractions to generate heat. Each skeletal muscle is an organ that consists of various integrated tissues. These tissues include the skeletal muscle fibers, blood vessels, nerve fibers, and connective tissue. Each skeletal muscle has three layers of connective tissue (called “mysia”) that enclose it and provide structure to the muscle as a whole, and also compartmentalize the muscle fibers within the muscle (Figure 10.3). Each muscle is wrapped in a sheath of dense, irregular connective tissue called the epimysium, which allows a muscle to contract and move powerfully while maintaining its structural integrity. The epimysium also separates muscle from other tissues and organs in the area, allowing the muscle to move independently. Figure 10.3 The Three Connective Tissue Layers Bundles of muscle fibers, called fascicles, are covered by the perimysium. Muscle fibers are covered by the endomysium. Inside each skeletal muscle, muscle fibers are organized into individual bundles, each called a fascicle, by a middle layer of connective tissue called the perimysium. This fascicular organization is common in muscles of the limbs; it allows the nervous system to trigger a specific movement of a muscle by activating a subset of muscle fibers within a bundle, or fascicle of the muscle. Inside each fascicle, each muscle fiber is encased in a thin connective tissue layer of collagen and reticular fibers called the endomysium. The endomysium contains the extracellular fluid and nutrients to support the muscle fiber. These nutrients are supplied via blood to the muscle tissue. In skeletal muscles that work with tendons to pull on bones, the collagen in the three tissue layers (the mysia) intertwines with the collagen of a tendon. At the other end of the tendon, it fuses with the periosteum coating the bone. The tension created by contraction of the muscle fibers is then transferred though the mysia, to the tendon, and then to the periosteum to pull on the bone for movement of the skeleton. In other places, the mysia may fuse with a broad, tendon-like sheet called an aponeurosis, or to fascia, the connective tissue between skin and bones. The broad sheet of connective tissue in the lower back that the latissimus dorsi muscles (the “lats”) fuse into is an example of an aponeurosis. Every skeletal muscle is also richly supplied by blood vessels for nourishment, oxygen delivery, and waste removal. In addition, every muscle fiber in a skeletal muscle is supplied by the axon branch of a somatic motor neuron, which signals the fiber to contract. Unlike cardiac and smooth muscle, the only way to functionally contract a skeletal muscle is through signaling from the nervous system. Skeletal Muscle Fibers Because skeletal muscle cells are long and cylindrical, they are commonly referred to as muscle fibers. Skeletal muscle fibers can be quite large for human cells, with diameters up to 100 μm and lengths up to 30 cm (11.8 in) in the Sartorius of the upper leg. During early development, embryonic myoblasts, each with its own nucleus, fuse with up to hundreds of other myoblasts to form the multinucleated skeletal muscle fibers. Multiple nuclei mean multiple copies of genes, permitting the production of the large amounts of proteins and enzymes needed for muscle contraction. Some other terminology associated with muscle fibers is rooted in the Greek sarco, which means “flesh.” The plasma membrane of muscle fibers is called the sarcolemma, the cytoplasm is referred to as sarcoplasm, and the specialized smooth endoplasmic reticulum, which stores, releases, and retrieves calcium ions (Ca++) is called the sarcoplasmic reticulum (SR)(Figure 10.4). As will soon be described, the functional unit of a skeletal muscle fiber is the sarcomere, a highly organized arrangement of the contractile myofilaments actin (thin filament) and myosin (thick filament), along with other support proteins. Figure 10.4 Muscle Fiber A skeletal muscle fiber is surrounded by a plasma membrane called the sarcolemma, which contains sarcoplasm, the cytoplasm of muscle cells. A muscle fiber is composed of many fibrils, which give the cell its striated appearance. The Sarcomere The striated appearance of skeletal muscle fibers is due to the arrangement of the myofilaments of actin and myosin in sequential order from one end of the muscle fiber to the other. Each packet of these microfilaments and their regulatory proteins, troponin and tropomyosin (along with other proteins) is called a sarcomere. INTERACTIVE LINK Watch this video to learn more about macro- and microstructures of skeletal muscles. (a) What are the names of the “junction points” between sarcomeres? (b) What are the names of the “subunits” within the myofibrils that run the length of skeletal muscle fibers? (c) What is the “double strand of pearls” described in the video? (d) What gives a skeletal muscle fiber its striated appearance? The sarcomere is the functional unit of the muscle fiber. The sarcomere itself is bundled within the myofibril that runs the entire length of the muscle fiber and attaches to the sarcolemma at its end. As myofibrils contract, the entire muscle cell contracts. Because myofibrils are only approximately 1.2 μm in diameter, hundreds to thousands (each with thousands of sarcomeres) can be found inside one muscle fiber. Each sarcomere is approximately 2 μm in length with a three-dimensional cylinder-like arrangement and is bordered by structures called Z-discs (also called Z-lines, because pictures are two-dimensional), to which the actin myofilaments are anchored (Figure 10.5). Because the actin and its troponin-tropomyosin complex (projecting from the Z-discs toward the center of the sarcomere) form strands that are thinner than the myosin, it is called the thin filament of the sarcomere. Likewise, because the myosin strands and their multiple heads (projecting from the center of the sarcomere, toward but not all to way to, the Z-discs) have more mass and are thicker, they are called the thick filament of the sarcomere. Figure 10.5 The Sarcomere The sarcomere, the region from one Z-line to the next Z-line, is the functional unit of a skeletal muscle fiber. The Neuromuscular Junction Another specialization of the skeletal muscle is the site where a motor neuron’s terminal meets the muscle fiber—called the neuromuscular junction (NMJ). This is where the muscle fiber first responds to signaling by the motor neuron. Every skeletal muscle fiber in every skeletal muscle is innervated by a motor neuron at the NMJ. Excitation signals from the neuron are the only way to functionally activate the fiber to contract. INTERACTIVE LINK Every skeletal muscle fiber is supplied by a motor neuron at the NMJ. Watch this video to learn more about what happens at the NMJ. (a) What is the definition of a motor unit? (b) What is the structural and functional difference between a large motor unit and a small motor unit? (c) Can you give an example of each? (d) Why is the neurotransmitter acetylcholine degraded after binding to its receptor? Excitation-Contraction Coupling All living cells have membrane potentials, or electrical gradients across their membranes. The inside of the membrane is usually around -60 to -90 mV, relative to the outside. This is referred to as a cell’s membrane potential. Neurons and muscle cells can use their membrane potentials to generate electrical signals. They do this by controlling the movement of charged particles, called ions, across their membranes to create electrical currents. This is achieved by opening and closing specialized proteins in the membrane called ion channels. Although the currents generated by ions moving through these channel proteins are very small, they form the basis of both neural signaling and muscle contraction. Both neurons and skeletal muscle cells are electrically excitable, meaning that they are able to generate action potentials. An action potential is a special type of electrical signal that can travel along a cell membrane as a wave. This allows a signal to be transmitted quickly and faithfully over long distances. Although the term excitation-contraction coupling confuses or scares some students, it comes down to this: for a skeletal muscle fiber to contract, its membrane must first be “excited”—in other words, it must be stimulated to fire an action potential. The muscle fiber action potential, which sweeps along the sarcolemma as a wave, is “coupled” to the actual contraction through the release of calcium ions (Ca++) from the SR. Once released, the Ca++ interacts with the shielding proteins, forcing them to move aside so that the actin-binding sites are available for attachment by myosin heads. The myosin then pulls the actin filaments toward the center, shortening the muscle fiber. In skeletal muscle, this sequence begins with signals from the somatic motor division of the nervous system. In other words, the “excitation” step in skeletal muscles is always triggered by signaling from the nervous system (Figure 10.6). Figure 10.6 Motor End-Plate and Innervation At the NMJ, the axon terminal releases ACh. The motor end-plate is the location of the ACh-receptors in the muscle fiber sarcolemma. When ACh molecules are released, they diffuse across a minute space called the synaptic cleft and bind to the receptors. The motor neurons that tell the skeletal muscle fibers to contract originate in the spinal cord, with a smaller number located in the brainstem for activation of skeletal muscles of the face, head, and neck. These neurons have long processes, called axons, which are specialized to transmit action potentials long distances— in this case, all the way from the spinal cord to the muscle itself (which may be up to three feet away). The axons of multiple neurons bundle together to form nerves, like wires bundled together in a cable. Signaling begins when a neuronal action potential travels along the axon of a motor neuron, and then along the individual branches to terminate at the NMJ. At the NMJ, the axon terminal releases a chemical messenger, or neurotransmitter, called acetylcholine (ACh). The ACh molecules diffuse across a minute space called the synaptic cleft and bind to ACh receptors located within the motor end-plate of the sarcolemma on the other side of the synapse. Once ACh binds, a channel in the ACh receptor opens and positively charged ions can pass through into the muscle fiber, causing it to depolarize, meaning that the membrane potential of the muscle fiber becomes less negative (closer to zero.) As the membrane depolarizes, another set of ion channels called voltage-gated sodium channels are triggered to open. Sodium ions enter the muscle fiber, and an action potential rapidly spreads (or “fires”) along the entire membrane to initiate excitation-contraction coupling. Things happen very quickly in the world of excitable membranes (just think about how quickly you can snap your fingers as soon as you decide to do it). Immediately following depolarization of the membrane, it repolarizes, re-establishing the negative membrane potential. Meanwhile, the ACh in the synaptic cleft is degraded by the enzyme acetylcholinesterase (AChE) so that the ACh cannot rebind to a receptor and reopen its channel, which would cause unwanted extended muscle excitation and contraction. Propagation of an action potential along the sarcolemma is the excitation portion of excitation-contraction coupling. Recall that this excitation actually triggers the release of calcium ions (Ca++) from its storage in the cell’s SR. For the action potential to reach the membrane of the SR, there are periodic invaginations in the sarcolemma, called T-tubules (“T” stands for “transverse”). You will recall that the diameter of a muscle fiber can be up to 100 μm, so these T-tubules ensure that the membrane can get close to the SR in the sarcoplasm. The arrangement of a T-tubule with the membranes of SR on either side is called a triad (Figure 10.7). The triad surrounds the cylindrical structure called a myofibril, which contains actin and myosin. Figure 10.7 The T-tubule Narrow T-tubules permit the conduction of electrical impulses. The SR functions to regulate intracellular levels of calcium. Two terminal cisternae (where enlarged SR connects to the T-tubule) and one T-tubule comprise a triad—a “threesome” of membranes, with those of SR on two sides and the T-tubule sandwiched between them. The T-tubules carry the action potential into the interior of the cell, which triggers the opening of calcium channels in the membrane of the adjacent SR, causing Ca++ to diffuse out of the SR and into the sarcoplasm. It is the arrival of Ca++ in the sarcoplasm that initiates contraction of the muscle fiber by its contractile units, or sarcomeres. Muscle Fiber Contraction and Relaxation - Describe the components involved in a muscle contraction - Explain how muscles contract and relax - Describe the sliding filament model of muscle contraction The sequence of events that result in the contraction of an individual muscle fiber begins with a signal—the neurotransmitter, ACh—from the motor neuron innervating that fiber. The local membrane of the fiber will depolarize as positively charged sodium ions (Na+) enter, triggering an action potential that spreads to the rest of the membrane which will depolarize, including the T-tubules. This triggers the release of calcium ions (Ca++) from storage in the sarcoplasmic reticulum (SR). The Ca++ then initiates contraction, which is sustained by ATP (Figure 10.8). As long as Ca++ ions remain in the sarcoplasm to bind to troponin, which keeps the actin-binding sites “unshielded,” and as long as ATP is available to drive the cross-bridge cycling and the pulling of actin strands by myosin, the muscle fiber will continue to shorten to an anatomical limit. Figure 10.8 Contraction of a Muscle Fiber A cross-bridge forms between actin and the myosin heads triggering contraction. As long as Ca++ ions remain in the sarcoplasm to bind to troponin, and as long as ATP is available, the muscle fiber will continue to shorten. Muscle contraction usually stops when signaling from the motor neuron ends, which repolarizes the sarcolemma and T-tubules, and closes the voltage-gated calcium channels in the SR. Ca++ ions are then pumped back into the SR, which causes the tropomyosin to reshield (or re-cover) the binding sites on the actin strands. A muscle also can stop contracting when it runs out of ATP and becomes fatigued (Figure 10.9). Figure 10.9 Relaxation of a Muscle Fiber Ca++ ions are pumped back into the SR, which causes the tropomyosin to reshield the binding sites on the actin strands. A muscle may also stop contracting when it runs out of ATP and becomes fatigued. INTERACTIVE LINK The release of calcium ions initiates muscle contractions. Watch this video to learn more about the role of calcium. (a) What are “T-tubules” and what is their role? (b) Please describe how actin-binding sites are made available for cross-bridging with myosin heads during contraction. The molecular events of muscle fiber shortening occur within the fiber’s sarcomeres (see Figure 10.10). The contraction of a striated muscle fiber occurs as the sarcomeres, linearly arranged within myofibrils, shorten as myosin heads pull on the actin filaments. The region where thick and thin filaments overlap has a dense appearance, as there is little space between the filaments. This zone where thin and thick filaments overlap is very important to muscle contraction, as it is the site where filament movement starts. Thin filaments, anchored at their ends by the Z-discs, do not extend completely into the central region that only contains thick filaments, anchored at their bases at a spot called the M-line. A myofibril is composed of many sarcomeres running along its length; thus, myofibrils and muscle cells contract as the sarcomeres contract. The Sliding Filament Model of Contraction When signaled by a motor neuron, a skeletal muscle fiber contracts as the thin filaments are pulled and then slide past the thick filaments within the fiber’s sarcomeres. This process is known as the sliding filament model of muscle contraction (Figure 10.10). The sliding can only occur when myosin-binding sites on the actin filaments are exposed by a series of steps that begins with Ca++ entry into the sarcoplasm. Figure 10.10 The Sliding Filament Model of Muscle Contraction When a sarcomere contracts, the Z lines move closer together, and the I band becomes smaller. The A band stays the same width. At full contraction, the thin and thick filaments overlap completely. Tropomyosin is a protein that winds around the chains of the actin filament and covers the myosin-binding sites to prevent actin from binding to myosin. Tropomyosin binds to troponin to form a troponin-tropomyosin complex. The troponin-tropomyosin complex prevents the myosin “heads” from binding to the active sites on the actin microfilaments. Troponin also has a binding site for Ca++ ions. To initiate muscle contraction, tropomyosin has to expose the myosin-binding site on an actin filament to allow cross-bridge formation between the actin and myosin microfilaments. The first step in the process of contraction is for Ca++ to bind to troponin so that tropomyosin can slide away from the binding sites on the actin strands. This allows the myosin heads to bind to these exposed binding sites and form cross-bridges. The thin filaments are then pulled by the myosin heads to slide past the thick filaments toward the center of the sarcomere. But each head can only pull a very short distance before it has reached its limit and must be “re-cocked” before it can pull again, a step that requires ATP. ATP and Muscle Contraction For thin filaments to continue to slide past thick filaments during muscle contraction, myosin heads must pull the actin at the binding sites, detach, re-cock, attach to more binding sites, pull, detach, re-cock, etc. This repeated movement is known as the cross-bridge cycle. This motion of the myosin heads is similar to the oars when an individual rows a boat: The paddle of the oars (the myosin heads) pull, are lifted from the water (detach), repositioned (re-cocked) and then immersed again to pull (Figure 10.11). Each cycle requires energy, and the action of the myosin heads in the sarcomeres repetitively pulling on the thin filaments also requires energy, which is provided by ATP. Figure 10.11 Skeletal Muscle Contraction (a) The active site on actin is exposed as calcium binds to troponin. (b) The myosin head is attracted to actin, and myosin binds actin at its actin-binding site, forming the cross-bridge. (c) During the power stroke, the phosphate generated in the previous contraction cycle is released. This results in the myosin head pivoting toward the center of the sarcomere, after which the attached ADP and phosphate group are released. (d) A new molecule of ATP attaches to the myosin head, causing the cross-bridge to detach. (e) The myosin head hydrolyzes ATP to ADP and phosphate, which returns the myosin to the cocked position. Cross-bridge formation occurs when the myosin head attaches to the actin while adenosine diphosphate (ADP) and inorganic phosphate (Pi) are still bound to myosin (Figure 10.11a,b). Pi is then released, causing myosin to form a stronger attachment to the actin, after which the myosin head moves toward the M-line, pulling the actin along with it. As actin is pulled, the filaments move approximately 10 nm toward the M-line. This movement is called the power stroke, as movement of the thin filament occurs at this step (Figure 10.11c). In the absence of ATP, the myosin head will not detach from actin. One part of the myosin head attaches to the binding site on the actin, but the head has another binding site for ATP. ATP binding causes the myosin head to detach from the actin (Figure 10.11d). After this occurs, ATP is converted to ADP and Pi by the intrinsic ATPase activity of myosin. The energy released during ATP hydrolysis changes the angle of the myosin head into a cocked position (Figure 10.11e). The myosin head is now in position for further movement. When the myosin head is cocked, myosin is in a high-energy configuration. This energy is expended as the myosin head moves through the power stroke, and at the end of the power stroke, the myosin head is in a low-energy position. After the power stroke, ADP is released; however, the formed cross-bridge is still in place, and actin and myosin are bound together. As long as ATP is available, it readily attaches to myosin, the cross-bridge cycle can recur, and muscle contraction can continue. Note that each thick filament of roughly 300 myosin molecules has multiple myosin heads, and many cross-bridges form and break continuously during muscle contraction. Multiply this by all of the sarcomeres in one myofibril, all the myofibrils in one muscle fiber, and all of the muscle fibers in one skeletal muscle, and you can understand why so much energy (ATP) is needed to keep skeletal muscles working. In fact, it is the loss of ATP that results in the rigor mortis observed soon after someone dies. With no further ATP production possible, there is no ATP available for myosin heads to detach from the actin-binding sites, so the cross-bridges stay in place, causing the rigidity in the skeletal muscles. Sources of ATP ATP supplies the energy for muscle contraction to take place. In addition to its direct role in the cross-bridge cycle, ATP also provides the energy for the active-transport Ca++ pumps in the SR. Muscle contraction does not occur without sufficient amounts of ATP. The amount of ATP stored in muscle is very low, only sufficient to power a few seconds worth of contractions. As it is broken down, ATP must therefore be regenerated and replaced quickly to allow for sustained contraction. There are three mechanisms by which ATP can be regenerated: creatine phosphate metabolism, anaerobic glycolysis, and fermentation and aerobic respiration. Creatine phosphate is a molecule that can store energy in its phosphate bonds. In a resting muscle, excess ATP transfers its energy to creatine, producing ADP and creatine phosphate. This acts as an energy reserve that can be used to quickly create more ATP. When the muscle starts to contract and needs energy, creatine phosphate transfers its phosphate back to ADP to form ATP and creatine. This reaction is catalyzed by the enzyme creatine kinase and occurs very quickly; thus, creatine phosphate-derived ATP powers the first few seconds of muscle contraction. However, creatine phosphate can only provide approximately 15 seconds worth of energy, at which point another energy source has to be used (Figure 10.12). Figure 10.12 Muscle Metabolism (a) Some ATP is stored in a resting muscle. As contraction starts, it is used up in seconds. More ATP is generated from creatine phosphate for about 15 seconds. (b) Each glucose molecule produces two ATP and two molecules of pyruvic acid, which can be used in aerobic respiration or converted to lactic acid. If oxygen is not available, pyruvic acid is converted to lactic acid, which may contribute to muscle fatigue. This occurs during strenuous exercise when high amounts of energy are needed but oxygen cannot be sufficiently delivered to muscle. (c) Aerobic respiration is the breakdown of glucose in the presence of oxygen (O2) to produce carbon dioxide, water, and ATP. Approximately 95 percent of the ATP required for resting or moderately active muscles is provided by aerobic respiration, which takes place in mitochondria. As the ATP produced by creatine phosphate is depleted, muscles turn to glycolysis as an ATP source. Glycolysis is an anaerobic (non-oxygen-dependent) process that breaks down glucose (sugar) to produce ATP; however, glycolysis cannot generate ATP as quickly as creatine phosphate. Thus, the switch to glycolysis results in a slower rate of ATP availability to the muscle. The sugar used in glycolysis can be provided by blood glucose or by metabolizing glycogen that is stored in the muscle. The breakdown of one glucose molecule produces two ATP and two molecules of pyruvic acid, which can be used in aerobic respiration or when oxygen levels are low, converted to lactic acid (Figure 10.12b). If oxygen is available, pyruvic acid is used in aerobic respiration. However, if oxygen is not available, pyruvic acid is converted to lactic acid, which may contribute to muscle fatigue. This conversion allows the recycling of the enzyme NAD+ from NADH, which is needed for glycolysis to continue. This occurs during strenuous exercise when high amounts of energy are needed but oxygen cannot be sufficiently delivered to muscle. Glycolysis itself cannot be sustained for very long (approximately 1 minute of muscle activity), but it is useful in facilitating short bursts of high-intensity output. This is because glycolysis does not utilize glucose very efficiently, producing a net gain of two ATPs per molecule of glucose, and the end product of lactic acid, which may contribute to muscle fatigue as it accumulates. Aerobic respiration is the breakdown of glucose or other nutrients in the presence of oxygen (O2) to produce carbon dioxide, water, and ATP. Approximately 95 percent of the ATP required for resting or moderately active muscles is provided by aerobic respiration, which takes place in mitochondria. The inputs for aerobic respiration include glucose circulating in the bloodstream, pyruvic acid, and fatty acids. Aerobic respiration is much more efficient than anaerobic glycolysis, producing approximately 36 ATPs per molecule of glucose versus four from glycolysis. However, aerobic respiration cannot be sustained without a steady supply of O2 to the skeletal muscle and is much slower (Figure 10.12c). To compensate, muscles store small amount of excess oxygen in proteins call myoglobin, allowing for more efficient muscle contractions and less fatigue. Aerobic training also increases the efficiency of the circulatory system so that O2 can be supplied to the muscles for longer periods of time. Muscle fatigue occurs when a muscle can no longer contract in response to signals from the nervous system. The exact causes of muscle fatigue are not fully known, although certain factors have been correlated with the decreased muscle contraction that occurs during fatigue. ATP is needed for normal muscle contraction, and as ATP reserves are reduced, muscle function may decline. This may be more of a factor in brief, intense muscle output rather than sustained, lower intensity efforts. Lactic acid buildup may lower intracellular pH, affecting enzyme and protein activity. Imbalances in Na+ and K+ levels as a result of membrane depolarization may disrupt Ca++ flow out of the SR. Long periods of sustained exercise may damage the SR and the sarcolemma, resulting in impaired Ca++ regulation. Intense muscle activity results in an oxygen debt, which is the amount of oxygen needed to compensate for ATP produced without oxygen during muscle contraction. Oxygen is required to restore ATP and creatine phosphate levels, convert lactic acid to pyruvic acid, and, in the liver, to convert lactic acid into glucose or glycogen. Other systems used during exercise also require oxygen, and all of these combined processes result in the increased breathing rate that occurs after exercise. Until the oxygen debt has been met, oxygen intake is elevated, even after exercise has stopped. Relaxation of a Skeletal Muscle Relaxing skeletal muscle fibers, and ultimately, the skeletal muscle, begins with the motor neuron, which stops releasing its chemical signal, ACh, into the synapse at the NMJ. The muscle fiber will repolarize, which closes the gates in the SR where Ca++ was being released. ATP-driven pumps will move Ca++ out of the sarcoplasm back into the SR. This results in the “reshielding” of the actin-binding sites on the thin filaments. Without the ability to form cross-bridges between the thin and thick filaments, the muscle fiber loses its tension and relaxes. Muscle Strength The number of skeletal muscle fibers in a given muscle is genetically determined and does not change. Muscle strength is directly related to the amount of myofibrils and sarcomeres within each fiber. Factors, such as hormones and stress (and artificial anabolic steroids), acting on the muscle can increase the production of sarcomeres and myofibrils within the muscle fibers, a change called hypertrophy, which results in the increased mass and bulk in a skeletal muscle. Likewise, decreased use of a skeletal muscle results in atrophy, where the number of sarcomeres and myofibrils disappear (but not the number of muscle fibers). It is common for a limb in a cast to show atrophied muscles when the cast is removed, and certain diseases, such as polio, show atrophied muscles. DISORDERS OF THE... Muscular System Duchenne muscular dystrophy (DMD) is a progressive weakening of the skeletal muscles. It is one of several diseases collectively referred to as “muscular dystrophy.” DMD is caused by a lack of the protein dystrophin, which helps the thin filaments of myofibrils bind to the sarcolemma. Without sufficient dystrophin, muscle contractions cause the sarcolemma to tear, causing an influx of Ca++, leading to cellular damage and muscle fiber degradation. Over time, as muscle damage accumulates, muscle mass is lost, and greater functional impairments develop. DMD is an inherited disorder caused by an abnormal X chromosome. It primarily affects males, and it is usually diagnosed in early childhood. DMD usually first appears as difficulty with balance and motion, and then progresses to an inability to walk. It continues progressing upward in the body from the lower extremities to the upper body, where it affects the muscles responsible for breathing and circulation. It ultimately causes death due to respiratory failure, and those afflicted do not usually live past their 20s. Because DMD is caused by a mutation in the gene that codes for dystrophin, it was thought that introducing healthy myoblasts into patients might be an effective treatment. Myoblasts are the embryonic cells responsible for muscle development, and ideally, they would carry healthy genes that could produce the dystrophin needed for normal muscle contraction. This approach has been largely unsuccessful in humans. A recent approach has involved attempting to boost the muscle’s production of utrophin, a protein similar to dystrophin that may be able to assume the role of dystrophin and prevent cellular damage from occurring. Nervous System Control of Muscle Tension - Explain concentric, isotonic, and eccentric contractions - Describe the length-tension relationship - Describe the three phases of a muscle twitch - Define wave summation, tetanus, and treppe To move an object, referred to as load, the sarcomeres in the muscle fibers of the skeletal muscle must shorten. The force generated by the contraction of the muscle (or shortening of the sarcomeres) is called muscle tension. However, muscle tension also is generated when the muscle is contracting against a load that does not move, resulting in two main types of skeletal muscle contractions: isotonic contractions and isometric contractions. In isotonic contractions, where the tension in the muscle stays constant, a load is moved as the length of the muscle changes (shortens). There are two types of isotonic contractions: concentric and eccentric. A concentric contraction involves the muscle shortening to move a load. An example of this is the biceps brachii muscle contracting when a hand weight is brought upward with increasing muscle tension. As the biceps brachii contract, the angle of the elbow joint decreases as the forearm is brought toward the body. Here, the biceps brachii contracts as sarcomeres in its muscle fibers are shortening and cross-bridges form; the myosin heads pull the actin. An eccentric contraction occurs as the muscle tension diminishes and the muscle lengthens. In this case, the hand weight is lowered in a slow and controlled manner as the amount of cross-bridges being activated by nervous system stimulation decreases. In this case, as tension is released from the biceps brachii, the angle of the elbow joint increases. Eccentric contractions are also used for movement and balance of the body. An isometric contraction occurs as the muscle produces tension without changing the angle of a skeletal joint. Isometric contractions involve sarcomere shortening and increasing muscle tension, but do not move a load, as the force produced cannot overcome the resistance provided by the load. For example, if one attempts to lift a hand weight that is too heavy, there will be sarcomere activation and shortening to a point, and ever-increasing muscle tension, but no change in the angle of the elbow joint. In everyday living, isometric contractions are active in maintaining posture and maintaining bone and joint stability. However, holding your head in an upright position occurs not because the muscles cannot move the head, but because the goal is to remain stationary and not produce movement. Most actions of the body are the result of a combination of isotonic and isometric contractions working together to produce a wide range of outcomes (Figure 10.13). Figure 10.13 Types of Muscle Contractions During isotonic contractions, muscle length changes to move a load. During isometric contractions, muscle length does not change because the load exceeds the tension the muscle can generate. All of these muscle activities are under the exquisite control of the nervous system. Neural control regulates concentric, eccentric and isometric contractions, muscle fiber recruitment, and muscle tone. A crucial aspect of nervous system control of skeletal muscles is the role of motor units. Motor Units As you have learned, every skeletal muscle fiber must be innervated by the axon terminal of a motor neuron in order to contract. Each muscle fiber is innervated by only one motor neuron. The actual group of muscle fibers in a muscle innervated by a single motor neuron is called a motor unit. The size of a motor unit is variable depending on the nature of the muscle. A small motor unit is an arrangement where a single motor neuron supplies a small number of muscle fibers in a muscle. Small motor units permit very fine motor control of the muscle. The best example in humans is the small motor units of the extraocular eye muscles that move the eyeballs. There are thousands of muscle fibers in each muscle, but every six or so fibers are supplied by a single motor neuron, as the axons branch to form synaptic connections at their individual NMJs. This allows for exquisite control of eye movements so that both eyes can quickly focus on the same object. Small motor units are also involved in the many fine movements of the fingers and thumb of the hand for grasping, texting, etc. A large motor unit is an arrangement where a single motor neuron supplies a large number of muscle fibers in a muscle. Large motor units are concerned with simple, or “gross,” movements, such as powerfully extending the knee joint. The best example is the large motor units of the thigh muscles or back muscles, where a single motor neuron will supply thousands of muscle fibers in a muscle, as its axon splits into thousands of branches. There is a wide range of motor units within many skeletal muscles, which gives the nervous system a wide range of control over the muscle. The small motor units in the muscle will have smaller, lower-threshold motor neurons that are more excitable, firing first to their skeletal muscle fibers, which also tend to be the smallest. Activation of these smaller motor units, results in a relatively small degree of contractile strength (tension) generated in the muscle. As more strength is needed, larger motor units, with bigger, higher-threshold motor neurons are enlisted to activate larger muscle fibers. This increasing activation of motor units produces an increase in muscle contraction known as recruitment. As more motor units are recruited, the muscle contraction grows progressively stronger. In some muscles, the largest motor units may generate a contractile force of 50 times more than the smallest motor units in the muscle. This allows a feather to be picked up using the biceps brachii arm muscle with minimal force, and a heavy weight to be lifted by the same muscle by recruiting the largest motor units. When necessary, the maximal number of motor units in a muscle can be recruited simultaneously, producing the maximum force of contraction for that muscle, but this cannot last for very long because of the energy requirements to sustain the contraction. To prevent complete muscle fatigue, motor units are generally not all simultaneously active, but instead some motor units rest while others are active, which allows for longer muscle contractions. The nervous system uses recruitment as a mechanism to efficiently utilize a skeletal muscle. The Length-Tension Range of a Sarcomere When a skeletal muscle fiber contracts, myosin heads attach to actin to form cross-bridges followed by the thin filaments sliding over the thick filaments as the heads pull the actin, and this results in sarcomere shortening, creating the tension of the muscle contraction. The cross-bridges can only form where thin and thick filaments already overlap, so that the length of the sarcomere has a direct influence on the force generated when the sarcomere shortens. This is called the length-tension relationship. The ideal length of a sarcomere to produce maximal tension occurs at 80 percent to 120 percent of its resting length, with 100 percent being the state where the medial edges of the thin filaments are just at the most-medial myosin heads of the thick filaments (Figure 10.14). This length maximizes the overlap of actin-binding sites and myosin heads. If a sarcomere is stretched past this ideal length (beyond 120 percent), thick and thin filaments do not overlap sufficiently, which results in less tension produced. If a sarcomere is shortened beyond 80 percent, the zone of overlap is reduced with the thin filaments jutting beyond the last of the myosin heads and shrinks the H zone, which is normally composed of myosin tails. Eventually, there is nowhere else for the thin filaments to go and the amount of tension is diminished. If the muscle is stretched to the point where thick and thin filaments do not overlap at all, no cross-bridges can be formed, and no tension is produced in that sarcomere. This amount of stretching does not usually occur, as accessory proteins and connective tissue oppose extreme stretching. Figure 10.14 The Ideal Length of a Sarcomere Sarcomeres produce maximal tension when thick and thin filaments overlap between about 80 percent to 120 percent. The Frequency of Motor Neuron Stimulation A single action potential from a motor neuron will produce a single contraction in the muscle fibers of its motor unit. This isolated contraction is called a twitch. A twitch can last for a few milliseconds or 100 milliseconds, depending on the muscle type. The tension produced by a single twitch can be measured by a myogram, an instrument that measures the amount of tension produced over time (Figure 10.15). Each twitch undergoes three phases. The first phase is the latent period, during which the action potential is being propagated along the sarcolemma and Ca++ ions are released from the SR. This is the phase during which excitation and contraction are being coupled but contraction has yet to occur. The contraction phase occurs next. The Ca++ ions in the sarcoplasm have bound to troponin, tropomyosin has shifted away from actin-binding sites, cross-bridges formed, and sarcomeres are actively shortening to the point of peak tension. The last phase is the relaxation phase, when tension decreases as contraction stops. Ca++ ions are pumped out of the sarcoplasm into the SR, and cross-bridge cycling stops, returning the muscle fibers to their resting state. Figure 10.15 A Myogram of a Muscle Twitch A single muscle twitch has a latent period, a contraction phase when tension increases, and a relaxation phase when tension decreases. During the latent period, the action potential is being propagated along the sarcolemma. During the contraction phase, Ca++ ions in the sarcoplasm bind to troponin, tropomyosin moves from actin-binding sites, cross-bridges form, and sarcomeres shorten. During the relaxation phase, tension decreases as Ca++ ions are pumped out of the sarcoplasm and cross-bridge cycling stops. Although a person can experience a muscle “twitch,” a single twitch does not produce any significant muscle activity in a living body. A series of action potentials to the muscle fibers is necessary to produce a muscle contraction that can produce work. Normal muscle contraction is more sustained, and it can be modified by input from the nervous system to produce varying amounts of force; this is called a graded muscle response. The frequency of action potentials (nerve impulses) from a motor neuron and the number of motor neurons transmitting action potentials both affect the tension produced in skeletal muscle. The rate at which a motor neuron fires action potentials affects the tension produced in the skeletal muscle. If the fibers are stimulated while a previous twitch is still occurring, the second twitch will be stronger. This response is called wave summation, because the excitation-contraction coupling effects of successive motor neuron signaling is summed, or added together (Figure 10.16a). At the molecular level, summation occurs because the second stimulus triggers the release of more Ca++ ions, which become available to activate additional sarcomeres while the muscle is still contracting from the first stimulus. Summation results in greater contraction of the motor unit. Figure 10.16 Wave Summation and Tetanus (a) The excitation-contraction coupling effects of successive motor neuron signaling is added together which is referred to as wave summation. The bottom of each wave, the end of the relaxation phase, represents the point of stimulus. (b) When the stimulus frequency is so high that the relaxation phase disappears completely, the contractions become continuous; this is called tetanus. If the frequency of motor neuron signaling increases, summation and subsequent muscle tension in the motor unit continues to rise until it reaches a peak point. The tension at this point is about three to four times greater than the tension of a single twitch, a state referred to as incomplete tetanus. During incomplete tetanus, the muscle goes through quick cycles of contraction with a short relaxation phase for each. If the stimulus frequency is so high that the relaxation phase disappears completely, contractions become continuous in a process called complete tetanus (Figure 10.16b). During tetanus, the concentration of Ca++ ions in the sarcoplasm allows virtually all of the sarcomeres to form cross-bridges and shorten, so that a contraction can continue uninterrupted (until the muscle fatigues and can no longer produce tension). Treppe When a skeletal muscle has been dormant for an extended period and then activated to contract, with all other things being equal, the initial contractions generate about one-half the force of later contractions. The muscle tension increases in a graded manner that to some looks like a set of stairs. This tension increase is called treppe, a condition where muscle contractions become more efficient. It’s also known as the “staircase effect” (Figure 10.17). Figure 10.17 Treppe When muscle tension increases in a graded manner that looks like a set of stairs, it is called treppe. The bottom of each wave represents the point of stimulus. It is believed that treppe results from a higher concentration of Ca++ in the sarcoplasm resulting from the steady stream of signals from the motor neuron. It can only be maintained with adequate ATP. Muscle Tone Skeletal muscles are rarely completely relaxed, or flaccid. Even if a muscle is not producing movement, it is contracted a small amount to maintain its contractile proteins and produce muscle tone. The tension produced by muscle tone allows muscles to continually stabilize joints and maintain posture. Muscle tone is accomplished by a complex interaction between the nervous system and skeletal muscles that results in the activation of a few motor units at a time, most likely in a cyclical manner. In this manner, muscles never fatigue completely, as some motor units can recover while others are active. The absence of the low-level contractions that lead to muscle tone is referred to as hypotonia, and can result from damage to parts of the central nervous system (CNS), such as the cerebellum, or from loss of innervations to a skeletal muscle, as in poliomyelitis. Hypotonic muscles have a flaccid appearance and display functional impairments, such as weak reflexes. Conversely, excessive muscle tone is referred to as hypertonia, accompanied by hyperreflexia (excessive reflex responses), often the result of damage to upper motor neurons in the CNS. Hypertonia can present with muscle rigidity (as seen in Parkinson’s disease) or spasticity, a phasic change in muscle tone, where a limb will “snap” back from passive stretching (as seen in some strokes). Types of Muscle Fibers - Describe the types of skeletal muscle fibers - Explain fast and slow muscle fibers Two criteria to consider when classifying the types of muscle fibers are how fast some fibers contract relative to others, and how fibers produce ATP. Using these criteria, there are three main types of skeletal muscle fibers. Slow oxidative (SO) fibers contract relatively slowly and use aerobic respiration (oxygen and glucose) to produce ATP. Fast oxidative (FO) fibers have fast contractions and primarily use aerobic respiration, but because they may switch to anaerobic respiration (glycolysis), can fatigue more quickly than SO fibers. Lastly, fast glycolytic (FG) fibers have fast contractions and primarily use anaerobic glycolysis. The FG fibers fatigue more quickly than the others. Most skeletal muscles in a human contain(s) all three types, although in varying proportions. The speed of contraction is dependent on how quickly myosin’s ATPase hydrolyzes ATP to produce cross-bridge action. Fast fibers hydrolyze ATP approximately twice as quickly as slow fibers, resulting in much quicker cross-bridge cycling (which pulls the thin filaments toward the center of the sarcomeres at a faster rate). The primary metabolic pathway used by a muscle fiber determines whether the fiber is classified as oxidative or glycolytic. If a fiber primarily produces ATP through aerobic pathways it is oxidative. More ATP can be produced during each metabolic cycle, making the fiber more resistant to fatigue. Glycolytic fibers primarily create ATP through anaerobic glycolysis, which produces less ATP per cycle. As a result, glycolytic fibers fatigue at a quicker rate. The oxidative fibers contain many more mitochondria than the glycolytic fibers, because aerobic metabolism, which uses oxygen (O2) in the metabolic pathway, occurs in the mitochondria. The SO fibers possess a large number of mitochondria and are capable of contracting for longer periods because of the large amount of ATP they can produce, but they have a relatively small diameter and do not produce a large amount of tension. SO fibers are extensively supplied with blood capillaries to supply O2 from the red blood cells in the bloodstream. The SO fibers also possess myoglobin, an O2-carrying molecule similar to O2-carrying hemoglobin in the red blood cells. The myoglobin stores some of the needed O2 within the fibers themselves (and gives SO fibers their red color). All of these features allow SO fibers to produce large quantities of ATP, which can sustain muscle activity without fatiguing for long periods of time. The fact that SO fibers can function for long periods without fatiguing makes them useful in maintaining posture, producing isometric contractions, stabilizing bones and joints, and making small movements that happen often but do not require large amounts of energy. They do not produce high tension, and thus they are not used for powerful, fast movements that require high amounts of energy and rapid cross-bridge cycling. FO fibers are sometimes called intermediate fibers because they possess characteristics that are intermediate between fast fibers and slow fibers. They produce ATP relatively quickly, more quickly than SO fibers, and thus can produce relatively high amounts of tension. They are oxidative because they produce ATP aerobically, possess high amounts of mitochondria, and do not fatigue quickly. However, FO fibers do not possess significant myoglobin, giving them a lighter color than the red SO fibers. FO fibers are used primarily for movements, such as walking, that require more energy than postural control but less energy than an explosive movement, such as sprinting. FO fibers are useful for this type of movement because they produce more tension than SO fibers but they are more fatigue-resistant than FG fibers. FG fibers primarily use anaerobic glycolysis as their ATP source. They have a large diameter and possess high amounts of glycogen, which is used in glycolysis to generate ATP quickly to produce high levels of tension. Because they do not primarily use aerobic metabolism, they do not possess substantial numbers of mitochondria or significant amounts of myoglobin and therefore have a white color. FG fibers are used to produce rapid, forceful contractions to make quick, powerful movements. These fibers fatigue quickly, permitting them to only be used for short periods. Most muscles possess a mixture of each fiber type. The predominant fiber type in a muscle is determined by the primary function of the muscle. Exercise and Muscle Performance - Describe hypertrophy and atrophy - Explain how resistance exercise builds muscle - Explain how performance-enhancing substances affect muscle Physical training alters the appearance of skeletal muscles and can produce changes in muscle performance. Conversely, a lack of use can result in decreased performance and muscle appearance. Although muscle cells can change in size, new cells are not formed when muscles grow. Instead, structural proteins are added to muscle fibers in a process called hypertrophy, so cell diameter increases. The reverse, when structural proteins are lost and muscle mass decreases, is called atrophy. Age-related muscle atrophy is called sarcopenia. Cellular components of muscles can also undergo changes in response to changes in muscle use. Endurance Exercise Slow fibers are predominantly used in endurance exercises that require little force but involve numerous repetitions. The aerobic metabolism used by slow-twitch fibers allows them to maintain contractions over long periods. Endurance training modifies these slow fibers to make them even more efficient by producing more mitochondria to enable more aerobic metabolism and more ATP production. Endurance exercise can also increase the amount of myoglobin in a cell, as increased aerobic respiration increases the need for oxygen. Myoglobin is found in the sarcoplasm and acts as an oxygen storage supply for the mitochondria. The training can trigger the formation of more extensive capillary networks around the fiber, a process called angiogenesis, to supply oxygen and remove metabolic waste. To allow these capillary networks to supply the deep portions of the muscle, muscle mass does not greatly increase in order to maintain a smaller area for the diffusion of nutrients and gases. All of these cellular changes result in the ability to sustain low levels of muscle contractions for greater periods without fatiguing. The proportion of SO muscle fibers in muscle determines the suitability of that muscle for endurance, and may benefit those participating in endurance activities. Postural muscles have a large number of SO fibers and relatively few FO and FG fibers, to keep the back straight (Figure 10.18). Endurance athletes, like marathon-runners also would benefit from a larger proportion of SO fibers, but it is unclear if the most-successful marathoners are those with naturally high numbers of SO fibers, or whether the most successful marathon runners develop high numbers of SO fibers with repetitive training. Endurance training can result in overuse injuries such as stress fractures and joint and tendon inflammation. Figure 10.18 Marathoners Long-distance runners have a large number of SO fibers and relatively few FO and FG fibers. (credit: “Tseo2”/Wikimedia Commons) Resistance Exercise Resistance exercises, as opposed to endurance exercise, require large amounts of FG fibers to produce short, powerful movements that are not repeated over long periods. The high rates of ATP hydrolysis and cross-bridge formation in FG fibers result in powerful muscle contractions. Muscles used for power have a higher ratio of FG to SO/FO fibers, and trained athletes possess even higher levels of FG fibers in their muscles. Resistance exercise affects muscles by increasing the formation of myofibrils, thereby increasing the thickness of muscle fibers. This added structure causes hypertrophy, or the enlargement of muscles, exemplified by the large skeletal muscles seen in body builders and other athletes (Figure 10.19). Because this muscular enlargement is achieved by the addition of structural proteins, athletes trying to build muscle mass often ingest large amounts of protein. Figure 10.19 Hypertrophy Body builders have a large number of FG fibers and relatively few FO and SO fibers. (credit: Lin Mei/flickr) Except for the hypertrophy that follows an increase in the number of sarcomeres and myofibrils in a skeletal muscle, the cellular changes observed during endurance training do not usually occur with resistance training. There is usually no significant increase in mitochondria or capillary density. However, resistance training does increase the development of connective tissue, which adds to the overall mass of the muscle and helps to contain muscles as they produce increasingly powerful contractions. Tendons also become stronger to prevent tendon damage, as the force produced by muscles is transferred to tendons that attach the muscle to bone. For effective strength training, the intensity of the exercise must continually be increased. For instance, continued weight lifting without increasing the weight of the load does not increase muscle size. To produce ever-greater results, the weights lifted must become increasingly heavier, making it more difficult for muscles to move the load. The muscle then adapts to this heavier load, and an even heavier load must be used if even greater muscle mass is desired. If done improperly, resistance training can lead to overuse injuries of the muscle, tendon, or bone. These injuries can occur if the load is too heavy or if the muscles are not given sufficient time between workouts to recover or if joints are not aligned properly during the exercises. Cellular damage to muscle fibers that occurs after intense exercise includes damage to the sarcolemma and myofibrils. This muscle damage contributes to the feeling of soreness after strenuous exercise, but muscles gain mass as this damage is repaired, and additional structural proteins are added to replace the damaged ones. Overworking skeletal muscles can also lead to tendon damage and even skeletal damage if the load is too great for the muscles to bear. Performance-Enhancing Substances Some athletes attempt to boost their performance by using various agents that may enhance muscle performance. Anabolic steroids are one of the more widely known agents used to boost muscle mass and increase power output. Anabolic steroids are a form of testosterone, a male sex hormone that stimulates muscle formation, leading to increased muscle mass. Endurance athletes may also try to boost the availability of oxygen to muscles to increase aerobic respiration by using substances such as erythropoietin (EPO), a hormone normally produced in the kidneys, which triggers the production of red blood cells. The extra oxygen carried by these blood cells can then be used by muscles for aerobic respiration. Human growth hormone (hGH) is another supplement, and although it can facilitate building muscle mass, its main role is to promote the healing of muscle and other tissues after strenuous exercise. Increased hGH may allow for faster recovery after muscle damage, reducing the rest required after exercise, and allowing for more sustained high-level performance. Although performance-enhancing substances often do improve performance, most are banned by governing bodies in sports and are illegal for nonmedical purposes. Their use to enhance performance raises ethical issues of cheating because they give users an unfair advantage over nonusers. A greater concern, however, is that their use carries serious health risks. The side effects of these substances are often significant, nonreversible, and in some cases fatal. The physiological strain caused by these substances is often greater than what the body can handle, leading to effects that are unpredictable and dangerous. Anabolic steroid use has been linked to infertility, aggressive behavior, cardiovascular disease, and brain cancer. Similarly, some athletes have used creatine to increase power output. Creatine phosphate provides quick bursts of ATP to muscles in the initial stages of contraction. Increasing the amount of creatine available to cells is thought to produce more ATP and therefore increase explosive power output, although its effectiveness as a supplement has been questioned. EVERYDAY CONNECTION Aging and Muscle Tissue Although atrophy due to disuse can often be reversed with exercise, muscle atrophy with age, referred to as sarcopenia, is irreversible. This is a primary reason why even highly trained athletes succumb to declining performance with age. This decline is noticeable in athletes whose sports require strength and powerful movements, such as sprinting, whereas the effects of age are less noticeable in endurance athletes such as marathon runners or long-distance cyclists. As muscles age, muscle fibers die, and they are replaced by connective tissue and adipose tissue (Figure 10.20). Because those tissues cannot contract and generate force as muscle can, muscles lose the ability to produce powerful contractions. The decline in muscle mass causes a loss of strength, including the strength required for posture and mobility. This may be caused by a reduction in FG fibers that hydrolyze ATP quickly to produce short, powerful contractions. Muscles in older people sometimes possess greater numbers of SO fibers, which are responsible for longer contractions and do not produce powerful movements. There may also be a reduction in the size of motor units, resulting in fewer fibers being stimulated and less muscle tension being produced. Figure 10.20 Atrophy Muscle mass is reduced as muscles atrophy with disuse. Sarcopenia can be delayed to some extent by exercise, as training adds structural proteins and causes cellular changes that can offset the effects of atrophy. Increased exercise can produce greater numbers of cellular mitochondria, increase capillary density, and increase the mass and strength of connective tissue. The effects of age-related atrophy are especially pronounced in people who are sedentary, as the loss of muscle cells is displayed as functional impairments such as trouble with locomotion, balance, and posture. This can lead to a decrease in quality of life and medical problems, such as joint problems because the muscles that stabilize bones and joints are weakened. Problems with locomotion and balance can also cause various injuries due to falls. Cardiac Muscle Tissue - Describe intercalated discs and gap junctions - Describe a desmosome Cardiac muscle tissue is only found in the heart. Highly coordinated contractions of cardiac muscle pump blood into the vessels of the circulatory system. Similar to skeletal muscle, cardiac muscle is striated and organized into sarcomeres, possessing the same banding organization as skeletal muscle (Figure 10.21). However, cardiac muscle fibers are shorter than skeletal muscle fibers and usually contain only one nucleus, which is located in the central region of the cell. Cardiac muscle fibers also possess many mitochondria and myoglobin, as ATP is produced primarily through aerobic metabolism. Cardiac muscle fibers cells also are extensively branched and are connected to one another at their ends by intercalated discs. An intercalated disc allows the cardiac muscle cells to contract in a wave-like pattern so that the heart can work as a pump. Figure 10.21 Cardiac Muscle Tissue Cardiac muscle tissue is only found in the heart. LM × 1600. (Micrograph provided by the Regents of University of Michigan Medical School © 2012) INTERACTIVE LINK View the University of Michigan WebScope to explore the tissue sample in greater detail. Intercalated discs are part of the sarcolemma and contain two structures important in cardiac muscle contraction: gap junctions and desmosomes. A gap junction forms channels between adjacent cardiac muscle fibers that allow the depolarizing current produced by cations to flow from one cardiac muscle cell to the next. This joining is called electric coupling, and in cardiac muscle it allows the quick transmission of action potentials and the coordinated contraction of the entire heart. This network of electrically connected cardiac muscle cells creates a functional unit of contraction called a syncytium. The remainder of the intercalated disc is composed of desmosomes. A desmosome is a cell structure that anchors the ends of cardiac muscle fibers together so the cells do not pull apart during the stress of individual fibers contracting (Figure 10.22). Figure 10.22 Cardiac Muscle Intercalated discs are part of the cardiac muscle sarcolemma and they contain gap junctions and desmosomes. Contractions of the heart (heartbeats) are controlled by specialized cardiac muscle cells called pacemaker cells that directly control heart rate. Although cardiac muscle cannot be consciously controlled, the pacemaker cells respond to signals from the autonomic nervous system (ANS) to speed up or slow down the heart rate. The pacemaker cells can also respond to various hormones that modulate heart rate to control blood pressure. The wave of contraction that allows the heart to work as a unit, called a functional syncytium, begins with the pacemaker cells. This group of cells is self-excitable and able to depolarize to threshold and fire action potentials on their own, a feature called autorhythmicity; they do this at set intervals which determine heart rate. Because they are connected with gap junctions to surrounding muscle fibers and the specialized fibers of the heart’s conduction system, the pacemaker cells are able to transfer the depolarization to the other cardiac muscle fibers in a manner that allows the heart to contract in a coordinated manner. Another feature of cardiac muscle is its relatively long action potentials in its fibers, having a sustained depolarization “plateau.” The plateau is produced by Ca++ entry though voltage-gated calcium channels in the sarcolemma of cardiac muscle fibers. This sustained depolarization (and Ca++ entry) provides for a longer contraction than is produced by an action potential in skeletal muscle. Unlike skeletal muscle, a large percentage of the Ca++ that initiates contraction in cardiac muscles comes from outside the cell rather than from the SR. Smooth Muscle - Describe a dense body - Explain how smooth muscle works with internal organs and passageways through the body - Explain how smooth muscles differ from skeletal and cardiac muscles - Explain the difference between single-unit and multi-unit smooth muscle Smooth muscle (so-named because the cells do not have striations) is present in the walls of hollow organs like the urinary bladder, uterus, stomach, intestines, and in the walls of passageways, such as the arteries and veins of the circulatory system, and the tracts of the respiratory, urinary, and reproductive systems (Figure 10.23ab). Smooth muscle is also present in the eyes, where it functions to change the size of the iris and alter the shape of the lens; and in the skin where it causes hair to stand erect in response to cold temperature or fear. Figure 10.23 Smooth Muscle Tissue Smooth muscle tissue is found around organs in the digestive, respiratory, reproductive tracts and the iris of the eye. LM × 1600. (Micrograph provided by the Regents of University of Michigan Medical School © 2012) INTERACTIVE LINK View the University of Michigan WebScope to explore the tissue sample in greater detail. Smooth muscle fibers are spindle-shaped (wide in the middle and tapered at both ends, somewhat like a football) and have a single nucleus; they range from about 30 to 200 μm (thousands of times shorter than skeletal muscle fibers), and they produce their own connective tissue, endomysium. Although they do not have striations and sarcomeres, smooth muscle fibers do have actin and myosin contractile proteins, and thick and thin filaments. These thin filaments are anchored by dense bodies. A dense body is analogous to the Z-discs of skeletal and cardiac muscle fibers and is fastened to the sarcolemma. Calcium ions are supplied by the SR in the fibers and by sequestration from the extracellular fluid through membrane indentations called calveoli. Because smooth muscle cells do not contain troponin, cross-bridge formation is not regulated by the troponin-tropomyosin complex but instead by the regulatory protein calmodulin. In a smooth muscle fiber, external Ca++ ions passing through opened calcium channels in the sarcolemma, and additional Ca++ released from SR, bind to calmodulin. The Ca++-calmodulin complex then activates an enzyme called myosin (light chain) kinase, which, in turn, activates the myosin heads by phosphorylating them (converting ATP to ADP and Pi, with the Pi attaching to the head). The heads can then attach to actin-binding sites and pull on the thin filaments. The thin filaments also are anchored to the dense bodies; the structures invested in the inner membrane of the sarcolemma (at adherens junctions) that also have cord-like intermediate filaments attached to them. When the thin filaments slide past the thick filaments, they pull on the dense bodies, structures tethered to the sarcolemma, which then pull on the intermediate filaments networks throughout the sarcoplasm. This arrangement causes the entire muscle fiber to contract in a manner whereby the ends are pulled toward the center, causing the midsection to bulge in a corkscrew motion (Figure 10.24). Figure 10.24 Muscle Contraction The dense bodies and intermediate filaments are networked through the sarcoplasm, which cause the muscle fiber to contract. Although smooth muscle contraction relies on the presence of Ca++ ions, smooth muscle fibers have a much smaller diameter than skeletal muscle cells. T-tubules are not required to reach the interior of the cell and therefore not necessary to transmit an action potential deep into the fiber. Smooth muscle fibers have a limited calcium-storing SR but have calcium channels in the sarcolemma (similar to cardiac muscle fibers) that open during the action potential along the sarcolemma. The influx of extracellular Ca++ ions, which diffuse into the sarcoplasm to reach the calmodulin, accounts for most of the Ca++ that triggers contraction of a smooth muscle cell. Muscle contraction continues until ATP-dependent calcium pumps actively transport Ca++ ions back into the SR and out of the cell. However, a low concentration of calcium remains in the sarcoplasm to maintain muscle tone. This remaining calcium keeps the muscle slightly contracted, which is important in certain tracts and around blood vessels. Because most smooth muscles must function for long periods without rest, their power output is relatively low, but contractions can continue without using large amounts of energy. Some smooth muscle can also maintain contractions even as Ca++ is removed and myosin kinase is inactivated/dephosphorylated. This can happen as a subset of cross-bridges between myosin heads and actin, called latch-bridges, keep the thick and thin filaments linked together for a prolonged period, and without the need for ATP. This allows for the maintaining of muscle “tone” in smooth muscle that lines arterioles and other visceral organs with very little energy expenditure. Smooth muscle is not under voluntary control; thus, it is called involuntary muscle. The triggers for smooth muscle contraction include hormones, neural stimulation by the ANS, and local factors. In certain locations, such as the walls of visceral organs, stretching the muscle can trigger its contraction (the stress-relaxation response). Axons of neurons in the ANS do not form the highly organized NMJs with smooth muscle, as seen between motor neurons and skeletal muscle fibers. Instead, there is a series of neurotransmitter-filled bulges called varicosities as an axon courses through smooth muscle, loosely forming motor units (Figure 10.25). A varicosity releases neurotransmitters into the synaptic cleft. Also, visceral muscle in the walls of the hollow organs (except the heart) contains pacesetter cells. A pacesetter cell can spontaneously trigger action potentials and contractions in the muscle. Figure 10.25 Motor Units A series of axon-like swelling, called varicosities or “boutons,” from autonomic neurons form motor units through the smooth muscle. Smooth muscle is organized in two ways: as single-unit smooth muscle, which is much more common; and as multiunit smooth muscle. The two types have different locations in the body and have different characteristics. Single-unit muscle has its muscle fibers joined by gap junctions so that the muscle contracts as a single unit. This type of smooth muscle is found in the walls of all visceral organs except the heart (which has cardiac muscle in its walls), and so it is commonly called visceral muscle. Because the muscle fibers are not constrained by the organization and stretchability limits of sarcomeres, visceral smooth muscle has a stress-relaxation response. This means that as the muscle of a hollow organ is stretched when it fills, the mechanical stress of the stretching will trigger contraction, but this is immediately followed by relaxation so that the organ does not empty its contents prematurely. This is important for hollow organs, such as the stomach or urinary bladder, which continuously expand as they fill. The smooth muscle around these organs also can maintain a muscle tone when the organ empties and shrinks, a feature that prevents “flabbiness” in the empty organ. In general, visceral smooth muscle produces slow, steady contractions that allow substances, such as food in the digestive tract, to move through the body. Multiunit smooth muscle cells rarely possess gap junctions, and thus are not electrically coupled. As a result, contraction does not spread from one cell to the next, but is instead confined to the cell that was originally stimulated. Stimuli for multiunit smooth muscles come from autonomic nerves or hormones but not from stretching. This type of tissue is found around large blood vessels, in the respiratory airways, and in the eyes. Hyperplasia in Smooth Muscle Similar to skeletal and cardiac muscle cells, smooth muscle can undergo hypertrophy to increase in size. Unlike other muscle, smooth muscle can also divide to produce more cells, a process called hyperplasia. This can most evidently be observed in the uterus at puberty, which responds to increased estrogen levels by producing more uterine smooth muscle fibers, and greatly increases the size of the myometrium. Development and Regeneration of Muscle Tissue - Describe the function of satellite cells - Define fibrosis - Explain which muscle has the greatest regeneration ability Most muscle tissue of the body arises from embryonic mesoderm. Paraxial mesodermal cells adjacent to the neural tube form blocks of cells called somites. Skeletal muscles, excluding those of the head and limbs, develop from mesodermal somites, whereas skeletal muscle in the head and limbs develop from general mesoderm. Somites give rise to myoblasts. A myoblast is a muscle-forming stem cell that migrates to different regions in the body and then fuse(s) to form a syncytium, or myotube. As a myotube is formed from many different myoblast cells, it contains many nuclei, but has a continuous cytoplasm. This is why skeletal muscle cells are multinucleate, as the nucleus of each contributing myoblast remains intact in the mature skeletal muscle cell. However, cardiac and smooth muscle cells are not multinucleate because the myoblasts that form their cells do not fuse. Gap junctions develop in the cardiac and single-unit smooth muscle in the early stages of development. In skeletal muscles, ACh receptors are initially present along most of the surface of the myoblasts, but spinal nerve innervation causes the release of growth factors that stimulate the formation of motor end-plates and NMJs. As neurons become active, electrical signals that are sent through the muscle influence the distribution of slow and fast fibers in the muscle. Although the number of muscle cells is set during development, satellite cells help to repair skeletal muscle cells. A satellite cellis similar to a myoblast because it is a type of stem cell; however, satellite cells are incorporated into muscle cells and facilitate the protein synthesis required for repair and growth. These cells are located outside the sarcolemma and are stimulated to grow and fuse with muscle cells by growth factors that are released by muscle fibers under certain forms of stress. Satellite cells can regenerate muscle fibers to a very limited extent, but they primarily help to repair damage in living cells. If a cell is damaged to a greater extent than can be repaired by satellite cells, the muscle fibers are replaced by scar tissue in a process called fibrosis. Because scar tissue cannot contract, muscle that has sustained significant damage loses strength and cannot produce the same amount of power or endurance as it could before being damaged. Smooth muscle tissue can regenerate from a type of stem cell called a pericyte, which is found in some small blood vessels. Pericytes allow smooth muscle cells to regenerate and repair much more readily than skeletal and cardiac muscle tissue. Similar to skeletal muscle tissue, cardiac muscle does not regenerate to a great extent. Dead cardiac muscle tissue is replaced by scar tissue, which cannot contract. As scar tissue accumulates, the heart loses its ability to pump because of the loss of contractile power. However, some minor regeneration may occur due to stem cells found in the blood that occasionally enter cardiac tissue. CAREER CONNECTION Physical Therapist As muscle cells die, they are not regenerated but instead are replaced by connective tissue and adipose tissue, which do not possess the contractile abilities of muscle tissue. Muscles atrophy when they are not used, and over time if atrophy is prolonged, muscle cells die. It is therefore important that those who are susceptible to muscle atrophy exercise to maintain muscle function and prevent the complete loss of muscle tissue. In extreme cases, when movement is not possible, electrical stimulation can be introduced to a muscle from an external source. This acts as a substitute for endogenous neural stimulation, stimulating the muscle to contract and preventing the loss of proteins that occurs with a lack of use. Physiotherapists work with patients to maintain muscles. They are trained to target muscles susceptible to atrophy, and to prescribe and monitor exercises designed to stimulate those muscles. There are various causes of atrophy, including mechanical injury, disease, and age. After breaking a limb or undergoing surgery, muscle use is impaired and can lead to disuse atrophy. If the muscles are not exercised, this atrophy can lead to long-term muscle weakness. A stroke can also cause muscle impairment by interrupting neural stimulation to certain muscles. Without neural inputs, these muscles do not contract and thus begin to lose structural proteins. Exercising these muscles can help to restore muscle function and minimize functional impairments. Age-related muscle loss is also a target of physical therapy, as exercise can reduce the effects of age-related atrophy and improve muscle function. The goal of a physiotherapist is to improve physical functioning and reduce functional impairments; this is achieved by understanding the cause of muscle impairment and assessing the capabilities of a patient, after which a program to enhance these capabilities is designed. Some factors that are assessed include strength, balance, and endurance, which are continually monitored as exercises are introduced to track improvements in muscle function. Physiotherapists can also instruct patients on the proper use of equipment, such as crutches, and assess whether someone has sufficient strength to use the equipment and when they can function without it. Key Terms - acetylcholine (ACh) - neurotransmitter that binds at a motor end-plate to trigger depolarization - actin - protein that makes up most of the thin myofilaments in a sarcomere muscle fiber - action potential - change in voltage of a cell membrane in response to a stimulus that results in transmission of an electrical signal; unique to neurons and muscle fibers - aerobic respiration - production of ATP in the presence of oxygen - angiogenesis - formation of blood capillary networks - aponeurosis - broad, tendon-like sheet of connective tissue that attaches a skeletal muscle to another skeletal muscle or to a bone - ATPase - enzyme that hydrolyzes ATP to ADP - atrophy - loss of structural proteins from muscle fibers - autorhythmicity - heart’s ability to control its own contractions - calmodulin - regulatory protein that facilitates contraction in smooth muscles - cardiac muscle - striated muscle found in the heart; joined to one another at intercalated discs and under the regulation of pacemaker cells, which contract as one unit to pump blood through the circulatory system. Cardiac muscle is under involuntary control. - concentric contraction - muscle contraction that shortens the muscle to move a load - contractility - ability to shorten (contract) forcibly - contraction phase - twitch contraction phase when tension increases - creatine phosphate - phosphagen used to store energy from ATP and transfer it to muscle - dense body - sarcoplasmic structure that attaches to the sarcolemma and shortens the muscle as thin filaments slide past thick filaments - depolarize - to reduce the voltage difference between the inside and outside of a cell’s plasma membrane (the sarcolemma for a muscle fiber), making the inside less negative than at rest - desmosome - cell structure that anchors the ends of cardiac muscle fibers to allow contraction to occur - eccentric contraction - muscle contraction that lengthens the muscle as the tension is diminished - elasticity - ability to stretch and rebound - endomysium - loose, and well-hydrated connective tissue covering each muscle fiber in a skeletal muscle - epimysium - outer layer of connective tissue around a skeletal muscle - excitability - ability to undergo neural stimulation - excitation-contraction coupling - sequence of events from motor neuron signaling to a skeletal muscle fiber to contraction of the fiber’s sarcomeres - extensibility - ability to lengthen (extend) - fascicle - bundle of muscle fibers within a skeletal muscle - fast glycolytic (FG) - muscle fiber that primarily uses anaerobic glycolysis - fast oxidative (FO) - intermediate muscle fiber that is between slow oxidative and fast glycolytic fibers - fibrosis - replacement of muscle fibers by scar tissue - glycolysis - anaerobic breakdown of glucose to ATP - graded muscle response - modification of contraction strength - hyperplasia - process in which one cell splits to produce new cells - hypertonia - abnormally high muscle tone - hypertrophy - addition of structural proteins to muscle fibers - hypotonia - abnormally low muscle tone caused by the absence of low-level contractions - intercalated disc - part of the sarcolemma that connects cardiac tissue, and contains gap junctions and desmosomes - isometric contraction - muscle contraction that occurs with no change in muscle length - isotonic contraction - muscle contraction that involves changes in muscle length - lactic acid - product of anaerobic glycolysis - latch-bridges - subset of a cross-bridge in which actin and myosin remain locked together - latent period - the time when a twitch does not produce contraction - motor end-plate - sarcolemma of muscle fiber at the neuromuscular junction, with receptors for the neurotransmitter acetylcholine - motor unit - motor neuron and the group of muscle fibers it innervates - muscle tension - force generated by the contraction of the muscle; tension generated during isotonic contractions and isometric contractions - muscle tone - low levels of muscle contraction that occur when a muscle is not producing movement - myoblast - muscle-forming stem cell - myofibril - long, cylindrical organelle that runs parallel within the muscle fiber and contains the sarcomeres - myogram - instrument used to measure twitch tension - myosin - protein that makes up most of the thick cylindrical myofilament within a sarcomere muscle fiber - myotube - fusion of many myoblast cells - neuromuscular junction (NMJ) - synapse between the axon terminal of a motor neuron and the section of the membrane of a muscle fiber with receptors for the acetylcholine released by the terminal - neurotransmitter - signaling chemical released by nerve terminals that bind to and activate receptors on target cells - oxygen debt - amount of oxygen needed to compensate for ATP produced without oxygen during muscle contraction - pacesetter cell - cell that triggers action potentials in smooth muscle - pericyte - stem cell that regenerates smooth muscle cells - perimysium - connective tissue that bundles skeletal muscle fibers into fascicles within a skeletal muscle - power stroke - action of myosin pulling actin inward (toward the M line) - pyruvic acid - product of glycolysis that can be used in aerobic respiration or converted to lactic acid - recruitment - increase in the number of motor units involved in contraction - relaxation phase - period after twitch contraction when tension decreases - sarcolemma - plasma membrane of a skeletal muscle fiber - sarcomere - longitudinally, repeating functional unit of skeletal muscle, with all of the contractile and associated proteins involved in contraction - sarcopenia - age-related muscle atrophy - sarcoplasm - cytoplasm of a muscle cell - sarcoplasmic reticulum (SR) - specialized smooth endoplasmic reticulum, which stores, releases, and retrieves Ca++ - satellite cell - stem cell that helps to repair muscle cells - skeletal muscle - striated, multinucleated muscle that requires signaling from the nervous system to trigger contraction; most skeletal muscles are referred to as voluntary muscles that move bones and produce movement - slow oxidative (SO) - muscle fiber that primarily uses aerobic respiration - smooth muscle - nonstriated, mononucleated muscle in the skin that is associated with hair follicles; assists in moving materials in the walls of internal organs, blood vessels, and internal passageways - somites - blocks of paraxial mesoderm cells - stress-relaxation response - relaxation of smooth muscle tissue after being stretched - synaptic cleft - space between a nerve (axon) terminal and a motor end-plate - T-tubule - projection of the sarcolemma into the interior of the cell - tetanus - a continuous fused contraction - thick filament - the thick myosin strands and their multiple heads projecting from the center of the sarcomere toward, but not all to way to, the Z-discs - thin filament - thin strands of actin and its troponin-tropomyosin complex projecting from the Z-discs toward the center of the sarcomere - treppe - stepwise increase in contraction tension - triad - the grouping of one T-tubule and two terminal cisternae - tropomyosin - regulatory protein that covers myosin-binding sites to prevent actin from binding to myosin - troponin - regulatory protein that binds to actin, tropomyosin, and calcium - twitch - single contraction produced by one action potential - varicosity - enlargement of neurons that release neurotransmitters into synaptic clefts - visceral muscle - smooth muscle found in the walls of visceral organs - voltage-gated sodium channels - membrane proteins that open sodium channels in response to a sufficient voltage change, and initiate and transmit the action potential as Na+ enters through the channel - wave summation - addition of successive neural stimuli to produce greater contraction Chapter Review 10.1 Overview of Muscle Tissues Muscle is the tissue in animals that allows for active movement of the body or materials within the body. There are three types of muscle tissue: skeletal muscle, cardiac muscle, and smooth muscle. Most of the body’s skeletal muscle produces movement by acting on the skeleton. Cardiac muscle is found in the wall of the heart and pumps blood through the circulatory system. Smooth muscle is found in the skin, where it is associated with hair follicles; it also is found in the walls of internal organs, blood vessels, and internal passageways, where it assists in moving materials. 10.2 Skeletal Muscle Skeletal muscles contain connective tissue, blood vessels, and nerves. There are three layers of connective tissue: epimysium, perimysium, and endomysium. Skeletal muscle fibers are organized into groups called fascicles. Blood vessels and nerves enter the connective tissue and branch in the cell. Muscles attach to bones directly or through tendons or aponeuroses. Skeletal muscles maintain posture, stabilize bones and joints, control internal movement, and generate heat. Skeletal muscle fibers are long, multinucleated cells. The membrane of the cell is the sarcolemma; the cytoplasm of the cell is the sarcoplasm. The sarcoplasmic reticulum (SR) is a form of endoplasmic reticulum. Muscle fibers are composed of myofibrils. The striations are created by the organization of actin and myosin resulting in the banding pattern of myofibrils. 10.3 Muscle Fiber Contraction and Relaxation A sarcomere is the smallest contractile portion of a muscle. Myofibrils are composed of thick and thin filaments. Thick filaments are composed of the protein myosin; thin filaments are composed of the protein actin. Troponin and tropomyosin are regulatory proteins. Muscle contraction is described by the sliding filament model of contraction. ACh is the neurotransmitter that binds at the neuromuscular junction (NMJ) to trigger depolarization, and an action potential travels along the sarcolemma to trigger calcium release from SR. The actin sites are exposed after Ca++ enters the sarcoplasm from its SR storage to activate the troponin-tropomyosin complex so that the tropomyosin shifts away from the sites. The cross-bridging of myposin heads docking into actin-binding sites is followed by the “power stroke”—the sliding of the thin filaments by thick filaments. The power strokes are powered by ATP. Ultimately, the sarcomeres, myofibrils, and muscle fibers shorten to produce movement. 10.4 Nervous System Control of Muscle Tension The number of cross-bridges formed between actin and myosin determines the amount of tension produced by a muscle. The length of a sarcomere is optimal when the zone of overlap between thin and thick filaments is greatest. Muscles that are stretched or compressed too greatly do not produce maximal amounts of power. A motor unit is formed by a motor neuron and all of the muscle fibers that are innervated by that same motor neuron. A single contraction is called a twitch. A muscle twitch has a latent period, a contraction phase, and a relaxation phase. A graded muscle response allows variation in muscle tension. Summation occurs as successive stimuli are added together to produce a stronger muscle contraction. Tetanus is the fusion of contractions to produce a continuous contraction. Increasing the number of motor neurons involved increases the amount of motor units activated in a muscle, which is called recruitment. Muscle tone is the constant low-level contractions that allow for posture and stability. 10.5 Types of Muscle Fibers ATP provides the energy for muscle contraction. The three mechanisms for ATP regeneration are creatine phosphate, anaerobic glycolysis, and aerobic metabolism. Creatine phosphate provides about the first 15 seconds of ATP at the beginning of muscle contraction. Anaerobic glycolysis produces small amounts of ATP in the absence of oxygen for a short period. Aerobic metabolism utilizes oxygen to produce much more ATP, allowing a muscle to work for longer periods. Muscle fatigue, which has many contributing factors, occurs when muscle can no longer contract. An oxygen debt is created as a result of muscle use. The three types of muscle fiber are slow oxidative (SO), fast oxidative (FO) and fast glycolytic (FG). SO fibers use aerobic metabolism to produce low power contractions over long periods and are slow to fatigue. FO fibers use aerobic metabolism to produce ATP but produce higher tension contractions than SO fibers. FG fibers use anaerobic metabolism to produce powerful, high-tension contractions but fatigue quickly. 10.6 Exercise and Muscle Performance Hypertrophy is an increase in muscle mass due to the addition of structural proteins. The opposite of hypertrophy is atrophy, the loss of muscle mass due to the breakdown of structural proteins. Endurance exercise causes an increase in cellular mitochondria, myoglobin, and capillary networks in SO fibers. Endurance athletes have a high level of SO fibers relative to the other fiber types. Resistance exercise causes hypertrophy. Power-producing muscles have a higher number of FG fibers than of slow fibers. Strenuous exercise causes muscle cell damage that requires time to heal. Some athletes use performance-enhancing substances to enhance muscle performance. Muscle atrophy due to age is called sarcopenia and occurs as muscle fibers die and are replaced by connective and adipose tissue. 10.7 Cardiac Muscle Tissue Cardiac muscle is striated muscle that is present only in the heart. Cardiac muscle fibers have a single nucleus, are branched, and joined to one another by intercalated discs that contain gap junctions for depolarization between cells and desmosomes to hold the fibers together when the heart contracts. Contraction in each cardiac muscle fiber is triggered by Ca++ ions in a similar manner as skeletal muscle, but here the Ca++ ions come from SR and through voltage-gated calcium channels in the sarcolemma. Pacemaker cells stimulate the spontaneous contraction of cardiac muscle as a functional unit, called a syncytium. 10.8 Smooth Muscle Smooth muscle is found throughout the body around various organs and tracts. Smooth muscle cells have a single nucleus, and are spindle-shaped. Smooth muscle cells can undergo hyperplasia, mitotically dividing to produce new cells. The smooth cells are nonstriated, but their sarcoplasm is filled with actin and myosin, along with dense bodies in the sarcolemma to anchor the thin filaments and a network of intermediate filaments involved in pulling the sarcolemma toward the fiber’s middle, shortening it in the process. Ca++ ions trigger contraction when they are released from SR and enter through opened voltage-gated calcium channels. Smooth muscle contraction is initiated when the Ca++ binds to intracellular calmodulin, which then activates an enzyme called myosin kinase that phosphorylates myosin heads so they can form the cross-bridges with actin and then pull on the thin filaments. Smooth muscle can be stimulated by pacesetter cells, by the autonomic nervous system, by hormones, spontaneously, or by stretching. The fibers in some smooth muscle have latch-bridges, cross-bridges that cycle slowly without the need for ATP; these muscles can maintain low-level contractions for long periods. Single-unit smooth muscle tissue contains gap junctions to synchronize membrane depolarization and contractions so that the muscle contracts as a single unit. Single-unit smooth muscle in the walls of the viscera, called visceral muscle, has a stress-relaxation response that permits muscle to stretch, contract, and relax as the organ expands. Multiunit smooth muscle cells do not possess gap junctions, and contraction does not spread from one cell to the next. 10.9 Development and Regeneration of Muscle Tissue Muscle tissue arises from embryonic mesoderm. Somites give rise to myoblasts and fuse to form a myotube. The nucleus of each contributing myoblast remains intact in the mature skeletal muscle cell, resulting in a mature, multinucleate cell. Satellite cells help to repair skeletal muscle cells. Smooth muscle tissue can regenerate from stem cells called pericytes, whereas dead cardiac muscle tissue is replaced by scar tissue. Aging causes muscle mass to decrease and be replaced by noncontractile connective tissue and adipose tissue. Interactive Link Questions Watch this video to learn more about macro- and microstructures of skeletal muscles. (a) What are the names of the “junction points” between sarcomeres? (b) What are the names of the “subunits” within the myofibrils that run the length of skeletal muscle fibers? (c) What is the “double strand of pearls” described in the video? (d) What gives a skeletal muscle fiber its striated appearance? 2.Every skeletal muscle fiber is supplied by a motor neuron at the NMJ. Watch this video to learn more about what happens at the neuromuscular junction. (a) What is the definition of a motor unit? (b) What is the structural and functional difference between a large motor unit and a small motor unit? Can you give an example of each? (c) Why is the neurotransmitter acetylcholine degraded after binding to its receptor? 3.The release of calcium ions initiates muscle contractions. Watch this video to learn more about the role of calcium. (a) What are “T-tubules” and what is their role? (b) Please also describe how actin-binding sites are made available for cross-bridging with myosin heads during contraction. Review Questions Muscle that has a striped appearance is described as being ________. - elastic - nonstriated - excitable - striated Which element is important in directly triggering contraction? - sodium (Na+) - calcium (Ca++) - potassium (K+) - chloride (Cl-) Which of the following properties is not common to all three muscle tissues? - excitability - the need for ATP - at rest, uses shielding proteins to cover actin-binding sites - elasticity The correct order for the smallest to the largest unit of organization in muscle tissue is ________. - fascicle, filament, muscle fiber, myofibril - filament, myofibril, muscle fiber, fascicle - muscle fiber, fascicle, filament, myofibril - myofibril, muscle fiber, filament, fascicle Depolarization of the sarcolemma means ________. - the inside of the membrane has become less negative as sodium ions accumulate - the outside of the membrane has become less negative as sodium ions accumulate - the inside of the membrane has become more negative as sodium ions accumulate - the sarcolemma has completely lost any electrical charge In relaxed muscle, the myosin-binding site on actin is blocked by ________. - titin - troponin - myoglobin - tropomyosin According to the sliding filament model, binding sites on actin open when ________. - creatine phosphate levels rise - ATP levels rise - acetylcholine levels rise - calcium ion levels rise The cell membrane of a muscle fiber is called ________. - myofibril - sarcolemma - sarcoplasm - myofilament Muscle relaxation occurs when ________. - calcium ions are actively transported out of the sarcoplasmic reticulum - calcium ions diffuse out of the sarcoplasmic reticulum - calcium ions are actively transported into the sarcoplasmic reticulum - calcium ions diffuse into the sarcoplasmic reticulum During muscle contraction, the cross-bridge detaches when ________. - the myosin head binds to an ADP molecule - the myosin head binds to an ATP molecule - calcium ions bind to troponin - calcium ions bind to actin Thin and thick filaments are organized into functional units called ________. - myofibrils - myofilaments - T-tubules - sarcomeres During which phase of a twitch in a muscle fiber is tension the greatest? - resting phase - repolarization phase - contraction phase - relaxation phase Muscle fatigue is caused by ________. - buildup of ATP and lactic acid levels - exhaustion of energy reserves and buildup of lactic acid levels - buildup of ATP and pyruvic acid levels - exhaustion of energy reserves and buildup of pyruvic acid levels A sprinter would experience muscle fatigue sooner than a marathon runner due to ________. - anaerobic metabolism in the muscles of the sprinter - anaerobic metabolism in the muscles of the marathon runner - aerobic metabolism in the muscles of the sprinter - glycolysis in the muscles of the marathon runner What aspect of creatine phosphate allows it to supply energy to muscles? - ATPase activity - phosphate bonds - carbon bonds - hydrogen bonds Drug X blocks ATP regeneration from ADP and phosphate. How will muscle cells respond to this drug? - by absorbing ATP from the bloodstream - by using ADP as an energy source - by using glycogen as an energy source - none of the above The muscles of a professional sprinter are most likely to have ________. - 80 percent fast-twitch muscle fibers and 20 percent slow-twitch muscle fibers - 20 percent fast-twitch muscle fibers and 80 percent slow-twitch muscle fibers - 50 percent fast-twitch muscle fibers and 50 percent slow-twitch muscle fibers - 40 percent fast-twitch muscle fibers and 60 percent slow-twitch muscle fibers The muscles of a professional marathon runner are most likely to have ________. - 80 percent fast-twitch muscle fibers and 20 percent slow-twitch muscle fibers - 20 percent fast-twitch muscle fibers and 80 percent slow-twitch muscle fibers - 50 percent fast-twitch muscle fibers and 50 percent slow-twitch muscle fibers - 40 percent fast-twitch muscle fibers and 60 percent slow-twitch muscle fibers Which of the following statements is true? - Fast fibers have a small diameter. - Fast fibers contain loosely packed myofibrils. - Fast fibers have large glycogen reserves. - Fast fibers have many mitochondria. Which of the following statements is false? - Slow fibers have a small network of capillaries. - Slow fibers contain the pigment myoglobin. - Slow fibers contain a large number of mitochondria. - Slow fibers contract for extended periods. Cardiac muscles differ from skeletal muscles in that they ________. - are striated - utilize aerobic metabolism - contain myofibrils - contain intercalated discs If cardiac muscle cells were prevented from undergoing aerobic metabolism, they ultimately would ________. - undergo glycolysis - synthesize ATP - stop contracting - start contracting Smooth muscles differ from skeletal and cardiac muscles in that they ________. - lack myofibrils - are under voluntary control - lack myosin - lack actin Which of the following statements describes smooth muscle cells? - They are resistant to fatigue. - They have a rapid onset of contractions. - They cannot exhibit tetanus. - They primarily use anaerobic metabolism. From which embryonic cell type does muscle tissue develop? - ganglion cells - myotube cells - myoblast cells - satellite cells Which cell type helps to repair injured muscle fibers? - ganglion cells - myotube cells - myoblast cells - satellite cells Critical Thinking Questions Why is elasticity an important quality of muscle tissue? 31.What would happen to skeletal muscle if the epimysium were destroyed? 32.Describe how tendons facilitate body movement. 33.What are the five primary functions of skeletal muscle? 34.What are the opposite roles of voltage-gated sodium channels and voltage-gated potassium channels? 35.How would muscle contractions be affected if skeletal muscle fibers did not have T-tubules? 36.What causes the striated appearance of skeletal muscle tissue? 37.How would muscle contractions be affected if ATP was completely depleted in a muscle fiber? 38.Why does a motor unit of the eye have few muscle fibers compared to a motor unit of the leg? 39.What factors contribute to the amount of tension produced in an individual muscle fiber? 40.Why do muscle cells use creatine phosphate instead of glycolysis to supply ATP for the first few seconds of muscle contraction? 41.Is aerobic respiration more or less efficient than glycolysis? Explain your answer. 42.What changes occur at the cellular level in response to endurance training? 43.What changes occur at the cellular level in response to resistance training? 44.What would be the drawback of cardiac contractions being the same duration as skeletal muscle contractions? 45.How are cardiac muscle cells similar to and different from skeletal muscle cells? 46.Why can smooth muscles contract over a wider range of resting lengths than skeletal and cardiac muscle? 47.Describe the differences between single-unit smooth muscle and multiunit smooth muscle. 48.Why is muscle that has sustained significant damage unable to produce the same amount of power as it could before being damaged? 49.Which muscle type(s) (skeletal, smooth, or cardiac) can regenerate new muscle cells/fibers? Explain your answer.	oercommons	2025-03-18T00:37:02.288715	07/23/2019	{ "license": "Creative Commons - Attribution - https://creativecommons.org/licenses/by/4.0/", "url": "https://oercommons.org/courseware/lesson/56369/overview", "title": "Anatomy and Physiology, Support and Movement, Muscle Tissue", "author": null }
https://oercommons.org/courseware/lesson/84551/overview	1.3 Components of Prokaryotic Cell 1.4 Components of Eukaryotic Cell 1.5 Components of a Plant Cell 1_The-Cell The Cell Overview Red and cyan fluorescent proteins marking plant cell nuclei. Fernan Federici CC-BY-NC-SA-2.0 Botany by Melissa Ha, Maria Morrow & Kammy Algiers https://bio.libretexts.org/Bookshelves/Botany/Botany_(Ha_Morrow_and_Algiers) A Photographic Atlas for Botany by Maria Morrow https://bio.libretexts.org/Bookshelves/Botany/A_Photographic_Atlas_for_Botany_(Morrow) Introduction to Botany By Alexey Shipunov https://bio.libretexts.org/Bookshelves/Botany/Introduction_to_Botany_(Shipunov) Plant Anatomy and Physiology by Sean Bellairs https://bio.libretexts.org/Bookshelves/Botany/Book%3A_Plant_Anatomy_and_Physiology_(Bellairs) Did you have an idea for improving this content? We’d love your input. Introduction Learning Objectives - Define cell. - Summarize the main components of a light microscope. - List the features of a prokaryotic cell. - Define cell theory. - Explain how the surface area to volume ratio regulates cell size. - List and describe the cellular components of a eukaryotic cell. - Identify characteristic features of a plant cell. - Explain the structure and function of the cell wall, chloroplast, central vacuole, and plasmodesmata in the plant cell. Key Terms cell theory/unified cell theory - a biological concept that states that all organisms are made up of cells; the cell is the basic unit of life, and new cells arise from existing cells cell wall - rigid cell covering comprised of various molecules that protect the cell, provides structural support, and give shape to the cell cellulose - the main component of cell wall, made up of glucose polymer central vacuole - large plant cell organelle that regulates the cell’s storage compartment, holds water, and plays a significant role in cell growth as the site of macromolecule degradation chlorophyll - the green pigment that captures the light energy that drives the light reactions of photosynthesis chloroplast - plant cell organelle that carries out photosynthesis endoplasmic reticulum (ER) - series of interconnected membranous structures within eukaryotic cells that collectively modify proteins and synthesize lipids eukaryotic cell - a cell that has a membrane-bound nucleus and several other membrane-bound compartments or sacs light microscope - an instrument that magnifies an object using a beam of visible light that passes and bends through a lens system to visualize a specimen lignin - phenolic polymer, a component of plant cell wall nucleus - cell organelle that houses the cell’s DNA and directs ribosome and protein synthesis pectin - polysaccharide commonly found in the primary cell wall of plants peptidoglycan - polysaccharide commonly found in the bacterial cell wall plasma membrane - phospholipid bilayer with embedded (integral) or attached (peripheral) proteins, and separates the cell's internal content from its surrounding environment plasmodesma - (plural = plasmodesmata) channel that passes between adjacent cell walls of plant cells, connects their cytoplasm, and allows transporting of materials from cell to cell primary cell wall - outermost cell wall in a plant cell, primary made up of cellulose and pectin; usually flexible and permeable prokaryote - a unicellular organism that lacks a nucleus or any other membrane-bound organelle secondary cell wall - cell wall between the primary cell wall and plasma membrane in a plant cell; usually rigid and impermeable Introduction Close your eyes and picture a brick wall. What is the wall's basic building block? It is a single brick. Like a brick wall, cells are the building blocks that make up our body. Our body has many kinds of cells, each specialized for a specific purpose. Just as we use a variety of materials to build a home, the human body is constructed from many cell types. Given their enormous variety, cells from all organisms—even ones as diverse as bacteria, onions, and humans—share certain fundamental characteristics. Microscopy, Cell Theory & Cell Size A cell is the smallest unit of all living things. We call “living things” – organism(s). Whether it is a single-cell organism (like bacteria) or a multi-cellular organism (like a human). Thus, cells are the basic building blocks of all organisms. Several cells of one kind that interconnect with each other and perform a shared function make a tissue. These tissues combine to form an organ (your stomach, heart, or brain), and several organs comprise an organ system (such as the digestive system, circulatory system, or nervous system). Several systems that function together form an organism (like a human being). Here, we will examine the structure and function of cells. All cells can be broadly categorized as prokaryotic and eukaryotic. For example, we classify both animal and plant cells as eukaryotic cells, whereas we classify bacterial cells as prokaryotic. Before discussing the criteria for determining whether a cell is prokaryotic or eukaryotic, we will first examine how biologists study cells. Microscopy Cells vary in size. To give you a sense of cell size, a typical human red blood cell is about eight-millionths of a meter or eight micrometers (abbreviated as eight µm) in diameter. A pinhead is about two-thousandths of a meter (two mm) in diameter. That means about 250 red blood cells could fit on a pinhead. With few exceptions, we cannot see individual cells with the naked eye, so scientists use microscopes (micro- ="small; -scope = "to look at") to study them. A microscope is an instrument that magnifies an object. We photograph most cells with a microscope, so we can call these images micrographs. The optics of a microscope’s lenses change the image orientation that the user sees. A specimen that is right-side up and facing right on the microscope slide will appear upside-down and facing left when one views through a microscope, and vice versa. Similarly, if one moves the slide left while looking through the microscope, it will appear to move right, and if one moves it down, it will seem to move up. This occurs because microscopes use two sets of lenses to magnify the image. Because of how light travels through the lenses, this two-lens system produces an inverted image (binocular, or dissecting microscopes, work in a similar manner, but include an additional magnification system that makes the final image appear to be upright). Light Microscope Most student microscopes are light microscopes (figure 1.1a). In this type of microscope, visible light passes and bends through the lens system to enable the user to see the specimen. Light microscopes are advantageous for viewing living organisms, but since individual cells are generally transparent, their components are not distinguishable unless they are colored with special stains. Staining, however, usually kills the cells. Two parameters that are important in microscopy are magnification and resolving power. Magnification is the process of enlarging an object in appearance. Resolving power is the microscope's ability to distinguish two adjacent structures as separate: the higher the resolution, the better the image's clarity and detail. Light microscopes that students commonly use in the laboratory magnify up to approximately 400 times. Light microscopes can magnify up to 1,000 times when oil immersion lenses are used. To gain a better understanding of cellular structure and function, scientists typically use electron microscopes. Electron Microscope In contrast to light microscopes, electron microscopes (figure 1.1.1b) use a beam of electrons instead of a beam of light. Not only does this allow for higher magnification and, thus, more detail, but it also provides higher resolving power. There are two main types of electron microscopes, transmission electron microscope (TEM) and scanning electron microscope (SEM). In a scanning electron microscope, a beam of electrons moves back and forth across a cell’s surface, creating details of cell surface characteristics. In a transmission electron microscope, the electron beam penetrates the cell and provides details of a cell’s internal structures. As you might imagine, electron microscopes are significantly bulkier and more expensive than light microscopes. To learn more about light microscopes, visit this site. Cell theory The microscopes we use today are far more complex than those that Dutch shopkeeper Antony van Leeuwenhoek, used in the 1600s. Skilled in crafting lenses, van Leeuwenhoek observed the movements of single-celled organisms, which he collectively termed “animalcules.” In the 1665 publication Micrographia, experimental scientist Robert Hooke coined the term “cell” for the box-like structures he observed when viewing cork tissue through a lens. In the 1670s, van Leeuwenhoek discovered bacteria and protozoa. Later advances in lenses, microscope construction, and staining techniques enabled other scientists to see some components inside cells. By the late 1830s, botanist Matthias Schleiden and zoologist Theodor Schwann were studying tissues and proposed the unified cell theory, which states that one or more cells comprise all living things, the cell is the basic unit of life, and new cells arise from existing cells. Rudolf Virchow later made important contributions to this theory. Cells fall into one of two broad categories: prokaryotic and eukaryotic. We classify only the predominantly single-celled organisms Bacteria and Archaea as prokaryotes (pro- = “before”; -Kary- = “nucleus”). Animal cells, plants, fungi, and protists (protozoa) are all eukaryotes (EU- = “true”). Cell Size At 0.1 to 5.0 µm in diameter, prokaryotic cells are significantly smaller than eukaryotic cells, which have diameters ranging from 10 to 100 µm. The prokaryotes' small size allows ions and organic molecules that enter them to quickly diffuse to other parts of the cell. Similarly, any waste produced within a prokaryotic cell can quickly diffuse. This is not the case in eukaryotic cells, which have developed different structural adaptations to enhance intracellular transport. Small size, in general, is necessary for all cells, whether prokaryotic or eukaryotic. Let’s examine why that is so. First, we’ll consider the area and volume of a typical cell. Not all cells are spherical in shape, but most tend to approximate a sphere. You may remember from your high school geometry course that the formula for the surface area of a sphere is 4πr2, while the formula for its volume is 4πr3/3. Thus, as the radius of a cell increases, its surface area increases as the square of its radius, but its volume increases as the cube of its radius (much more rapidly). Therefore, as a cell increases in size, it's surface area-to-volume ratio decreases. This same principle would apply if the cell had a cube shape (figure 1.1.2). If the cell grows too large, the plasma membrane will not have sufficient surface area to support the rate of diffusion required for the increased volume. In other words, as a cell grows, it becomes less efficient. One way to become more efficient is to divide. Other ways are to increase surface area by creating inward or outward projections of the cell membrane, becoming flat or thin and elongated, or by developing organelles that perform specific tasks. These adaptations lead to the development of more sophisticated cells, which we call eukaryotic cells. For another perspective on cell size, try the HowBig interactive at this site. Access for free at https://openstax.org/books/biology-2e/pages/4-1-studying-cells Components of Prokaryotic Cell All cells share four common components: 1) a plasma membrane, an outer covering that separates the cell’s interior from its surrounding environment; 2) cytoplasm, consisting of a jelly-like cytosol within the cell in which there are other cellular components; 3) DNA, the cell's genetic material; and 4) ribosome, which synthesize proteins. However, prokaryotes differ from eukaryotic cells in several ways. A prokaryote is a simple, mostly single-celled (unicellular) organism that lacks a nucleus, or any other membrane-bound organelle. We will shortly come to see that this is significantly different in eukaryotes. Prokaryotic DNA is in the cell's central part: the nucleoid (figure 1.1.3) Most prokaryotes have a Peptidoglycan cell wall, and many have a polysaccharide capsule (figure 1.1.3). The cell wall acts as an extra layer of protection, helps the cell maintain its shape, and prevents dehydration. The capsule enables the cell to attach to surfaces in its environment. Some prokaryotes have flagella, pili, or fimbriae. Flagella are used for locomotion. Pili exchange genetic material during conjugation, the process by which one bacterium transfers genetic material to another through direct contact. Bacteria use Fimbriae to attach to a host cell. Access for free at https://openstax.org/books/biology-2e/pages/4-2-prokaryotic-cells Components of Eukaryotic Cell Have you ever heard the phrase “form follows function?” It’s a philosophy that many industries follow. In architecture, this means that buildings should be constructed to support the activities that will be carried out inside them. For example, a skyscraper should include several elevator banks. A hospital should place its emergency room where it is easily accessible. Our natural world also utilizes the principle of form following function, especially in cell biology, and this will become clear as we explore eukaryotic (figure 1.1.4). Unlike prokaryote cells, eukaryotic cells have 1) a membrane-bound nucleus; 2) numerous membrane-bound organelles, such as the endoplasmic reticulum, Golgi apparatus, chloroplast, mitochondria, and others; and 3) several, rod-shaped chromosomes. Because a membrane surrounds the eukaryotic cell’s nucleus, it has a “true nucleus.” The word “organelle” means “little organ,” and, as we already mentioned, organelles have specialized cellular functions, just as your body's organs have specialized functions. At this point, it should be clear to you that eukaryotic cells have a more complex structure than prokaryotic cells. Organelles allow different functions to be compartmentalized in different areas of the cell. Before turning to organelles, let’s first examine two important components of the cell: the plasma membrane and the cytoplasm. The Plasma Membrane Like prokaryotes, eukaryotic cells have a plasma membrane (figure 1.1.5), a phospholipid bilayer with embedded proteins that separate the internal contents of the cell from its surrounding environment. A phospholipid is a lipid molecule with two fatty acid chains and a phosphate-containing group. The plasma membrane controls the passage of organic molecules, ions, water, and oxygen into and out of the cell. Wastes (such as carbon dioxide and ammonia) also leave the cell by passing through the plasma membrane. The Cytoplasm The cytoplasm is the cell's entire region between the plasma membrane and the nuclear envelope (a structure we will discuss shortly). It is comprised of organelles suspended in the gel-like cytosol, the cytoskeleton, and various chemicals (figure 1.1.4). Even though the cytoplasm consists of 70 to 80 percent water, it has a semi-solid consistency, which comes from the proteins within it. However, proteins are not the only organic molecules in the cytoplasm. Glucose and other simple sugars, polysaccharides, amino acids, nucleic acids, fatty acids, and derivatives of glycerol are also there. Ions of sodium, potassium, calcium and many other elements also dissolve in the cytoplasm. Many metabolic reactions, including protein synthesis, take place in the cytoplasm. The Nucleus Typically, the nucleus is the most prominent organelle in a cell (figure 1.1.4). The nucleus (plural = nuclei) houses the cell’s DNA and directs the synthesis of ribosomes and proteins. Let’s look at it in more detail (figure 1.1.6). The Nuclear Envelope The nuclear envelope is a double-membrane structure that constitutes the nucleus' outermost portion (figure 1.1.6). Both the nuclear envelope's inner and outer membranes are phospholipid bilayers. The nuclear envelope is punctuated with pores that control the passage of ions, molecules, and RNA between the nucleoplasm and cytoplasm. The nucleoplasm is the semi-solid fluid inside the nucleus, where we find the chromatin and the nucleolus. Chromatin and Chromosomes To understand chromatin, it is helpful to first explore chromosomes, structures within the nucleus that are made up of DNA, the hereditary material. You may remember that in prokaryotes, DNA is organized into a single circular chromosome. In eukaryotes, chromosomes are linear structures. Every eukaryotic species has a specific number of chromosomes in the nucleus of each cell. For example, in humans, the chromosome number is 46, while in fruit flies, it is 8. Chromosomes are only visible and distinguishable from one another when the cell is getting ready to divide. When the cell is in the growth and maintenance phases of its life cycle, proteins attach to chromosomes. During this stage, they resemble an unwound, jumbled bunch of threads. We call these unwound protein-chromosome complexes chromatin (figure1.1.6 & 1.1.7). Chromatin describes the material that makes up the chromosomes both when condensed and decondensed. The Nucleolus We already know that the nucleus directs the synthesis of ribosomes, but how does it do this? Some chromosomes have sections of DNA that encode ribosomal RNA. A darkly staining area within the nucleus called the nucleolus (plural = nucleoli) aggregates the ribosomal RNA with associated proteins to assemble the ribosomal subunits that are then transported out through the pores in the nuclear envelope to the cytoplasm (figure 1.1.6). Ribosomes Ribosomes are the cellular structures responsible for protein synthesis. When we view them through an electron microscope, ribosomes appear either as clusters (polyribosomes) or as single, tiny dots that float freely in the cytoplasm. They may be attached to the cytoplasmic surfaces of the plasma membrane, on the endoplasmic reticulum, and the nuclear envelope (figure 1.1.4). Electron microscopy shows us that ribosomes, which are large protein and RNA complexes, consist of two subunits: large and small (figure 1.1.8). Ribosomes receive their “orders” for protein synthesis from the nucleus where the DNA transcribes into messenger RNA (mRNA). The mRNA travels to the ribosomes, which translate the code, provided by the sequence of the nitrogenous bases in the mRNA, into a specific order of amino acids in a protein. Amino acids are the building blocks of proteins. Because protein synthesis is an essential function of all cells (including enzymes, hormones, antibodies, pigments, structural components, and surface receptors), there are ribosomes in practically every cell. Ribosomes are particularly abundant in cells that synthesize large amounts of protein. For example, the pancreas is responsible for creating several digestive enzymes and the cells that produce these enzymes contain many ribosomes. Thus, we see another example of the structure following function. Mitochondria Scientists often call mitochondria (singular = mitochondrion) “powerhouses” or “energy factories” of both plant and animal cells because they are responsible for making adenosine triphosphate (ATP) — the cell’s main energy-carrying molecule. Cellular respiration is the process of making ATP using the chemical energy in glucose and other nutrients. In mitochondria, this process uses oxygen and produces carbon dioxide as a waste product. Mitochondria are oval-shaped, double-membrane organelles (figure 1.1.9) that have their own ribosomes and DNA. Each membrane is a phospholipid bilayer embedded with proteins. The inner layer has inward projections or folds called cristae. The inner lumen of mitochondria is filled with viscous fluid called matrix, made up of enzymes, certain vitamins & minerals in different forms, ions, small and large proteins, DNA, and ribosomes. Peroxisomes Peroxisomes are small, round organelles enclosed by single membranes. They carry out oxidation reactions that break down fatty acids and amino acids. They also detoxify many poisons that may enter the body. (Many of these oxidation reactions release hydrogen peroxide H2O2, which would be damaging to cells; however, when these reactions are confined to peroxisomes, enzymes safely break down the H2O2 into oxygen and water.) For example, peroxisomes in liver cells detoxify alcohol. Glyoxysomes, which are specialized peroxisomes in plants, are responsible for converting stored fats into sugars. Plant cells contain many different types of peroxisomes that play a role in metabolism, pathogen defense, and stress response, to mention a few. Vesicles and Vacuoles Vesicles and vacuoles are membrane-bound sacs that function in storage and transport. Other than the fact that vacuoles are somewhat larger than vesicles, there is a very subtle distinction between them. Vesicle membranes can fuse with either the plasma membrane or other membrane systems within the cell. The vacuole's membrane does not fuse with the membranes of other cellular components. Additionally, some agents such as enzymes within plant vacuoles break down macromolecules. Endomembrane System Scientists have long noticed that bacteria, mitochondria, and chloroplast are similar in size. We also know that bacteria have DNA and ribosomes, just like mitochondria and chloroplasts. Scientists believe that host cells and bacteria formed an endosymbiotic relationship when the host cells ingested both aerobic and autotrophic bacteria (cyanobacteria) but did not destroy them. Through many millions of years of evolution, these ingested bacteria became more specialized in their functions, with the aerobic bacteria becoming mitochondria and the autotrophic bacteria becoming chloroplasts. The endomembrane system (endo = “within”) is a group of membranes and organelles (figure 1.1.4) in eukaryotic cells that works together to modify, package, and transport lipids and proteins. It includes the nuclear envelope, lysosomes, and vesicles, which we have already mentioned, as well as the endoplasmic reticulum and Golgi apparatus, which we will cover shortly. Although not technically within the cell, the plasma membrane is included in the endomembrane system because, as you will see, it interacts with the other endomembranous organelles. The endomembrane system does not include either mitochondria or chloroplast membranes. The Endoplasmic Reticulum The endoplasmic reticulum (ER) (figure 1.1.4) is a series of interconnected membranous sacs and tubules. The ER's membrane, which is a phospholipid bilayer embedded with proteins, is continuous with the nuclear envelope. The inner hollow space of ER is called lumen or cisternal space. ER is responsible for modifying proteins, and their transportation as well as for synthesizing lipids. However, these two functions take place in two different areas of the ER: the rough ER and the smooth ER, respectively. Rough Endoplasmic Reticulum Scientists have named the rough endoplasmic reticulum (RER) as such because the ribosomes attached to its cytoplasmic surface give it a studded appearance when viewing it through an electron microscope (figure 1.1.10). Ribosomes transfer their newly synthesized proteins into the RER's lumen where they undergo structural modifications, such as folding or acquiring side chains. These modified proteins incorporate into cellular membranes—the ER or the ER's or other organelles' membranes. The proteins can also secrete from the cell (such as protein hormones, and enzymes). The RER also makes phospholipids for cellular membranes. If the phospholipids or modified proteins are not destined to stay in the RER, they will reach their destinations via transport vesicles that bud from the RER’s membrane (figure 1.1.11). Since the RER is engaged in modifying proteins (such as enzymes, for example) that secrete from the cell, you would be correct in assuming that the RER is abundant in cells that secrete proteins. Smooth Endoplasmic Reticulum The smooth endoplasmic reticulum (SER) is continuous with the RER but has few or no ribosomes on its cytoplasmic surface (figure 1.1.11). SER functions include the synthesis of carbohydrates, lipids, and steroid hormones; detoxification of medications and poisons; and storing calcium ions. In muscle cells, a specialized SER, the sarcoplasmic reticulum, is responsible for storing calcium ions that are needed to trigger the muscle cells' coordinated contractions. The Golgi Apparatus We have already mentioned that vesicles can bud from the ER and transport their contents elsewhere, but where do the vesicles go? Before reaching their final destination, the lipids or proteins within the transport vesicles still need sorting, packaging, and tagging so that they end up in the right place. Sorting, tagging, packaging, and distributing lipids and proteins takes place in the Golgi apparatus (also called the Golgi body), a series of flattened membranous sacs (figure 1.1.12). The side of the Golgi apparatus that is closer to the ER is called the cis face. The opposite side is the trans face. The transport vesicles that formed from the ER travel to the cis face, fuse with it, and empty their contents into the lumen of the Golgi apparatus. As the proteins and lipids travel through the Golgi, they undergo further modifications that allow them to be sorted. The most frequent modification is adding short-chain sugar molecules. These newly modified proteins and lipids are then tagged with phosphate groups or other small molecules to travel to their target destinations. Finally, the modified and tagged proteins are packaged into secretory vesicles that bud from the Golgi's trans face. While some of these vesicles deposit their contents into other cell parts where they will be used, other secretory vesicles fuse with the plasma membrane and release their contents outside the cell. In another example of form following function, cells that engage in a great deal of secretory activity (such as salivary gland cells that secrete digestive enzymes or immune system cells that secrete antibodies) have an abundance of Golgi. In a plant cell, the Golgi apparatus has the additional role of synthesizing polysaccharides, some of which are incorporated into the cell wall and some of which other cell parts use. Lysosomes The lysosomes are the cell’s “garbage disposal.” Enzymes within the lysosomes aid in breaking down proteins, polysaccharides, lipids, nucleic acids, and even worn-out organelles. Most plant cells do not have lysosomes, though many of these lysosomal enzymes are present in the vacuole of the plant cell. Lysosomes are also part of the endomembrane system. You can watch an excellent animation of the endomembrane system here. At the end of the animation, there is a short self-assessment. Cytoskeleton If you were to remove all the organelles from a cell, would the plasma membrane and the cytoplasm be the only components left? No. Within the cytoplasm, there would still be ions and organic molecules, plus a network of protein fibers that help maintain the cell's shape, secure some organelles in specific positions, allow cytoplasm and vesicles to move within the cell, and enable cells within the all eukaryotic organisms to move. Collectively, scientists call this network of protein fibers the cytoskeleton. There are three types of fibers within the cytoskeleton: microfilaments, intermediate filaments, and microtubules (figure 1.1.13). Here, we will examine each. Microfilaments Also called actin filaments (figure 1.1.14), microfilaments are the narrowest. They function in cellular movement, have a diameter of about 7 nm, and are made up of intertwined strands of two globular proteins. Microfilaments also provide some rigidity and help cells to change their shape. Microfilaments function in muscle contraction, cytoplasmic streaming, maintaining the cell shape, internal transport and cytokinesis. Intermediate Filaments Intermediate filaments are filaments with a diameter of about 8 to 10 nm (figure 1.1.15). You are probably most familiar with keratin, the fibrous protein that strengthens your hair, nails, and the skin's epidermis. Intermediate filaments have no role in cell movement. Their function is purely structural. They bear tension, thus maintaining the cell's shape, and anchor the nucleus and other organelles in place. The intermediate filaments are the most diverse group of cytoskeletal elements. The research is ongoing to understand the function of intermediate filaments in plants. Microtubules As their name implies, microtubules are small hollow tubes. With a diameter of about 25 nm, microtubules are the widest component of cytoskeletons. Two globular proteins, α-tubulin and β-tubulin are polymerized as dimers, which then associate with other such dimers laterally to form tubular structures called protofilaments. One of the common arrangements is of 13 protofilaments joined to each other, side by side, to form a microtubule (figure 1.1.16). They help the cell resist compression, provide a track along which vesicles move through the cell, and pull replicated chromosomes to opposite ends of a dividing cell. Like microfilaments, microtubules can disassemble and reform quickly. Microtubules participate in cell division in plant cells. You have now completed a broad survey of prokaryotic and eukaryotic cell components. For a summary of cellular components in prokaryotic and eukaryotic cells, see table 1.1 Cell Component \| Function \| Present in Prokaryotes? \| Present in Animal Cells? \| Present in Plant Cells? \| Plasma membrane \| Separates cell from the external environment; controls passage of organic molecules, ions, water, oxygen, and wastes into and out of a cell \| Yes \| Yes \| Yes \| Cytoplasm \| Provides turgor pressure to plant cells as the fluid inside the central vacuole; site of many metabolic reactions; medium in which organelles are found \| Yes \| Yes \| Yes \| Nucleolus \| The darkened area within the nucleus where ribosomal subunits are synthesized. \| No \| Yes \| Yes \| Nucleus \| A cell organelle that houses DNA and directs the synthesis of ribosomes and proteins \| No \| Yes \| Yes \| Ribosomes \| Protein synthesis \| Yes \| Yes \| Yes \| Mitochondria \| ATP production/cellular respiration \| No \| Yes \| Yes \| Peroxisomes \| Oxidize and thus break down fatty acids and amino acids, and detoxify poisons \| No \| Yes \| Yes \| Vesicles and vacuoles \| Storage and transport; digestive function in plant cells \| No \| Yes \| Yes \| Centrosome \| Unspecified role in cell division in animal cells; microtubule source in animal cells \| No \| Yes \| No \| Lysosomes \| Digestion of macromolecules; recycling of worn-out organelles \| No \| Yes \| Some \| Cell wall \| Protection, structural support, and maintenance of cell shape \| Yes, primarily peptidoglycan \| No \| Yes, primarily cellulose \| Chloroplasts \| Photosynthesis \| No \| No \| Yes \| Endoplasmic reticulum \| Modifies proteins and synthesizes lipids \| No \| Yes \| Yes \| Golgi apparatus \| Modifies, sorts, tags, packages, and distributes lipids and proteins \| No \| Yes \| Yes \| Cytoskeleton \| Maintains cell’s shape, secures organelles in specific positions, allows cytoplasm and vesicles to move within the cell, and enables unicellular organisms to move independently \| Yes \| Yes \| Yes \| Flagella \| Cellular locomotion \| Some \| Some \| No, except for some plant sperm cells \| Cilia \| Cellular locomotion, movement of particles along plasma membrane's extracellular surface, and filtration \| Some \| Some \| No \| Extracellular Structure If you work on a group project, you need to communicate with others (at least your group members and the teacher). As you might expect, if cells are to work together, they must communicate with each other. Let’s look at how cells communicate with each other. Animal cells release materials into the extracellular space. The primary component of these materials is collagen. Collagen fibers are interwoven with proteoglycans, which are carbohydrate-containing protein molecules. Collectively, we call these materials the extracellular matrix. Plant cells do not secrete collagen but produce a rigid cell wall. Access for free at https://openstax.org/books/biology-2e/pages/4-3-eukaryotic-cells Components of a Plant Cell At this point, you know that all eukaryotic cell has a plasma membrane, cytoplasm, a nucleus, ribosomes, mitochondria, peroxisomes, and in some vacuoles, microtubule organizing centers (MTOCs). Animal cells and plant cells have lysosomes, though lysosomes in plants operate differently and are not very common. There are some striking differences between animal and plant cells. In animal cells centrioles are associated with the MTOC, a complex we call the centrosome. Plant cells lack centrioles. Plant cells have a cell wall, chloroplasts, and other specialized plastids, and a large central vacuole, whereas animal cells do not. The Cell Wall If you examine figure 1.1.4 b, the plant cell diagram, you will see a structure external to the plasma membrane. This is the cell wall, a rigid covering that protects the cell, provides structural support, and gives shape to the cell. Fungal and some protistan cells also have cell walls. While the prokaryotic cell walls' chief component is peptidoglycan, the major organic molecule in the plant’s (and some protists') cell wall is cellulose — a polysaccharide comprised of glucose units (figure 1.1.17). Have you ever noticed that when you bite into a raw vegetable, like celery, it crunches? That’s because you are tearing the rigid cell walls of a celery stalk with your teeth. Central Vacuole Previously, we mentioned vacuoles as essential components of plant cells. If you look at figure 1.1.4b, you will see that each plant cell has a large central vacuole that occupies most of the space inside the cell. The central vacuole plays a key role in regulating the cell’s concentration of water in changing environmental conditions. Have you ever noticed that if you forget to water a plant for a few days, it wilts? That’s because as the water concentration in the soil becomes lower than the water concentration in the plant, water moves out of the central vacuoles and cytoplasm. As the central vacuole shrinks, it leaves the cell wall unsupported. This loss of support to the plant's cell walls results in a wilted appearance. The central vacuole also supports the cell's expansion. When the central vacuole holds more water, the cell becomes larger without having to invest considerable energy in synthesizing new cytoplasm. Chloroplasts Like the mitochondria, chloroplasts have their own DNA and ribosomes, but chloroplasts have an entirely different function. Chloroplasts are plant cell organelles that carry out photosynthesis. Photosynthesis is the series of reactions that use carbon dioxide, water, and light energy to make glucose and oxygen. This is a major difference between plants and animals. Plants (autotrophs) can make their own food, like sugars that is used in cellular respiration to provide ATP energy generated in the plant mitochondria. Animals (heterotrophs) must ingest their food. Like mitochondria, chloroplasts have outer and inner membranes, but within the space enclosed by a chloroplast’s inner membrane is a set of interconnected and stacked fluid-filled membrane sacs we call thylakoids (figure 1.1.18). Each thylakoid stack is a granum (plural = grana). We call the fluid enclosed by the inner membrane that surrounds the grana the stroma. The chloroplasts contain a green pigment, chlorophyll, which captures the light energy that drives the reactions of photosynthesis. Like plant cells, photosynthetic protists also have chloroplasts. Some bacteria perform photosynthesis, but their chlorophyll is different from that of plants and is not present inside an organelle. Intercellular Junctions Cells can also communicate with each other via direct contact or intercellular junctions. There are differences in the ways that plant and animal and fungal cells communicate. Plasmodesmata are junctions between plant cells, whereas, animal cell contacts include tight junctions, gap junctions, and desmosomes. Only plasmodesmata are discussed here. Plasmodesmata In general, long stretches of the plasma membranes of neighboring plant cells cannot touch one another because the cell wall that surrounds each cell separates them (figure 1.1.4b). How then, can a plant transfer water and other soil nutrients from its roots, through its stems, and to its leaves? Such transport uses the vascular tissues (xylem and phloem) primarily. There also exist structural modifications, which we call plasmodesmata (singular = plasmodesma). Numerous channels pass between adjacent cell walls of plant cells connecting their cytoplasm, and enabling the transport of materials from cell to cell, and thus throughout the plant (figure 1.1.19). Access for free at https://openstax.org/books/biology-2e/pages/4-3-eukaryotic-cells Attributions Biology 2e by Clark Mary Ann, Douglas Matthew, Choi Jung. OpenStax is licensed under Creative Commons Attribution License V 4.0 Introduction to Organismal Biology at https://sites.gatech.edu/organismalbio/ is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 3.0 Unported License. Botany by Melissa Ha, Maria Morrow, and Kammy Algiers is shared under a CC BY-NC 4.0 license and was authored, remixed, and/or curated by Melissa Ha, Maria Morrow, & Kammy Algiers.	oercommons	2025-03-18T00:37:02.442441	null	{ "license": "Creative Commons - Attribution - https://creativecommons.org/licenses/by/4.0/", "url": "https://oercommons.org/courseware/lesson/84551/overview", "title": "Statewide Dual Credit Introduction to Plant Science, Plant Form", "author": null }
https://oercommons.org/courseware/lesson/89185/overview	2.3 Plant Organ System - Roots 2.4 Plant Organ System - Stems 2.5 Plant Organ System - Leaf 2.6 Plant Organ System - Flower 2_Parts-of-a-Plant Parts of a Plant Overview Common ash (Fraxinus excelsior), a deciduous broad-leaved (angiosperm tree) By Brian Green, CC BY-SA 2.0, https://commons.wikimedia.org/w/index.php?curid=13127021 Did you have an idea for improving this content? We’d love your input. Introduction Learning Objectives - Describe the angiosperms or flowering plants. - Identify the root & shoot system of a plant. - Differentiate between a monocot and a eudicot plant. - Describe the external structure of roots and various modifications of the roots. - Describe the external structure of the stem and various modifications of the stem. - Explain the external structure of a typical leaf. - Define phyllotaxy. - Differentiate between simple and compound leaves. - Describe the internal structure of a typical dicot leaf. - List and describe the parts of a typical angiosperm flower. - Differentiate between perfect and imperfect flower flowers. - Differentiate between complete and incomplete flowers. - Differentiate between monoecious and dioecious plants. Key Terms androecium - the sum of all the stamens in a flower angiosperms - a group of seed-bearing plants that produce flowers and fruits anther - sac-like structure at the tip of the stamen in which pollen grains are produced bract - modified leaf associated with a flower bulb - a modified underground stem that consists of a large bud surrounded by numerous leaf scales calyx - whorl of sepals carpel - a single unit of the pistil complete flower - flower with all four parts, sepals, petals, stamens, and carpels compound leaf - a leaf in which the leaf blade is subdivided to form leaflets, all attached to the midrib corm - rounded, fleshy underground stem that contains stored food corolla - a collection of petals dicot - (also, eudicot) related group of angiosperms whose embryos possess two cotyledons dioecious - describes a species in which the male and female reproductive organs are carried on separate specimens filament - thin stalk that links the anther to the base of the flower guard cell - paired cells on either side of a stoma that control the stomatal opening and thereby regulate the movement of gases and water vapor gynoecium - (also, carpel) structure that constitutes the female reproductive organs imperfect flower - a flower that only carries either male or female reproductive organ monocot - a related group of angiosperms that produce embryos with one cotyledon and pollen with a single ridge monoecious - describes a species in which the male and female reproductive organs are on the same plant ovary - a chamber that contains and protects the ovule or female megasporangium palisade mesophyll - an area of a typical dicot leaf comprising column-shaped tightly packed parenchyma cells found underneath the upper epidermis perfect flower - a flower that carries both male and female reproductive organs petal - modified leaf interior to the sepals; colorful petals attract animal pollinators phyllotaxy - arrangement of leaves on a stem pistil - a fused group of carpels pistillate flower - a flower that only carries female reproductive organs pneumatophore - roots participating in gas exchange rhizome - a modified underground stem that grows horizontally to the soil surface and has nodes and internodes root - belowground portion of the plant that supports the plant and absorbs water and minerals runner/stolen - a modified stem that runs parallel to the ground and can give rise to new plants at the nodes sepal - a modified leaf that encloses the bud; the outermost structure of a flower simple leaf - leaf type in which the lamina is completely undivided spongy mesophyll - an area of a typical dicot leaf comprising large air spaces and loosely packed irregularly shaped parenchyma cells found underneath the palisade parenchyma cells staminate flower - a flower that only carries male reproductive organs stem - aboveground portion of the plant; consists of nonreproductive plant parts, such as leaves and stems, and reproductive parts, such as flowers and fruits stigma - the uppermost structure of the carpel where pollen is deposited style - long, thin structure that links the sigma to the ovary Introduction Plants are as essential to human existence as land, water, and air. Without plants, our day-to-day lives would be impossible because, without oxygen from photosynthesis, aerobic life cannot be sustained. From providing food and shelter to serving as a source of medicines, oils, perfumes, and industrial products, plants provide humans with numerous valuable resources. When you think of plants, most of the organisms that come to mind are vascular plants. These plants have tissues that conduct food and water, and most of them have seeds. Seed plants are divided into gymnosperms and angiosperms. Gymnosperms include the needle-leaved conifers—spruce, fir, and pine—as well as less familiar plants, such as ginkgo and cycads. Their seeds are not enclosed by fleshy fruit. Angiosperms, constitute seed plants with flowers, also called flowering plants. They include broadleaved trees (such as maple, oak, and elm), vegetables (such as potatoes, lettuce, and carrots), grasses, and plants known for the beauty of their flowers (roses, irises, and daffodils, for example). While individual plant species are unique, all share a common structure: a plant body consisting of stems, roots, and leaves. They all transport water, minerals, and sugars produced through photosynthesis through the plant body in a similar manner. All plant species also respond to environmental factors, such as light, gravity, competition, temperature, and predation. Angiosperms or flowering plants From their humble and still obscure beginning during the early Jurassic period, the angiosperms—or flowering plants—have evolved to dominate most terrestrial ecosystems (Figure 1.2.1). With more than 300,000 species, the angiosperm phylum (Anthophyta) is second only to insects in terms of diversification. The success of angiosperms is due to two novel reproductive structures: flowers and fruits. The function of the flower is to ensure pollination, often by insects, as well as to protect a developing embryo. The colors and patterns on flowers offer specific signals to many pollinating insects or birds and bats that have coevolved with them. For example, some patterns are visible only in the ultraviolet range of light, which can be seen by insect pollinators. For some pollinators, flowers advertise themselves as a reliable source of nectar. Flower scent also helps to select pollinators. Sweet scents tend to attract bees and butterflies and moths, but some flies and beetles might prefer scents that signal fermentation or putrefaction. Flowers also provide protection for the ovule and developing embryo inside a receptacle. The function of the fruit is seed protection and dispersal. Different fruit structures or tissues on fruit—such as sweet flesh, wings, parachutes, or spines that grab—reflect the dispersal strategies that help spread seeds. Access for free at https://openstax.org/books/biology-2e/pages/30-introduction Diversity of Angiosperms Diversity of Angiosperms Within the angiosperms are three major groups: basal angiosperms, monocots, and dicots. Basal angiosperms are a group of plants that are believed to have branched off before the separation of the monocots and dicots, because they exhibit traits from both groups. They are categorized separately in most classification schemes. The basal angiosperms include Amborella, water lilies, the Magnoliids (magnolia trees, laurels, and spice peppers), and a group called the Austrobaileyales, which includes the star anise. The monocots and dicots are differentiated on the basis of the structure of the cotyledons, pollen grains, and other structures. Monocots include grasses and lilies, and the dicots form a multi-branched group that includes (among many others) roses, cabbages, sunflowers, and mints. Monocots Plants in the monocot group are primarily identified by the presence of a single cotyledon in the seedling. Other anatomical features shared by monocots include veins that run parallel to and along the length of the leaves, and flower parts that are arranged in a three- or six-fold symmetry. True woody tissue is rarely found in monocots. In palm trees, vascular and parenchyma tissues produced by the primary and secondary thickening meristems form the trunk. The pollen from the first angiosperms was likely monosulcate, containing a single furrow or pore through the outer layer. This feature is still seen in modern monocots. The vascular tissue of the stem is scattered, not arranged in any particular pattern, but is organized in a ring in the roots. The root system consists of multiple fibrous roots, with no major taproot. Adventitious roots often emerge from the stem or leaves. The monocots include familiar plants such as the true lilies (Liliopsida), orchids, yucca, asparagus, grasses, and palms. Many important crops are monocots, such as rice and other cereals, corn, sugar cane, and tropical fruits like bananas and pineapples (figure 1.2.2 a, b, c). Eudicots Eudicots, or true dicots, are characterized by the presence of two cotyledons in the developing shoot. Veins form a network in leaves, and flower parts come in four, five, or many whorls. Vascular tissue forms a ring in the stem; in monocots, the vascular tissue is scattered in the stem. Eudicots can be herbaceous (not woody) or produce woody tissues. Most eudicots produce pollen that is trisulcate or triporate, with three furrows or pores. The root system is usually anchored by one main root developed from the embryonic radicle. Eudicots comprise two-thirds of all flowering plants. The major differences between monocots and eudicots are summarized in table 2.1. However, some species may exhibit characteristics usually associated with the other group, so the identification of a plant as a monocot or a eudicot is not always straightforward (figure 1.2.2. d, e, f). Characteristic \| Monocot \| Eudicot \| Cotyledon \| One \| Two \| Veins in Leaves \| Parallel \| Network (branched) \| Stem Vascular Tissue \| Scattered \| Arranged in a ring pattern \| Roots \| Network of fibrous roots \| Taproot with many lateral roots \| Pollen \| Monosulcate \| Trisulcate \| Flower Parts \| Three or multiple of three \| Four, five, multiple of four or five and whorls \| Access for free at https://openstax.org/books/biology-2e/pages/26-3-angiosperms Plant Organ System - Roots In plants, just as in animals, similar cells working together form a tissue. When different types of tissues work together to perform a unique function, they form an organ; organs working together form organ systems. Vascular plants have two distinct organ systems: a shoot system and a root system. The shoot system consists of two portions: the vegetative (non-reproductive) parts of the plant, such as the leaves and the stems, and the reproductive parts of the plant, which include flowers and fruits. The shoot system generally grows above ground, where it absorbs the light needed for photosynthesis. The root system, which supports the plants and absorbs water and minerals, is usually underground. Figure 1.2.3 shows the organ systems of a typical plant. Roots The roots of seed plants have three major functions: anchoring the plant to the soil, absorbing water and minerals, transporting them upwards, and storing the products of photosynthesis. Some roots are modified to absorb moisture and exchange gases. Most roots are underground. Some plants, however, also have adventitious roots, which emerge above the ground from the shoot. Types of Root Systems Root systems are mainly of two types (figure 1.2.4). Dicots have a taproot system, while monocots have a fibrous root system. A tap root system has a main root that grows down vertically, from which many smaller lateral roots arise. Dandelions are a good example; their tap roots usually break off when trying to pull these weeds, and they can regrow another shoot from the remaining root. A tap root system penetrates deep into the soil. In contrast, a fibrous root system is located closer to the soil surface and forms a dense network of roots that also helps prevent soil erosion (lawn grasses are a good example, as are wheat, rice, and corn). Some plants have a combination of tap roots and fibrous roots. Plants that grow in dry areas often have deep root systems, whereas plants growing in areas with abundant water are likely to have shallower root systems. Root Modifications Root structures may be modified for specific purposes. For example, some roots are bulbous and store starch. Aerial roots and prop roots are two forms of aboveground roots that provide additional support to anchor the plant. Tap roots, such as carrots, turnips, and beets, are examples of roots that are modified for food storage (figure 1.2.5). Epiphytic roots enable a plant to grow on another plant. For example, the epiphytic roots of orchids develop spongy tissue to absorb moisture. The banyan tree (Ficus sp.) begins as an epiphyte, germinating in the branches of a host tree; aerial roots develop from the branches and eventually reach the ground, providing additional support (figure 1.2.6). In screwpine (Pandanus sp.), a palm-like tree that grows in sandy tropical soils, aboveground prop roots develop from the nodes to provide additional support. Access for free at https://openstax.org/books/biology-2e/pages/30-3-roots Plant Organ System - Stems Stems are a part of the shoot system of a plant. They may range in length from a few millimeters to hundreds of meters, and vary in diameter, depending on the plant type. Stems are usually above ground, although the stems of some plants, such as the potato, also grow underground. Stems may be herbaceous (green & soft) or woody in nature. Their main function is to provide support to the plant, holding leaves, flowers, and buds; in some cases, stems also store food for the plant. A stem may be unbranched, like that of a palm tree, or it may be highly branched, like that of a magnolia tree. The stem of the plant connects the roots to the leaves, helping to transport absorbed water and minerals to different parts of the plant. It also helps to transport the products of photosynthesis, namely sugars, from the leaves to the rest of the plant. Plant stems, whether above or below ground, are characterized by the presence of nodes and internodes (figure 1.2.7). Nodes are points of attachment for leaves, aerial roots, and flowers. The stem region between two nodes is called an internode. The stalk that extends from the stem to the base of the leaf is the petiole. An axillary bud is usually found in the axil—the area between the base of a leaf and the stem—where it can give rise to a branch or a flower. The apex (tip) of the shoot contains the apical meristem within the apical bud. Stem Modifications Some plant species have modified stems that are especially suited to a particular habitat and environment (figure 1.2.8). A rhizome is a modified stem that grows horizontally underground and has nodes and internodes. Vertical shoots may arise from the buds on the rhizome of some plants, such as ginger and ferns. Corms are like rhizomes; except they are more rounded and fleshier (such as in gladiolus). Corms contain stored food that enables some plants to survive the winter. Stolons are stems that run almost parallel to the ground, or just below the surface, and can give rise to new plants at the nodes. Runners are a type of stolon that runs above the ground and produces new clone plants at nodes at varying intervals: strawberries are an example. Tubers are modified stems that may store starch, as seen in the potato (Solanum sp.). Tubers arise as swollen ends of stolons and contain many adventitious or unusual buds (familiar to us as the “eyes” on potatoes). A bulb that functions as an underground storage unit is a modification of a stem that has the appearance of enlarged fleshy leaves emerging from the stem or surrounding the base of the stem, as seen in the iris. Some aerial modifications of stems are tendrils and thorns (figure 1.2.9). Tendrils are slender, twining strands that enable a plant (like a vine or pumpkin) to seek support by climbing on other surfaces. Thorns are modified branches appearing as sharp outgrowths that protect the plant; common examples include roses, Osage orange, and devil’s walking stick. Access for free at https://openstax.org/books/biology-2e/pages/30-2-stems Plant Organ System - Leaf Leaves are the main sites for photosynthesis: the process by which plants synthesize food. Most leaves are usually green, due to the presence of chlorophyll in the leaf cells. However, some leaves may have different colors, caused by other plant pigments that mask the green chlorophyll. The thickness, shape, and size of leaves are adapted to the environment. Each variation helps a plant species maximize its chances of survival in a particular habitat. Usually, the leaves of plants growing in tropical rainforests have larger surface areas than those of plants growing in deserts or very cold conditions, which are likely to have a smaller surface area to minimize water loss. Structure of a Typical Leaf The structure of a leaf is more complex than meets the naked eye. A leaf typically has a leaf blade also called the lamina, which is also the widest part of the leaf. Some leaves are attached to the plant stem by a petiole. Leaves that do not have a petiole and are directly attached to the plant stem are called sessile leaves. Small green appendages usually found at the base of the petiole are known as stipule(s). Most leaves have a midrib, which travels the length of the leaf and branches to each side to produce veins of vascular tissue. The edge of the leaf is called the margin. Figure 1.2.10 shows the structure of a typical eudicot leaf. Within each leaf, the vascular tissue forms veins. The arrangement of veins in a leaf is called the venation pattern. Monocots and dicots differ in their patterns of venation (figure 1.2.11). Monocots have parallel venation; the veins run in straight lines across the length of the leaf without converging at a point. In dicots, however, the veins of the leaf have a net-like appearance, forming a pattern known as reticulate venation. One extant plant, the Ginkgo biloba, has dichotomous venation where the veins fork. Leaf Arrangement The arrangement of leaves on a stem is known as phyllotaxy. The number and placement of a plant’s leaves will vary depending on the species, with each species exhibiting a characteristic leaf arrangement. Leaves are classified as either alternate, spiral, or opposite. Plants that have only one leaf per node have leaves that are said to be either alternate—meaning the leaves alternate on each side of the stem in a flat plane—or spiral, meaning the leaves are arrayed in a spiral along the stem. In an opposite leaf arrangement, two leaves arise at the same point, with the leaves connecting opposite each other along the branch. If there are three or more leaves connected at a node, the leaf arrangement is classified as whorled. Leaf Form Leaves may be simple or compound (figure 1.2.12). In a simple leaf, the blade is either completely undivided—as in the banana leaf—or it has lobes, but the separation does not reach the midrib, as in the maple leaf. In a compound leaf, the leaf blade is completely divided with the formation of leaflets (that may have a stalk), as in the locust tree, attached to the main axis or midrib in a simple leaf. This main axis is also called a rachis. A palmately compound leaf resembles the palm of a hand, with leaflets radiating outwards from one point. Examples include the leaves of poison ivy, the buckeye tree, or the familiar houseplant Schefflera sp. (common name “umbrella plant"). Pinnately compound leaves take their name from their feather-like appearance; the leaflets are arranged along the midrib, as in rose leaves (Rosa sp.), or the leaves of hickory, pecan, ash, or walnut trees. Internal Structure of a leaf The outermost layer of the leaf is the epidermis; it is present on both sides of the leaf and is called the upper and lower epidermis, respectively. Botanists call the upper side the adaxial surface (or adaxis) and the lower side the abaxial surface (or abaxis). The epidermis helps in the regulation of gas exchange. It contains stomata (figure 1.2.13): openings through which the exchange of gases takes place. Two guard cells surround each stoma, regulating its opening and closing. The epidermis is usually one cell layer thick; however, in plants that grow in very hot or very cold conditions, the epidermis may be several layers thick to protect against excessive water loss from transpiration. A waxy layer known as the cuticle covers the leaves of all plant species. The cuticle reduces the rate of water loss from the leaf surface. Other leaves may have small hairs called trichomes on the leaf surface. Trichomes help to deter herbivory by restricting insect movements, or by storing toxic or bad-tasting compounds; they can also reduce the rate of transpiration by blocking air flow across the leaf surface (figure 1.2.14). Below the epidermis of dicot leaves are layers of cells known as the mesophyll, or “middle leaf.” The mesophyll of most leaves typically contains two arrangements of parenchyma cells: the palisade parenchyma and spongy parenchyma (figure 1.2.15). The palisade parenchyma (also called the palisade mesophyll) has column-shaped, tightly packed cells, and may be present in one, two, or three layers. Below the palisade parenchyma is loosely arranged cells of irregular shape. These are the cells of the spongy parenchyma (or spongy mesophyll). The air space found between the spongy parenchyma cells allows gaseous exchange between the leaf and the outside atmosphere through the stomata. In aquatic plants, the intercellular spaces in the spongy parenchyma help the leaf float. Both layers of the mesophyll contain many chloroplasts. Guard cells are the only epidermal cells to contain chloroplasts. Like the stem, the leaf contains vascular bundles composed of the xylem and phloem (figure 1.2.16). The xylem consists of tracheids and vessels, which transport water and minerals to the leaves. The phloem transports the photosynthetic products from the leaf to the other parts of the plant. A single vascular bundle, no matter how large or small, always contains both the xylem and phloem tissues. Leaf Adaptations Coniferous plant species that thrive in cold environments—like spruce, fir, and pine—have leaves that are reduced in size and needle-like in appearance. These needle-like leaves have sunken stomata and a smaller surface area, which are two attributes that aid in reducing water loss. In hot climates, plants such as cacti have leaves that are reduced to spines that, in combination with their succulent stems, help to conserve water. Many aquatic plants have leaves with wide lamina that can float on the surface of the water, and a thick waxy cuticle on the leaf surface that repels water. Access for free at https://openstax.org/books/biology-2e/pages/30-4-leaves Plant Organ System - Flower Flowers are the sexual reproductive parts of a plant. Flowers are modified leaves, or sporophylls organized around a central receptacle. Although there is a remarkable variation in the appearance of flowers, virtually all flowers contain the sepals, petals, carpels, and stamens. A complete flower must have all four structures, otherwise, it is called an incomplete flower. The peduncle typically attaches the flower to the plant body. A whorl of sepals(collectively called the calyx) is located at the base of the peduncle and encloses the unopened floral bud. Sepals are usually photosynthetic organs, although there are some exceptions. For example, the corolla in lilies and tulips consists of three sepals and three petals that look virtually identical. Petals, collectively the corolla, are located inside the whorl of sepals and may display vivid colors to attract pollinators. Sepals and petals together form the perianth. The sexual organs—the female gynoecium and male androecium —are located at the center of the flower. Typically, the sepals, petals, and stamens are attached to the receptacle at the base of the gynoecium, but the gynoecium may also be located deeper in the receptacle, with the other floral structures attached above it. As illustrated in figure 1.2.17, the innermost part of a perfect flower is the gynoecium, the location in the flower where the eggs will form. The female reproductive unit consists of one or more carpels, each of which has a stigma, style, and ovary. The stigma is the location where the pollen is deposited either by wind or a pollinating arthropod. The sticky surface of the stigma traps pollen grains, and the style is a connecting structure through which the pollen tube will grow to reach the ovary. The ovary houses one or more ovules, each of which will ultimately develop into a seed. Flower structure is very diverse, and carpels may be singular, multiple, or fused. (Multiple fused carpels comprise a pistil.) The androecium, or male reproductive region, is composed of multiple stamens surrounding the central carpel. Stamens are composed of a thin stalk called a filament and a sac-like structure called the anther. The filament supports the anther, where the microspores are produced by meiosis and develop into haploid pollen grains, or male gametophytes. Most angiosperms have perfect flowers, which means that each flower carries both stamens and carpels (figure1.2.17), for example lilies. Many flowers are called imperfect since they are either staminate (with only male reproductive structure) or carpellate flowers (with only female reproductive structure). In monoecious plants, male (staminate) and female (pistillate/carpellate) flowers are separate but carried on the same plant, which can mature simultaneously or at different times (dichogamous) to ensure cross pollination, Sweetgums (Liquidambar spp.) and beeches (Betula spp.) are monoecious (figure 1.2.18). Family Rosaceae (rose) include many plants that show dichogamy. Monoecious plants also include many plants that produce bisexual flowers. In dioecious plants, male and female flowers are found on separate plants. Willows (Salix spp.), poplars (Populus spp.), papaya and asparagus are dioecious. Despite the predominance of perfect flowers, only a few species of angiosperms self-pollinate. Both anatomical and environmental barriers promote cross-pollination mediated by a physical agent (wind or water), or an animal, such as an insect or bird. Cross-pollination increases genetic diversity in a species. Access for free at https://openstax.org/books/biology-2e/pages/26-3-angiosperms Attributions Biology 2e by Clark Mary Ann, Douglas Matthew, Choi Jung. OpenStax is licensed under Creative Commons Attribution License V 4.0 Glossary adventitious root - an above-ground root that arises from a plant part other than the radicle of the plant embryo apical bud - bud formed at the tip of the shoot apical meristem - meristematic tissue located at the tips of stems and roots; enables a plant to extend in length axillary bud - bud located in the axil of a leaf, area of the stem where the petiole connects to the stem bark - the tough, waterproof, outer epidermal layer of cork cells bulb - modified underground stem that consists of a large bud surrounded by numerous leaf scales Casparian strip - waxy coating that forces water to cross endodermal plasma membranes before entering the vascular cylinder, instead of moving between endodermal cells collenchyma cell - elongated plant cell with unevenly thickened walls; provides structural support to the stem and leaves companion cell - phloem cell that is connected to sieve-tube cells; has large amounts of ribosomes and mitochondria compound leaf - a leaf in which the leaf blade is subdivided to form leaflets, all attached to the midrib corm - rounded, fleshy underground stem that contains stored food cortex - ground tissue found between the vascular tissue and the epidermis in a stem or root cuticle - waxy covering on the outside of the leaf and stem that prevents the loss of water dermal tissue - a protective plant tissue covering the outermost part of the plant; controls the gas exchange endodermis - a layer of cells in the root that forms a selective barrier between the ground tissue and the vascular tissue, allowing water and minerals to enter the root while excluding toxins and pathogens epidermis - a single layer of cells found in plant dermal tissue; covers and protects underlying tissue fibrous root system - type of root system in which the roots arise from the base of the stem in a cluster, forming a dense network of roots; found in monocots ground tissue - plant tissue involved in photosynthesis; provides support, and stores water and sugars guard cells - paired cells on either side of a stoma that control the stomatal opening and thereby regulate the movement of gases and water vapor intercalary meristem - meristematic tissue located at nodes and the bases of leaf blades; found only in monocots internode - region between nodes on the stem lamina - leaf blade lateral meristem - also called secondary meristem, meristematic tissue that enables a plant to increase in thickness or girth caused by the vascular cambium and cork cambium lenticel - opening on the surface of mature woody stems that facilitates gas exchange meristem - plant region of continuous growth meristematic tissue - tissue containing cells that constantly divide; contributes to plant growth node - point along the stem at which leaves, flowers, or aerial roots originate palmately compound leaf - leaf type with leaflets that emerge from a point, resembling the palm of a hand parenchyma cell - most common type of plant cell; found in the stem, root, leaf, and in fruit pulp; site of photosynthesis and starch storage pericycle - outer boundary of the stele from which lateral roots can arise periderm - outermost covering of woody stems; consists of the cork cambium, cork cells, and the phelloderm permanent tissue - plant tissue composed of cells that are no longer actively dividing petiole - stalk of the leaf phyllotaxy - arrangement of leaves on a stem pinnately compound leaf - leaf type with a divided leaf blade consisting of leaflets arranged on both sides of the midrib pith - ground tissue found towards the interior of the vascular tissue in a stem or root primary growth - growth resulting in an increase in length of the stem and the root; caused by cell division in the shoot or root apical meristem rhizome - modified underground stem that grows horizontally to the soil surface and has nodes and internodes root cap - protective cells covering the tip of the growing root root hair - hair-like structure that is an extension of epidermal cells; increases the root surface area and aids in absorption of water and minerals root system - belowground portion of the plant that supports the plant and absorbs water and minerals runner - stolon that runs above the ground and produces new clone plants at nodes sclerenchyma cell - plant cell that has thick secondary walls and provides structural support, usually dead at maturity sessile - leaf without a petiole that is attached directly to the plant stem shoot system - aboveground portion of the plant; consists of nonreproductive plant parts, such as leaves and stems, and reproductive parts, such as flowers and fruits sieve-tube cell - (sieve-tube members in angiosperms) phloem cell arranged end to end to form a sieve tube that transports organic substances, such as sugars and amino acids simple leaf - leaf type in which the lamina is completely undivided or merely lobed sink - growing parts of a plant, such as roots and young leaves, which require photosynthate source - organ that produces photosynthate for a plant stele - inner portion of the root containing the vascular tissue; surrounded by the endodermis stipule - small green structure found on either side of the leaf stalk or petiole stolon - modified stem that runs parallel to the ground and can give rise to new plants at the nodes tap root system - type of root system with a main root that grows vertically with few lateral roots; found in dicots tendril - modified stem consisting of slender, twining strands used for support or climbing thorn - modified stem branch appearing as a sharp outgrowth that protects the plant tracheid - xylem cell with thick secondary walls that helps transport water translocation - mass transport of photosynthates from source to sink in vascular plants transpiration - loss of water vapor to the atmosphere through stomata trichome - hair-like structure on the epidermal surface tuber - modified underground stem adapted for starch storage; has many adventitious buds vascular bundle - strands of plant tissue made up of xylem and phloem vascular stele - strands of root tissue made up of xylem and phloem vascular tissue - tissue made up of xylem and phloem that transports food and water throughout the plant venation - pattern of veins in a leaf; may be parallel (as in monocots), reticulate (as in dicots), or dichotomous (as in ginkgo biloba) vessel element - xylem cell that is shorter than a tracheid and has thinner walls whorled - pattern of leaf arrangement in which three or more leaves are connected at a node	oercommons	2025-03-18T00:37:02.593173	null	{ "license": "Creative Commons - Attribution - https://creativecommons.org/licenses/by/4.0/", "url": "https://oercommons.org/courseware/lesson/89185/overview", "title": "Statewide Dual Credit Introduction to Plant Science, Plant Form", "author": null }
https://oercommons.org/courseware/lesson/87592/overview	3.3 Vascular Tissue 3.4 Ground Tissue & Cell Types 3_Plant-Tissues-and-Cell-Types Plant Tissues and Cell Types Overview Introduction Learning Objectives - List three types of tissues in plants. - Describe the identifying features of dermal tissue. - List the most common modifications of dermal tissue. - List two types of vascular tissues. - Explain the structure of xylem tracheids and vessels. - Explain the structure of phloem sieve tube members and companion cells. - Differentiate between xylem and phloem. - List the three types of plant cells. - List the identifying features of parenchyma, collenchyma and sclerenchyma and their modifications. Key Terms adventitious root - an above ground root that arises from a plant part other than the radicle of the plant embryo apical bud - bud formed at the tip of the shoot apical meristem - meristematic tissue located at the tips of stems and roots; enables a plant to extend in length axillary bud - bud located in the axil of a leaf, area of the stem where the petiole connects to the stem bark - the tough, waterproof, outer epidermal layer of cork cells bulb - modified underground stem that consists of a large bud surrounded by numerous leaf scales Casparian strip - waxy coating that forces water to cross endodermal plasma membranes before entering the vascular cylinder, instead of moving between endodermal cells collenchyma cell - elongated plant cell with unevenly thickened walls; provides structural support to the stem and leaves companion cell - phloem cell that is connected to sieve-tube cells; has large amounts of ribosomes and mitochondria compound leaf - a leaf in which the leaf blade is subdivided to form leaflets, all attached to the midrib corm - rounded, fleshy underground stem that contains stored food cortex - ground tissue found between the vascular tissue and the epidermis in a stem or root cuticle - waxy covering on the outside of the leaf and stem that prevents the loss of water dermal tissue - a protective plant tissue covering the outermost part of the plant; controls the gas exchange endodermis - a layer of cells in the root that forms a selective barrier between the ground tissue and the vascular tissue, allowing water and minerals to enter the root while excluding toxins and pathogens epidermis - a single layer of cells found in plant dermal tissue; covers and protects underlying tissue fibrous root system - type of root system in which the roots arise from the base of the stem in a cluster, forming a dense network of roots; found in monocots ground tissue - plant tissue involved in photosynthesis; provides support, and stores water and sugars guard cells - paired cells on either side of a stoma that control the stomatal opening and thereby regulate the movement of gases and water vapor intercalary meristem - meristematic tissue located at nodes and the bases of leaf blades; found only in monocots internode - region between nodes on the stem lamina - leaf blade lateral meristem - also called secondary meristem, meristematic tissue that enables a plant to increase in thickness or girth caused by the vascular cambium and cork cambium lenticel - opening on the surface of mature woody stems that facilitates gas exchange meristem - plant region of continuous growth meristematic tissue - tissue containing cells that constantly divide; contributes to plant growth node - point along the stem at which leaves, flowers, or aerial roots originate palmately compound leaf - leaf type with leaflets that emerge from a point, resembling the palm of a hand parenchyma cell - most common type of plant cell; found in the stem, root, leaf, and in fruit pulp; site of photosynthesis and starch storage pericycle - outer boundary of the stele from which lateral roots can arise periderm - outermost covering of woody stems; consists of the cork cambium, cork cells, and the phelloderm permanent tissue - plant tissue composed of cells that are no longer actively dividing petiole - stalk of the leaf phyllotaxy - arrangement of leaves on a stem pinnately compound leaf - leaf type with a divided leaf blade consisting of leaflets arranged on both sides of the midrib pith - ground tissue found towards the interior of the vascular tissue in a stem or root primary growth - growth resulting in an increase in length of the stem and the root; caused by cell division in the shoot or root apical meristem rhizome - modified underground stem that grows horizontally to the soil surface and has nodes and internodes root cap - protective cells covering the tip of the growing root root hair - hair-like structure that is an extension of epidermal cells; increases the root surface area and aids in absorption of water and minerals root system - belowground portion of the plant that supports the plant and absorbs water and minerals runner - stolon that runs above the ground and produces new clone plants at nodes sclerenchyma cell - plant cell that has thick secondary walls and provides structural support, usually dead at maturity sessile - leaf without a petiole that is attached directly to the plant stem shoot system - aboveground portion of the plant; consists of nonreproductive plant parts, such as leaves and stems, and reproductive parts, such as flowers and fruits sieve-tube cell - (sieve-tube members in angiosperms) phloem cell arranged end to end to form a sieve tube that transports organic substances, such as sugars and amino acids simple leaf - leaf type in which the lamina is completely undivided or merely lobed sink - growing parts of a plant, such as roots and young leaves, which require photosynthate source - organ that produces photosynthate for a plant stele - inner portion of the root containing the vascular tissue; surrounded by the endodermis stipule - small green structure found on either side of the leaf stalk or petiole stolon - modified stem that runs parallel to the ground and can give rise to new plants at the nodes tap root system - type of root system with a main root that grows vertically with few lateral roots; found in dicots tendril - modified stem consisting of slender, twining strands used for support or climbing thorn - modified stem branch appearing as a sharp outgrowth that protects the plant tracheid - xylem cell with thick secondary walls that helps transport water translocation - mass transport of photosynthates from source to sink in vascular plants transpiration - loss of water vapor to the atmosphere through stomata trichome - hair-like structure on the epidermal surface tuber - modified underground stem adapted for starch storage; has many adventitious buds vascular bundle - strands of plant tissue made up of xylem and phloem vascular stele - strands of root tissue made up of xylem and phloem vascular tissue - tissue made up of xylem and phloem that transports food and water throughout the plant venation - pattern of veins in a leaf; may be parallel (as in monocots), reticulate (as in dicots), or dichotomous (as in ginkgo biloba) vessel element - xylem cell that is shorter than a tracheid and has thinner walls whorled - pattern of leaf arrangement in which three or more leaves are connected at a node Introduction Plants are multicellular eukaryotes with tissue systems made of various cell types that carry out specific functions. Plant tissue systems fall into one of two general types: meristematic tissue or permanent (or non-meristematic) tissue. Cells of the meristematic tissue are found in meristems, which are plant regions of continuous cell division and growth. Meristematic tissue cells are either undifferentiated or incompletely differentiated, and they continue to divide and contribute to the growth of the plant. In contrast, permanent tissue consists of plant cells that are no longer actively dividing. There are two types of meristematic tissues, based on their location in the plant. Apical meristem or primary meristem contain meristematic tissue located at the tips of stems and roots, which enable a plant to extend in length. Lateral meristem or secondary meristem facilitate growth in thickness or girth in a maturing woody plant. Intercalary meristem is found in some monocots such as grasses. Meristems produce cells that quickly differentiate, or specialize, and become permanent tissue. Such cells take on specific roles and lose their ability to divide further. They differentiate into three main types: dermal, vascular, and ground tissue. Permanent tissues are either simple (composed of similar cell types) or complex (composed of different cell types). Dermal tissue, for example, is a simple tissue that covers the outer surface of the plant and controls gas exchange. Dermal tissue covers and protects the plant, while vascular tissue transports water, minerals, and sugars to different parts of the plant. Vascular tissue is an example of a complex tissue and is made of two specialized conducting tissues: xylem and phloem. Xylem tissue transports water and nutrients from the roots to different parts of the plant and includes three different cell types: vessel elements and tracheids (both of which conduct water), and xylem parenchyma. Phloem tissue, which transports organic compounds from the site of photosynthesis to other parts of the plant, consists of four different cell types: sieve elements (which conduct photosynthates), companion cells, phloem parenchyma, and phloem fibers. Gymnosperms lack sieve elements and companion cells. Cells carrying out similar function in gymnosperms are called sieve cells. Unlike xylem conducting cells, phloem conducting cells are alive at maturity. The xylem and phloem always lie adjacent to each other (Figure 1.3.1). In stems, the xylem and the phloem form a structure called a vascular bundle; in roots, this is termed the vascular stele or vascular cylinder. Ground tissue serves as a site for photosynthesis, provides a supporting matrix for the vascular tissue, and helps to store water and sugars. Any part of a plant has three tissue systems: dermal, vascular, and ground tissue. Each is distinguished by characteristic cell types that perform specific tasks necessary for the plant’s growth and survival. Access for free at https://openstax.org/books/biology-2e/pages/30-1-the-plant-body Dermal Tissue Dermal Tissue The dermal tissue of the stem consists primarily of epidermis, a single layer of cells covering and protecting the underlying tissue. Woody plants have a tough, waterproof outer layer of cork cells commonly known as bark, which further protects the plant from damage. Epidermal cells are the most numerous and least differentiated of the cells in the epidermis. The epidermis of a leaf also contains openings known as stomata, through which the exchange of gases takes place (Figure 1.3.2). Two cells, known as guard cells, surround each leaf stoma, controlling its opening and closing and thus regulating the uptake of carbon dioxide and the release of oxygen and water vapor. Trichomes are hair-like structures on the epidermal surface. They help to reduce transpiration (the loss of water by aboveground plant parts), increase solar reflectance, and store compounds that defend the leaves against predation by herbivores. Access for free at https://openstax.org/books/biology-2e/pages/30-2-stems Vascular Tissue Vascular Tissue The xylem and phloem that make up the vascular tissue of the stem are arranged in distinct strands called vascular bundles, which run up and down the length of the stem. When the stem is viewed in cross section, the vascular bundles of dicot stems are arranged in a ring. In plants with stems that live for more than one year, the individual bundles grow together and produce the characteristic growth rings. In monocot stems, the vascular bundles are randomly scattered throughout the ground tissue (Figure 1.3.3). Xylem tissue has three types of cells: xylem parenchyma, tracheids, and vessel elements. The latter two types conduct water and are dead at maturity. Tracheids are xylem cells with thick secondary cell walls that are lignified. Water moves from one tracheid to another through regions on the side walls known as pits, where secondary walls are absent. Vessel elements are xylem cells with thinner walls; they are shorter than tracheids. Each vessel element is connected to the next by means of a perforation plate at the end walls of the element. Water moves through the perforation plates to travel up the plant. Phloem tissue is composed of sieve-tube cells, companion cells, phloem parenchyma, and phloem fibers. A series of sieve-elements (also called sieve-tube members) are arranged end to end to make up a long sieve tube, which transports organic substances such as sugars and amino acids. The sugars flow from one sieve-tube cell to the next through perforated sieve plates, which are found at the end junctions between two cells. Although still alive at maturity, the nucleus and other cell components of the sieve-tube cells have disintegrated. Companion cells are found alongside the sieve-tube cells, providing them with metabolic support. The companion cells contain more ribosomes and mitochondria than the sieve-tube cells, which lack some cellular organelles. Access for free at https://openstax.org/books/biology-2e/pages/30-2-stems Ground Tissue & Cell Types Ground Tissue Plant tissues that are not dermal or vascular are considered ground tissue. Cell of ground tisses perform many differnent types of functions, such as photosynthesis, storage, based on their location. In a stem ground tissue mostly contains parenchyma cells, but may also contain collenchyma and sclerenchyma cells that help support the stem. The ground tissue towards the interior of the vascular tissue in a stem or root is known as pith, while the layer of tissue between the vascular tissue and the epidermis is known as the cortex. Let us look at three types of plant cells, parenchyma, collenchyma, and sclerenchyma cells. Parenchyma cells are the most common plant cells (Figure 1.3.4). They are found in the stem, the root, the inside of the leaf, and the pulp of the fruit. These cells are somewhat spherical and have thin primary wall. This help in exchange of raw material and waste products between outside and the inside of the cell. Parenchyma cells are responsible for metabolic functions, such as photosynthesis, and they help repair and heal wounds. Some parenchyma cells also store starch. Parenchyma cells rarely show formation of secondary wall. Collenchyma cells are elongated cells with unevenly thickened walls (Figure 1.3.5). They provide structural support, mainly to the stem and leaves. These cells are alive at maturity and are usually found below the epidermis. The “strings” of a celery stalk are an example of collenchyma cells. Sclerenchyma cells also provide support to the plant, but unlike collenchyma cells, many of them are dead at maturity. There are two types of sclerenchyma cells: fibers and sclereids. Both types have secondary cell walls that are thickened with deposits of lignin—an organic compound that is a key component of wood. Fibers are long, slender cells; sclereids are smaller-sized. Sclereids give pears their gritty texture. Humans use sclerenchyma fibers to make linen and rope (Figure 1.3.6). Access for free at https://openstax.org/books/biology-2e/pages/30-2-stems Dig Deeper Watch Botany Without Borders, a video produced by the Botanical Society of America about the importance of plants. Attributions Title: Browallia americana L.: entire flowering plant with separate parts of fruit and seeds. Coloured etching by M. Bouchard, 1774. Work Type: Scientific illustrations Date: 1774 Description: Browallia demissa pedunculis unifloris. H.Cliff.318.t.17. - Hort.Ups.179. - Linn.Sp.Plant.773 Repository: Wellcome Collection Collection: Open Artstor: Wellcome Collection ID Number: V0042766ER Source: Image and original data from Wellcome Collection License: Creative Commons: Attribution Use of this image is in accordance with the applicable Terms & Conditions Biology 2e by Clark Mary Ann, Douglas Matthew, Choi Jung. OpenStax is licensed under Creative Commons Attribution License V 4.0	oercommons	2025-03-18T00:37:02.683448	null	{ "license": "Creative Commons - Attribution - https://creativecommons.org/licenses/by/4.0/", "url": "https://oercommons.org/courseware/lesson/87592/overview", "title": "Statewide Dual Credit Introduction to Plant Science, Plant Form", "author": null }
https://oercommons.org/courseware/lesson/87593/overview	4.3 Primary & Secondary Growth 4_Stages-of-Plant-Growth Exercise 1a Plant Dissection Exercise 1a Plant Dissection Stages of Plant Growth Overview Introduction Learning Objectives - Identify factors that influence transition of a plant from vegetative to reproductive phase. - List and describe primary and secondary meristem. - Differentiate between annual, biennial, and perennial plants. Key Terms adventitious root - an above ground root that arises from a plant part other than the radicle of the plant embryo apical bud - bud formed at the tip of the shoot apical meristem - meristematic tissue located at the tips of stems and roots; enables a plant to extend in length axillary bud - bud located in the axil of a leaf, the area of the stem where leaf petiole connects to the stem bark - the tough, waterproof, outer epidermal layer of cork cells Casparian strip - waxy coating that forces water to cross endodermal plasma membranes before entering the vascular cylinder, instead of moving between endodermal cells companion cell - phloem cell that is connected to sieve-tube cells; contain large amounts of ribosomes and mitochondria cortex - ground tissue found between the vascular tissue and the epidermis in a stem or root cuticle - waxy covering on the outside of the leaf and stem that prevents the loss of water endodermis - a layer of cells in the root that forms a selective barrier between the ground tissue and the vascular tissue, allowing water and minerals to enter the root while excluding toxins and pathogens epidermis - a single layer of cells found in plant dermal tissue; covers and protects underlying tissue fibrous root system - type of root system in which the roots arise from the base of the stem in a cluster, forming a dense network of roots; found in monocots ground tissue - plant tissue involved in photosynthesis; provides support, and stores water and sugars guard cells - paired cells on either side of a stoma that control the stomatal opening and thereby regulate the movement of gases and water vapor intercalary meristem - meristematic tissue located at nodes and the bases of leaf blades; found only in monocots internode - region between nodes on the stem lamina - leaf blade lateral meristem – also called secondary meristem, comprised of vascular cambium and cork cambium, meristematic tissue that enables a plant to increase in thickness or girth lenticel - opening on the surface of mature woody stems that facilitates gas exchange meristem - plant region of continuous growth meristematic tissue - tissue containing cells that constantly divide; contributes to plant growth node - point along the stem at which leaves, flowers, or aerial roots originate pericycle – cell layer present on the outer boundary of the stele; produce lateral roots periderm - outermost covering of woody stems; consists of the cork cambium, cork cells, and the phelloderm permanent tissue - plant tissue composed of cells that are no longer actively dividing petiole - stalk of the leaf pith - ground tissue found towards the interior of the vascular tissue in a stem or root primary growth - growth resulting in an increase in length of the stem and the root; caused by cell division in the shoot or root apical meristem root cap - protective cells covering the tip of the growing root root hair - hair-like structure that is an extension of epidermal cells; increases the root surface area and aids in the absorption of water and minerals root system - belowground portion of the plant that supports the plant and absorbs water and minerals shoot system - aboveground portion of the plant; consists of nonreproductive plant parts, such as leaves and stems, and reproductive parts, such as flowers and fruits sieve-tube cell - (sieve-tube members in angiosperms) phloem cell arranged end to end to form a sieve tube that transports organic substances such as sugars and amino acids stele - inner portion of the root containing the vascular tissue; surrounded by the endodermis tap-root system - type of root system with the main root that grows vertically with few lateral roots; found in dicots tendril - modified stem consisting of slender, twining strands used for support or climbing thorn - modified stem branch appearing as a sharp outgrowth that protects the plant tracheid - xylem cell with thick secondary walls that help transport water trichome - hair-like structure on the epidermal surface vascular bundle - strands of plant tissue made up of xylem and phloem vascular stele - strands of root tissue made up of xylem and phloem vascular tissue - tissue made up of xylem and phloem that transports food and water throughout the plant venation - a pattern of veins in a leaf; may be parallel (as in monocots), reticulate (as in dicots), or dichotomous (as in ginkgo) vessel element - xylem cell that is shorter than a tracheid and has thinner walls Introduction The lives of plants may be as short as a few weeks or months or as long as many years. All plants go through changes as they grow. We can identify these changes as stages of plant growth. These stages are more distinct in some plants compared to others. These stages can be roughly identified as germination or sprouting, seedling, vegetative growth, budding, flowering, fruiting, and ripening. The first three stages are vegetative and the last four stages are reproductive. The transition from vegetative stages to reproductive stages is called the phase transition and depends on internal genetic pathways that are regulated by environmental cues (temperature, day length) and internal factors (hormones, sugar accumulation). Meristems Meristems Meristematic cells are responsible for plant growth. Plant meristems are centers of mitotic cell division and are composed of a group of undifferentiated self-renewing cells from which most plant structures arise. The Shoot Apical Meristem (SAM) gives rise to organs like the leaves and flowers, while the Root Apical Meristem (RAM) provides the meristematic cells for future root growth. The cells of the shoot and root apical meristems divide rapidly and are indeterminate, which means that they do not possess any defined end fate. In that sense, the meristematic cells are frequently compared to the stem cells in animals, which have an analogous behavior and function. Meristem Tissue and Plant Development Meristematic tissues are cells or groups of cells that divide perpetually. These tissues in a plant consist of small, densely packed cells that can keep dividing to form new cells. Meristematic tissue is characterized by small cells, thin cell walls, large cell nuclei, absent or small vacuoles, and no intercellular spaces. Meristematic tissues are found in many locations, including: 1) near the tips of roots and stems (apical meristems), 2) in the buds and nodes of stems, 3) in the cambium between the xylem and phloem (vascular cambium) in dicotyledonous trees and shrubs, 4) under the epidermis of dicotyledonous trees and shrubs (cork cambium), and 5) in the pericycle layer of roots, producing lateral branches. The two types of meristems are primary meristems and secondary meristems. Primary meristem (apical meristems) initiates in the developing embryo and gives rise to three primary meristematic tissues: protoderm, procambium, and ground meristem. Primary meristem is responsible for the growth in length of a plant. All tissues that arise from primary meristem are identified as primary tissue. Secondary meristem (lateral meristem) is responsible for the growth in the girth of a plant. This growth in width of a plant is largely due to the meristematic action of the vascular cambium and to certain extent cork cambium. Any new cells arising from vascular cambium and or cork cambium are collectively called secondary tissues. Meristem Zones The apical meristem, also known as the “growing tip,” is an undifferentiated meristematic tissue found in the growing shoot tips or axillary buds and growing tips of roots (figure 1.4.1). Shoot apical meristems are organized into four zones: (1) the central zone, (2) the peripheral zone, (3) the medullary meristem, and (4) the medullary tissue (figure 1.4.2). The central zone is located at the meristem summit, where a small group of slowly dividing cells can be found. Cells of this zone have a stem cell function and are essential for meristem maintenance. The proliferation and growth rates at the meristem summit usually differ considerably from those at the periphery. Surrounding the central zone is the peripheral zone. The rate of cell division in the peripheral zone is higher than that of the central zone. Peripheral zone cells give rise to cells that contribute to the organs of the plant, including leaves (figure 1.4.4), inflorescence meristems, and floral meristems. The outermost layer is called the tunica, while the innermost layers are cumulatively called the corpus. An active root apical meristem consists of slow dividing cells in the region called the quiescent center, a mass of loosed packed cells in the region of the root cap, and the three primary meristems that may or may not be identifiable at low magnifications (figure 1.4.3). An active apical meristem lays down a growing root or shoot behind itself, pushing itself forward. Primary & Secondary Growth Plant Growth Growth in plants occurs as the stems and roots lengthen. Some plants, especially those that are woody, also increase in thickness during their life span. The increase in length of the shoot and the root is referred to as primary growth and is the result of cell division in the apical meristems. Secondary growth is characterized by an increase in thickness or girth of the plant and is caused by cell division in the lateral meristem. Figure 1.3.5 shows the areas of primary and secondary growth in a plant. Herbaceous plants mostly undergo primary growth, with hardly any secondary growth or increase in thickness. Secondary growth or “wood” is noticeable in woody plants; it occurs in some dicots but occurs very rarely in monocots. Some plant parts, such as stems and roots, continue to grow throughout a plant’s life: a phenomenon called indeterminate growth. Other plant parts, such as leaves and flowers, exhibit determinate growth, which ceases when a plant part reaches a particular size. Primary Growth Most primary growth occurs at the apices, or tips, of stems and roots. Primary growth is a result of rapidly dividing cells in the apical meristems at the shoot tip and root tip. Subsequent cell elongation also contributes to primary growth. The growth of shoots and roots during primary growth enables plants to continuously seek water (roots) or sunlight (shoots). The influence of the apical bud on overall plant growth is known as apical dominance, which diminishes the growth of axillary buds that form along the sides of branches and stems. Most coniferous trees (ex., pine) exhibit strong apical dominance, thus producing the typical conical Christmas tree shape. If the apical bud is removed, then the axillary buds will start forming lateral branches. Gardeners make use of this fact when they prune plants by cutting off the tops of branches, thus encouraging the axillary buds to grow out, giving the plant a bushy shape. Intercalary Meristem The intercalary meristem is located away from the growing shoot tip, usually between mature tissues. Have you ever wondered how lawn grasses regrow rapidly after mowing? Grasses regenerate their leaves rapidly after mowing because of the actions of the intercalary meristem located right above the base of the leaf. Grasses evolved in prairie habitats with many types of grazing animals. The ability to regrow quickly is critical to survival. Intercalary meristem is also present in other plants such as horsetails and welwitschia. Secondary Growth The increase in stem thickness that results from secondary growth is due to the activity of the lateral meristems, which are lacking in herbaceous plants. Lateral meristems include the vascular cambium and, in woody plants, the cork cambium (Figure 1.4.5.) The vascular cambium is located just outside the primary xylem and to the interior of the primary phloem. The cells of the vascular cambium divide and form secondary xylem (tracheids and vessel elements) to the inside and secondary phloem (sieve elements and companion cells) to the outside. The thickening of the stem that occurs in secondary growth is due to the formation of secondary phloem and secondary xylem by the vascular cambium, as well as the cork cambium. The cells of the secondary xylem contain lignin, which provides hardiness and strength. In woody plants, cork cambium is the outermost lateral meristem. It produces cork cells (bark) containing a waxy substance known as suberin that can repel water. The bark protects the plant against physical damage and helps reduce water loss. The cork cambium also produces a layer of cells known as phelloderm, which grows inward from the location of cork cambium. The cork cambium, cork cells, and phelloderm are collectively termed the periderm. The periderm substitutes for the epidermis in mature plants. In some plants, the periderm has many openings, known as lenticels, which allow the interior cells to exchange gases with the outside atmosphere (Figure 1.4.6). This supplies oxygen to the living and metabolically active cells of the cortex, xylem, and phloem. Annual Rings The activity of the vascular cambium gives rise to annual growth rings. During the spring growing season, cells of the secondary xylem have a large internal diameter and their primary cell walls are not extensively thickened. This is known as earlywood or springwood. During the fall season, the secondary xylem develops thickened cell walls, forming latewood, or autumn wood, which is denser than earlywood. This alternation of early and late wood is largely due to a seasonal decrease in the number of vessel elements and a seasonal increase in the number of tracheids. It results in the formation of an annual ring, which can be seen as a circular ring in the cross-section of the stem (Figure 1.4.7). An examination of the number of annual rings and their nature (such as their size and cell wall thickness) can reveal the age of the tree and the prevailing climatic conditions during each season. Growth in Roots Root growth begins with seed germination. When the plant embryo emerges from the seed, the radicle of the embryo forms the root system. The tip of the root is protected by the root cap, a structure exclusive to roots and unlike any other plant structure. The root cap is continuously replaced because it gets damaged easily as the root pushes through the soil. The root tip can be divided into three zones: a zone of cell division, a zone of elongation, and a zone of maturation & differentiation (Figure 1.4.8). The zone of cell division is closest to the root tip; it is made up of the actively dividing cells of the root meristem and quiescent center. The zone of elongation is where the newly formed cells increase in length, thereby lengthening the root. Beginning at the first root hair is the zone of cell maturation where the root cells begin to differentiate into specialized cell types. All three zones are in the first centimeter or so of the root tip. The root has an outer layer of cells called the epidermis, which surrounds areas of ground tissue and vascular tissue. The epidermis provides protection and helps in absorption. Root hairs, which are extensions of root epidermal cells, increase the surface area of the root, greatly contributing to the absorption of water and minerals. Inside the root, the ground tissue forms two regions: the cortex and the pith (Figure 1.4.9). Compared to stems, roots have lots of cortex and little pith. Both regions include cells that store photosynthetic products. The cortex is between the epidermis and the vascular tissue, whereas the pith lies between the vascular tissue and the center of the root. The vascular tissue in the root is arranged in the inner portion of the root, which is called the stele (Figure 1.4.10). A layer of cells known as the endodermis separates the stele from the ground tissue in the outer portion of the root. The endodermis is exclusive to roots and serves as a checkpoint for materials entering the root’s vascular system. A waxy substance called suberin is present on the walls of the endodermal cells. This waxy region, known as the Casparian strip, forces water and solutes to cross the plasma membranes of endodermal cells instead of slipping between the cells. This ensures that only materials required by the root pass through the endodermis, while toxic substances and pathogens are generally excluded. The outermost cell layer of the root’s vascular tissue is the pericycle, an area that can give rise to lateral roots. In dicot roots, the xylem and phloem of the stele are arranged alternately in an X shape, whereas in monocot roots, the vascular tissue is arranged in a ring around the pith. Unit 1 Lab Exercises Lab Exercises Notes for Instructors Each unit contains a section with two lab exercises provided to give students hands-on experience with the content in the SDC Plant Science course. They have been designed to be low-cost or free. The associated rubrics are guidelines for assessment and can be adapted based on specific classroom needs or standards. Safety: Some of these exercises require safety precautions. A student safety contract is included Instructors should keep the contract in their records for the length of the course. Safety concerns contain, but are not limited to - Handling glassware - Using sharp objects - Using Bromothymol blue solution - Proximity to possible allergens These concerns are addressed in the Student Laboratory Safety Contract. If you conduct the exercise that uses Bromothymol blue solution, post the MSDS that comes with the solution in the classroom and review the information with students. Schools and instructors are responsible for determining which exercises to use. Do not use an exercise if there is a high risk of harm. Exercise 1a: Plant Dissection Students dissect a plant to identify and study its various parts. This exercise helps students understand the structure and function of different plant components. Exercise 1b: Plant Cell DIagram Students create a detailed diagram of a plant cell, labeling its various parts, and understanding their functions. This exercise helps students visualize and comprehend the structure and components of plant cells. Attributions Title: A plant root cut to show growth rings, wood cells in longitudinal and transverse section and a root tip. Chromolithograph, c. 1850. Work Type: Chromolithographs. Date: [c. 1850] Material: chromolithograph. Description: 1 print : Pflanzenrich A. I. wurzelstock eines kieferstammes ... II. holzzellen im quer & la?ngsschnitte III. spitze, eines saugwurzel-chens ... Repository: Wellcome Collection Open Artstor: Wellcome Collection ID Number:V0044550 Source: Image and original data from Wellcome Collection License: Creative Commons: Attribution Use of this image is in accordance with the applicable Terms & Conditions File Name V0044550.jpg SSID 24897875 Biology 2e by Clark Mary Ann, Douglas Matthew, Choi Jung. OpenStax is licensed under Creative Commons Attribution License V 4.0 "Plant Development - Meristems" by LibreTexts is licensed under CC BY-SA. "Stems - Primary and Secondary Growth in Stems" by LibreTexts is licensed under CC BY-SA.	oercommons	2025-03-18T00:37:02.757230	null	{ "license": "Creative Commons - Attribution - https://creativecommons.org/licenses/by/4.0/", "url": "https://oercommons.org/courseware/lesson/87593/overview", "title": "Statewide Dual Credit Introduction to Plant Science, Plant Form", "author": null }
https://oercommons.org/courseware/lesson/75598/overview	French Level 1, Activity 14: Revision de la fin du semestre / Jeopardy Review (Online) Overview In this activity, students will play a game of Jeopardy to review various French vocabulary and grammar topics. Activity Information Did you know that you can access the complete collection of Pathways Project French activities in our new Let’s Chat! French pressbook? View the book here: https://boisestate.pressbooks.pub/pathwaysfrench Please Note: Many of our activities were created by upper-division students at Boise State University and serve as a foundation that our community of practice can build upon and refine. While they are polished, we welcome and encourage collaboration from language instructors to help modify grammar, syntax, and content where needed. Kindly contact pathwaysproject@boisestate.edu with any suggestions and we will update the content in a timely manner. Jeopardy Review / Revision de la fin du semestre Description In this activity, students will play a game of Jeopardy to review various French vocabulary and grammar topics. Semantic Topics Review, Jeopardy, end of the semester, revision, la fin du semestre Materials Needed Main Activity Main Activity *Note: If you'd like to customize this Jeopardy game, click "Edit." Once you've clicked edit, you will see an option that says, "If this isn't your template (or you forgot the password) then you can clone this template and edit the clone. Create a password for your clone below." 1. Log onto the jeopardy game and share your screen. Connectez-vous à votre ordinateur et cliquez sur le lien Jeopardy ci-dessus. 2. Have the students split into two teams. Demandez aux étudiants de former 2 équipes. 3. Play the Jeopardy review game. Jouez au jeu. Wrap-Up Wrap-Up - Avez-vous des questions ? (Have any questions?)	oercommons	2025-03-18T00:37:02.785257	Camille Daw	{ "license": "Creative Commons - Attribution - https://creativecommons.org/licenses/by/4.0/", "url": "https://oercommons.org/courseware/lesson/75598/overview", "title": "French Level 1, Activity 14: Revision de la fin du semestre / Jeopardy Review (Online)", "author": "Mimi Fahnstrom" }
https://oercommons.org/courseware/lesson/105114/overview	Creating Relationship Communication Portfolios as a Service-Learning Project Overview .To acquire objective information about the dynamics of interpersonal relationships—casual friendships, deeper friendships, family relationships and intimate relationships. Information learned will include theoretical material as well as research findings. Students will have better understanding of the nature of different interpersonal relationship dynamics, and be able to apply interpersonal relationship theories to practice. This objective will be achieved through class lectures, the reading of Brehm, and the achievement of this and related objectives will be assessed through service learning projects, journals, papers, etc. Semester-long Activites Title: Creating Communication Portfolios as a Service-Learning Project for teaching the Relationships Course Intended course: Interpersonal Communication/ Relationship Courses Learning goal/objectives: 1. To acquire objective information about the dynamics of interpersonal relationships—casual friendships, deeper friendships, family relationships and intimate relationships. Information learned will include theoretical material as well as research findings. Students will have better understanding of the nature of different interpersonal relationship dynamics, and be able to apply interpersonal relationship theories to practice. This objective will be achieved through class lectures, the reading of Brehm, and the achievement of this and related objectives will be assessed through service learning projects, journals, papers, etc. 2. To integrate this objective information with students’ self-knowledge about self-concept, interpersonal and relationship skills, attitudes toward friendship and closeness, ethical and moral values, and orientation toward others, who may be different from their background and socioeconomic status. Achieved through participation in class discussion, in-class experiential exercises, and class activities, and the course project; achievement assessed through quality of contributions to discussion and of term project. Students will have deeper understanding about diversity through communicating with different people, and about themselves, such as their conceptions of identity and self-esteem, through reflective activities. 3. To improve students’ skills in initiating, maintaining, deepening, repairing, and terminating relationships, and to increase students’ mindfulness in the use of these skills. They will work as consultants, and then provid plans about how to solve interpersonal communication problems, and how to improve interpersonal relationships in varies contexts. Achieved through in-class demonstrations, role-play practice, dramatic enactments of problem-solving episodes; achievement assessed by observation of progress in skill-development exercises, and the service learning project. Theoretical Rationale for conducting the activity Over the past few years, American college students are participating in service-learning projects in high amounts (Liu, Ruiz, DeAngelo, & Pryor, 2009). Service learning is a teaching method that merges traditional classroom formats with a related service to the community (Knapp & Fisher, 2010). It is effective because it connects theory to practice in real life in order to meet challenging social problems (Bringle & Julie, 1996). Kendall (1990, p. 20) noted that service learning are “needed tasks in the community with intentional learning goals and with conscious refection and critical analysis.” Students participate in an organized service activity that "reflect on the service activity in such a way as to gain further understanding of course content, a broader appreciation of the discipline, and an enhanced sense of civic responsibility” (Bringle & Hatcher, 1995, p. 112). The benefits of service learning make it one of the best ways to teach students. Service learning facilitates students’ personal development (Tomkovick, Lester, Flunker, & Wells, 2008) in many aspects, such as the influence on their conceptions of self, , self-esteem, and identity formation (Jones & Abes, 2004). Students who experience service-learning are more likely to value service as a great way to gain new perspectives, and cope with personal problems (Eppler, Ironsmith, Dingle, & Errickson, 2011). Eppler and his researchers (2011) believed that service learning is not only a valuable way to help students develop their identity within the context of the larger community, but also assist them adjust to college, adapt to social expectations, and define future career goals. Furthermore, most service-learning activities could promoted emotional intelligence and form a strong social climate in learning (Akujobi & Simmons, 1997). During service learning, students could learn much more beyound pure knowledge on textbook under teacher’s guidance. Moreover, another benefit researchers noticed in service learning is students’ increased interest in interacting with different cultural and people from diverse background (Simons & Cleary, 2006). Service learning encourages students to form bonds with adults other than teachers and parents (Billig, 2000), which could expand their insight and help them to explore the world. Therefore, students who engaged in community service offen reported better knowledge of diversity issues (Simons & Cleary, 2006), and ability to get along with people of different races and cultures (Astin & Sax, 1998). Service learning opens a window for students to have more direct connections and communication with the real world. Most importantly, service learning could produce the best outcomes when meaningful service activities are related to course contents through reflection activities such as project writings, group discussions, and class presentation (Bringle & Julie, 1996). Kohls (1996) discovered that when students have direct contact with their service recipients , then the students reported learning more than from their textbook. Eylers, Giles, Stenson, and Gray (2001) noted that service learning can help retention rates, comprehesion of material, and create better interpersonal relationships. In the same fashion, Kahne and Westheimer (2003) posited that students are more likely to learn from their service learning expereinces if there are several opportunities to refect on daunting expereinces. Faculties also discover that service learning could bring a new atmosphere to the classroom. It enhances performance of traditional learning method, increases student interest in the subject, provides new problem solving skills, and even makes teaching more enjoyable (Bringle & Julie, 1996). All and all, McKay and Estrella (2008) reported that service learning is very beneficial because of the increase interaction between students and faculty as well as comprehesion of the course material. It is neccesary for instructors to implement service learning for both students and themselves. Description of activity: The class will be divided in half with 1) one group focusing on romantic relationships and 2) the other half focusing on family relationships. In both sections, students will be put into several groups, and each group will be allowed to have three to four members. Within each group, they will conduct a project on how to improve relationships (family/romantic relationships). At this time, this project is like a proposal, which will include how are they going to evaluate/investigate the relationship, possible ways to solve the potential relationship problems, methods to improve the relationship, and researches/theories that can back up their project. Students will present their project first to the instructor, and then to the class/workshop for the community, such as Children and Family Services. After presenting the information, students will have to meet with one couple/ family to investigate their current communication patterns are and how to improve their communication. In other words, the students will act as consultants, with the instructor’s supervision, and provide a brief report on how communication can be effective and beneficial for these relationships. Instructor will meet with the group to facilitate their project, and provide necessary guidance and suggestions. In order to help the client to improve the relationship more effectively, students will need to sympathize their client, and stand on every client’s position to view the relationship and understand his/her concern. Only in this way, the suggestions students provided will be helpful to solve relationship problems, and satisfy every client. These reports, in turn, will be individualized to the specific couple/family, and help them to solve specific problems in certain context. Each group will create a portfolio, which consist of communication assessments, suggestions for the couple/family to get their desired communication behaviors, and research that can help the couple grow. The information could be used to help improve their communication, in turn their satisfaction with each other and their overall happiness. At the same time, the students reflect on their experiences in a journal. Much like a financial portfolio, the students create a communication portfolio, which provides their client with goals and ways to achieve them. Each group is required to meet with their service recipients for three separate times. The first time is to assess their communication skills and figure out what communication problems or goals that they have and would like to improve. The second time is to meet and show them the portfolio that they have created. They will have to meet with the individuals and explain the research as well as application of this material. They will offer exercises and strategies to help with their communication problems. The third time each group will do a follow-up meeting on their service learning recipients to see if any changes have occurred or to see if their portfolio was beneficial. Debriefing paragraph (including typical results) The most important aspect of this assisgnment is to allow input from student relefction. Eyler, Giles, and Schmiede (1996) that service learning is both connected and continuous. Student reflection allows for students to understand the bond between service and the knowledge learned in class. Instructions might allow students to respond to the following questions: - What have you learned from this project? - How do you think your project has impacted the client? - How has this project impacted you? - Do you think communication research is important? Why or why not? These answers will help instructors determine how much the students have learned and to improve for future semesters. These questions also allow for better comprehension of the material. In addition, the answers allow students to reflectively think the progress they have maded, the influence of this activity on themselves and their relationships, the nature of relationships and how the information is beneficial for others. This activity has been done for over three semesters. During this service learning activity, students are able to see the connection between classroom content and real-life application. Many of the students have selected career paths in family counseling and/or relationship specialists. This activitiy is important because it gives students practical experience and offers a way to present information in a professional manner. Often times, the beneficaries of the service are more satisfied in their relationships and are excited to learn new communication skills. Many of the recipients will offer money and gifts to the students for their services. Students’ transformation of their learning is significant. The skills students have learned in class but are unable to see the application of them are finally can be applied in this activity. Service learning does not have to be large scale. Some of biggest accomplishments are being able to tackle small problems. In turn, these can help the greater community. For instance, there was a parent who had difficulty talking to her child about bullying. The group offered strategies and creative games to play to increase the communication between parent-child. After the portfolio, the parent reported feeling a stronger connection with her child and the child felt a that we improved the lines of communication and understanding. As a result, the child had reported lower stress levels and a better sense of confidence. The parent stated that teachers of the child also noticed lower levels of attention seeking activites and fewer classroom disruptions. It is important to note, that some groups stated that their service recipients did not experience any changes in their communication behavior. There are some group projects that feel that their portfolio is a waste of time. They might express how it was busy work and may not be able to see the application of their knowledge. In addition, the groups that complain are also the ones that did not put as much effort into the project compared to their cohorts. At the end of the semester, each group will present their findings to the class so that the class can compare how they all did. The class will discuss about problems and pitfalls. Appraisal/Evaluation of the activity: Often times, students are only exposed to their personal relationships. Hence, they do not realize that communication in other relationships may be very different. This communication course has been taught for four semesters and teaching the course as a service-learning course greatly improves student learning and enhances their understanding of the course content, because the service learning opportunity will puts them in a situation, which will apply what they are learning to assist with the community. It provides the students with a valuable experience by exposing them to other communication and relationship styles. Moreover, it provides students with the opportunity to evaluate the material that they have learned. Overall, service learning improves the lives of some one who may really need these services. References and Suggested Readings Akujobi, C., & Simmons, R. (1997). An assessment of elementary school service-learning teaching methods: Using service-learning goals. National society for experiential education quarterly, (Winter), 19-27. Astin, A. W., & Sax, L. J. (1998). How undergraduates are affected by service participation. Journal of College Student Development, 39(3), 251-263. Batchelder, T. H., & Root, S. (1994). Effects of an undergraduate program to integrate academic learning and service: Cognitive, prosocial cognitive and identity outcomes. Journal of Adolescence, 17(4), 341-355. Bringle, R., & Hatcher, J. (1995). A service learning curriculum for faculty. The Michigan Journal of Community Service-Learning, 2(1), 112–122. Bringle, R. G., & Julie, A. H. (1996). Implementing service learning in higher education. The journal of higher education, 67 (2), 221-239. Billig, S. H. (2000). Research on school-based service-learning: The evidence builds. Phi delta kappan 81(9), 658-664. Eyler, J., Giles, D. E., Jr., & Schmiede, A. (1996). A practitioner’s guide to reflection in service learning: Student voices and reflections. Nashville, TN: Vanderbilt University. Eppler, M. A., Ironsmith, M., Dingle, S. H., & Errickson, M. A. (2011). Benefits of service-learning for freshmen college students and elementary school children. Journal of the scholarship of teaching and learning, 11 (4), 102-115. Jones, S. R., & Abes, E. S. (2004). Enduring influences of service-learning on college students' identity development. Journal of College Student Development, 45(2), 149-166. Kahne, J., & Westheimer, J. (2003). Teaching democracy. Phi Delta Kappan, 85(1), 34–40, 57–66. Kendall, J. (1990). Combining service and learning: An introduction. In J. Kendall (Ed.), Combining service and learning: A resource book for community and public service (pp. 1–33). Raleigh, NC: National Society for Internships and Experiential Education. Knapp, T.D., & Fisher, B. J. (2010). The effectiveness of service learning: It’s not always what you think. Journal of Experiential Education, 33(3), 208-224. Kohls, J. (1996). Student experiences with service-learning in a business ethics course. Journal of Business Ethics, 15, 45–57. Liu, A., Ruiz, S., DeAngelo, L., & Pryor, J. (2009). Findings from the 2008 administration of the College Senior Survey (CSS): National aggregates. Los Angeles: Higher Education Research Institute, UCLA. Mckay, V.C., & Estrella, J. (2008, July). First-generation student success: The role of faculty interaction in service learning courses. Communication Education, 57 (3), 356-372. Doi:10.1080/03634520801966123 Simons, L., & Cleary, B. (2006). The influence of service learning on students' personal and social development. College Teaching, 54(4), 307-319. Tomkovick, C., Lester, S.W., Flunker, L., & Wells, T.A. (2008). Linking collegiate service learning to future volunteerism: Implications for nonprofit organizations. Nonprofit Management and Leadership, 19(1), 3-26.	oercommons	2025-03-18T00:37:02.821472	06/12/2023	{ "license": "Creative Commons - Attribution - https://creativecommons.org/licenses/by/4.0/", "url": "https://oercommons.org/courseware/lesson/105114/overview", "title": "Creating Relationship Communication Portfolios as a Service-Learning Project", "author": "Narissra Punyanunt-Carter" }
https://oercommons.org/courseware/lesson/85122/overview	Chapter 2: Set Yourself Up for Success Overview LEARNING OBJECTIVES By the end of this chapter, you will be able to: - Define what success means to you. - Describe the qualities of a successful college student. - Compare and contrast a Growth Mindset vs. a Fixed Mindset. - Understand the concept of Self-Efficacy and how to apply it to your college success. - Identify campus resources to support your success. - Understand the principles of academic integrity. Set Yourself Up for Success Set Yourself Up for Success What Is Success? Personal Responsibility for Success A college education is aligned with greater success in many areas of life. While enrolled in college, most students are closely focused on making it through the next class or passing the next test. It can be easy to lose sight of the overall role that education plays in life. But sometimes it helps to recall what a truly great step forward you are taking! It’s also important to recognize, though, that some students do not succeed in college and drop out within the first year. Sometimes this is due to financial problems or a personal or family crisis. But most of the time students drop out because they’re having trouble passing their courses. In this section, we examine the elements of college success. Are there patterns of success you strive for but aren’t yet reaching? Where might you shore up your support? What strategies can you use to achieve success in your college endeavors? Defining Success in College How do you define college success? The definition really depends on you. You might think that “success” is earning an associate’s degree or attending classes in a four-year college. Maybe success is a bachelor’s or master’s degree or a Ph.D. Maybe success means receiving a certificate of completion or finishing skill-based training. You might be thinking of other measures of college success, too, like grades. For instance, you might be unhappy with anything less than an A in a course, although maybe this depends on the difficulty of the subject. As long as you pass with a C, you might be perfectly content. But no matter how you define success personally, you probably wouldn’t think it means earning a D or lower grade in a class. If most students believe that passing a class is the minimum requirement for “success,” and if most students want to be successful in their courses, why aren’t more college students consistently successful in the classroom? Perhaps some common misconceptions are at play. For example, we often hear students say, “I just can’t do it!” or “I’m not good at math,” or “I guess college isn’t for me.” But, these explanations for success or failure aren’t necessarily accurate. Considerable research into college success reveals that having difficulty in or failing in college courses usually has nothing to do with intellect. More often success depends on how fully a student embraces and masters the following seven strategies: - Learn how to listen actively in class and take effective notes (Chapters 10 and 11). - Review the text and your reading notes prior to class (Chapter 12). - Participate in class discussion and maybe even join a study group (Chapter 10.) - Go to office hours and ask your instructor questions. - Give yourself enough time to research, write, and edit your essays in manageable stages (Chapter 14). - Take advantage of online or on-campus academic support resources (Chapter 2). - Spend sufficient time studying (Chapter 5). So if you feel you are not smart enough for college, ask yourself if you can implement some of these skills. Overall, students struggle in college, not because of natural intellect or smarts, but because of time management, organization, and lack of quality study time. The good news is that there are ways to combat this, and this course and textbook will help you do just that. How Grades Play a Role in Shaping Success In a recent online discussion at a student-support Web site, a college freshman posted the following concern about how serious they should be about getting good grades: As a first semester freshman, I really have taken my education seriously. I’ve studied and done my homework nightly and have read all of the assignments. So far, I have all A’s in my classes, including calculus and programming. Now, with a month left to go in the semester, I feel myself slipping a bit on my studies. I blow off readings and homework more to go out at night during the week and I’ve even skipped a few classes to attend major sporting events. I also travel most weekends to visit my girlfriend. Still, I’ve gotten A’s on the exams even with these less extensive study habits, although not as high as before. So, my question really is this. Should I just be content with low A’s and B’s and enjoy myself during college, or should I strive to achieve all A’s? How would you answer this student’s question, given what you know and sense about college life? Grades do matter to your success, right? Or . . . do they? The answer depends on who you ask and what your college and career goals are. Consider these additional factors: - Undergraduate grades have been shown to have a positive impact on getting full-time employment in your career in a position appropriate to your degree. - Grades also have been shown to have a positive net impact on your occupational status and earnings. - Getting good grades, particularly in the first year of college, is important to your academic success throughout your college years. - Grades are probably the best predictors of your persistence, your ability to graduate, and your prospects for enrolling in graduate school. You stand to gain immeasurably when you get good grades. Understanding Your Grade-Point Average (GPA) Grades may not be the be-all and end-all in college life but, you should pay close attention to the GPA as it may be important to achieving your future goals. GPA is often an important criterion when applying for scholarships, specialized academic programs, internships, and transferring to a college or university. A grade point average is a number representing the average value of the accumulated final grades earned in courses over time. More commonly called a GPA, a student’s grade point average is calculated by adding up all accumulated final grades and dividing that figure by the number of credit hours awarded. This calculation results in a mathematical mean—or average—of all final grades. The most common form of GPA is based on a 0 to 4.0 scale (A = 4.0, B = 3.0, C = 2.0, D = 1.0, and F = 0), with a 4.0 representing a “perfect” GPA—or a student having earned straight As in every course. Austin Community College uses a standard letter grade system. When you finish your course, your instructor submits a letter grade of A, B, C, D or F that will then appear on your transcript. You can use this online GPA calculator to determine your GPA based on your grades and the number of credit hours for each course. You can check your official grades in MyACC by viewing your Unofficial Transcript. The following are two examples of semester GPAs at ACC. Please note how the number of credit hours of a course affects the points earned. For example, the first student has two classes that are each three credit hours (EDUC 1300 and ENGL 1301) and two classes that are four credit hours (BIOL 1408 and MATH 1414), for a total of 14 credit hours. The second student is also taking four classes but they are all three credit hour courses, for a total of 12 credit hours. \| Course \| Final Grade \| Numerical Equivalent \| Credit Hours \| Points Earned \| \| EDUC 1300 \| A \| 4 \| 3 \| 12 \| \| ENGL 1301 \| B \| 3 \| 3 \| 9 \| \| BIOL 1309 \| C \| 2 \| 4 \| 8 \| \| MATH 1414 \| A \| 4 \| 4 \| 16 \| \| TOTALS: \| 14 \| 45 \| \|\| \| GPA=Points Earned divided by Credit Hours \| GPA = 3.21 \| \| Course \| Final Grade \| Numerical Equivalent \| Credit Hours \| Points Earned \| \| EDUC 1300 \| A \| 4 \| 3 \| 12 \| \| ENGL 1301 \| B \| 3 \| 3 \| 9 \| \| BIOL 1408 \| C \| 2 \| 3 \| 6 \| \| PSYC 2301 \| A \| 4 \| 3 \| 12 \| \| TOTALS: \| 12 \| 39 \| \|\| \| GPA=Points Earned divided by Credit Hours \| GPA = 3.25 \| Each instructor has their own grading criteria for what constitutes an A, B, C, etc. Check your syllabus carefully to find this information. Some instructors issue an A for a grade average of 90% or higher while others will issue an A for an 88% or a 92% or higher. Other instructors may use a point system to determine final grades. For example, 450 out of 500 points is an A, etc. Be sure to read each syllabus carefully so you understand how your final grade for each course is determined. In addition to letter grades, there are also Incompletes. Withdrawals, and Pass/Fail. Students may request an Incomplete (I) due to extenuating circumstances that prevented them from completing the course work per the schedule. It is at the discretion of the instructor to determine whether to approve or deny the request. As a general rule, students must have been in good academic standing in the course prior to the request of an Incomplete. Students who receive an Incomplete will need to fulfill the requirements of the Incomplete contract as determined by agreement between the instructor and the student. If an Incomplete is not completed and resolved with a letter grade by the deadline, the I will automatically convert to an F. Students have the option of a Course Withdrawal, resulting in a W on their transcript. Students should always check with an advisor before withdrawing as there are potential consequences that may affect academic standing, financial aid, military benefits, etc. Instructors may also withdraw a student from a course due to poor attendance, missing assignments, etc. This also results in a W on the transcript. Lastly, some courses offer a Pass/Fail grading option. This is only available for a course if the college catalog specifies this option. If a given course permits two options of a letter grade or pass/fail grade, the student must declare the pass/fail option by the last day allowed for add/drop. Students may not change the pass/fail to a grade after the add/drop date. A passing grade is defined as the equivalent of a "C" grade or better and is not used when calculating GPA. However, An "F" (Failing) received in a course taken under a pass/fail option will be used in calculating GPA. Check with your advisor for specific information. Words of Wisdom It is important to know that college success is a responsibility shared with your institution. Above all, your college must provide you with stimulating classroom experiences that encourage you to devote more time and effort to your learning. Additional institutional factors in your success include the following: - High standards and expectations for your performance - Assessment and timely feedback - Peer support - Encouragement and support for you to explore human differences - Emphasis on your first college year - Respect for diverse ways of knowing - Integrating prior learning and experience - Academic support programs tailored to your needs - Ongoing application of learned skills - Active learning - Out-of-class contact with faculty[1] Ideally, you and your college collaborate to create success in every way possible. The cooperative nature of college life is echoed in the following practical advice from a college graduate, recounted in Foundations of Academic Success: Words of Wisdom: Professors do care about how you are doing in their class; they genuinely want you to succeed, but they will give you the grade you earn. There are people and resources on campus for you to utilize so you can earn the grade you want. Your professors are one of those resources, and are perhaps the most important. Go see them during office hours, ask them questions about the material and get extra help if you need it . . . Another resource to utilize can be found in the campus learning center . . . The first time I took a paper there, I recall standing outside the door for about ten minutes thinking of an excuse not to go in. Thankfully I saw a classmate walk in and I followed suit . . . Thanks to that first visit, I received an A- on the paper! Characteristics Of Successful Students Please take this quiz about successful students As you can see from the above quiz, it takes several qualities and habits to be successful in college. When we think about going to college, we think about learning a subject deeply, getting prepared for a profession. We tend to associate colleges and universities with knowledge, and we’re not wrong in that regard. But going to college, and doing well once we’re there, also relies heavily on our behaviors while we’re there. Professors and college administrators will expect you to behave in certain ways, without any explicit instructions on their part. For instance, professors will expect you to spend several hours a week working on class concepts (homework, writing, preparing for exams) on your own time. They will not tell you WHEN to spend those hours, but leave it up to you to recognize the need to put in the effort and schedule the time accordingly. Consider this short video from Richard St. John, who spent years interviewing people who reached the top of their fields, across a wide range of careers. He traces the core behaviors that were common to all of these successful people and distill them down into 8 key traits. To recap, those eight traits are: Passion, Work, Good Focus, Push, Serve, Ideas, and Persist All eight traits are things that you can put into practice immediately. With them, you’ll see improvement in your school successes, as well as what lies beyond. Keys to Success According to Tobin Quereau, a long-time professor of student success courses at Austin Community College, there are Seven Keys to College Success. You can build a strong foundation for college success by implementing the following seven behaviors: 1. Show Up - Be present mentally and physically for EVERY class. - Pay attention to your attention so that you stay focused during class and while studying rather than becoming distracted or daydreaming. - Establish a consistent, regular study schedule that takes priority over other activities. 2. Be Prepared - Develop an accurate, realistic picture of your academic strengths, weaknesses, skills and behaviors so that you know where to put your attention and how to do your best work. - Make a personal commitment to have ALL of your reading and studying done prior to each class and turn ALL of your assignments in ON TIME. - Look ahead prior to each class to see what will be covered and skim relevant chapters of the textbook so that you can take more effective notes during class. 3. Manage Your Time, Your Life, and Your Stress Levels Effectively - Make school a priority and keep a good balance between school, work, friends, and family. - Don’t let immediate pleasures get in the way of important long-term tasks. - Have back-up plans in place in case the unexpected happens. 4. Put in the Effort - Learning, like life, is not easy or automatic, you will need to work hard to get ahead. Plan on several hours of reading and study for each class each week to do well. - Be an active learner by studying regularly and learning as you go instead of putting it off until right before the exam. - Use effective strategies for deeper, more lasting learning rather than just memorization. 5. Stay Motivated - Be clear about the reasons you are here and what you can gain from continuing your education now and throughout your life. - Set some realistic academic goals for each day and week and monitor your progress on them. - Make a personal commitment to stay on course even when the going gets tough. 6. Seek Assistance Whenever Needed - You are here to learn, but you don’t need to do it alone. Make use of all the available resources: your instructors, the Learning Lab tutors, study groups, advising, etc. - When crisis strikes and life feels overwhelming, stay in touch with your instructor and get support from the free counseling services rather than just giving up and disappearing. 7. Finally, Learn from Everything! - When you succeed in learning and getting good grades, pay attention to what helped and keep doing those things. - And when things don’t turn out as you would like, figure out what went wrong or got in the way and make appropriate changes. - You are responsible for your successes in life and you can improve your performance with committed effort and persistence, so give it your best and keep on learning! Growth Mindset Vs. Fixed Mindset What is the difference between a student with a growth mindset versus a student with a fixed mindset? Students with a growth mindset believe that intelligence can be developed. These students focus on learning over just looking smart, see effort as the key to success, and thrive in the face of a challenge. On the other side, students with a fixed mindset believe that people are born with a certain amount of intelligence, and they can’t do much to change that. These students focus on looking smart over learning, see effort as a sign of low ability, and wilt in the face of a challenge. Carol Dweck, author of the 2006 book Mindset: The New Psychology of Success, defined both fixed and growth mindsets: “In a fixed mindset students believe their basic abilities, their intelligence, their talents, are just fixed traits. They have a certain amount and that’s that, and then their goal becomes to look smart all the time and never look dumb. In a growth mindset students understand that their talents and abilities can be developed through effort, good teaching and persistence. They don’t necessarily think everyone’s the same or anyone can be Einstein, but they believe everyone can get smarter if they work at it.” Which student do you think has more success in college? Think about this statement: You can learn new things, but you can’t really change your basic intelligence. People who really agree with this statement have a fixed mindset. People who really disagree with this statement have a growth mindset, and, of course, people might be somewhere in the middle. It turns out that the more students disagree with statements like these, the more they have a growth mindset, the better they do in school. This is because students with a growth mindset approach school differently than students with a fixed mindset. They have different goals in school. The main goal for students with a fixed mindset is to show how smart they are or to hide how unintelligent they are. This makes sense if you think that intelligence is something you either have or you don’t have. Students with a fixed mindset will avoid asking questions when they don’t understand something because they want to preserve the image that they are smart or hide that they’re not smart. But the main goal for students with a growth mindset is to learn. This also makes a lot of sense. If you think that intelligence is something that you can develop, the way you develop your intelligence is by learning new things. So students with a growth mindset will ask questions when they don’t understand something because that’s how they’ll learn. Similarly, students with a fixed mindset view effort negatively. They think, if I have to try, I must not be very smart at this. While students with a growth mindset view effort as the way that you learn, the way that you get smarter. Where you’ll really see a difference in students with fixed and growth mindsets is when they are faced with a challenge or setback. Students with a fixed mindset will give up because they think their setback means they’re not smart, but students with a growth mindset actually like challenges. If they already knew how to do something, it wouldn’t be an opportunity to learn, to develop their intelligence. Given that students with a growth mindset try harder in school, especially in the face of a challenge, it’s no surprise that they do better in school. Students with a growth mindset view mistakes as a challenge rather than a wall. Many students shy away from challenging schoolwork and get discouraged quickly when they make mistakes. These students are at a significant disadvantage in school—and in life more generally—because they end up avoiding the most difficult work. Making mistakes is one of the most useful ways to learn. Our brains develop when we make a mistake and think about the mistake. This brain activity doesn’t happen when we get the answers correct on the first try. What’s wrong with easy? According to Dweck, “it means you’re not learning as much as you could. If it was easy, well, you probably already knew how to do it.” Watch this supplemental video, Developing a Growth Mindset with Carol Dweck, to understand more about how you can develop your own Growth Mindset. And, remember, You Can Learn Anything! Supplemental Activity – Check Your Growth Mindset Take this quick assessment to learn about your own mindset. Self-Efficacy A concept that was first introduced by Albert Bandura in 1977, Self-efficacy is the belief that you are capable of carrying out a specific task or of reaching a specific goal (Bandura, 1977). Note that the belief and the action or goal are specific. Self-efficacy is a belief that you can write an acceptable term paper, for example, or repair an automobile, or make friends with the new student in the class. These are relatively specific beliefs and tasks. Self-efficacy is not about whether you believe that you are intelligent in general, whether you always like working with mechanical things, or think that you are generally a likable person. Self-efficacy is not a trait—there are not certain types of people with high self-efficacies and others with low self-efficacies (Stajkovic & Luthans, 1998). Rather, people have self-efficacy beliefs about specific goals and life domains. For example, if you believe that you have the skills necessary to do well in school and believe you can use those skills to excel, then you have high academic self-efficacy. Self-efficacy may sound similar to a concept you may be familiar with already—self-esteem—but these are very different notions. Self-esteem refers to how much you like or “esteem” yourself—to what extent you believe you are a good and worthwhile person. Self-efficacy, however, refers to your self-confidence to perform well and to achieve in specific areas of life such as school, work, and relationships. Self-efficacy does influence self-esteem because how you feel about yourself overall is greatly influenced by your confidence in your ability to perform well in areas that are important to you and to achieve valued goals. For example, if performing well in athletics is very important to you, then your self-efficacy for athletics will greatly influence your self-esteem; however, if performing well in athletics is not at all important to you, then your self-efficacy for athletics will probably have little impact on your self-esteem. Self-efficacy beliefs are not the same as “true” or documented skill or ability. They are self-constructed, meaning that they are personally developed perceptions. There can sometimes be discrepancies between a person’s self-efficacy beliefs and the person’s abilities. You can believe that you can write a good term paper, for example, without actually being able to do so, and vice versa: you can believe yourself incapable of writing a paper, but discover that you are in fact able to do so. In this way, self-efficacy is like the everyday idea of confidence, except that it is defined more precisely. And as with confidence, it is possible to have either too much or too little self-efficacy. The optimum level seems to be either at or slightly above true capacity (Bandura, 1997). Self-efficacy beliefs are influenced in five different ways (Bandura, 1997), which are summarized below. Influence \| Definition \| Performance Experiences \| When you do well and succeed at a particular task to attain a valued goal, you usually believe that you will succeed again at this task. When you fail, you often expect that you will fail again in the future if you try that task. \| Vicarious Performances \| If someone who seems similar to you succeeds, then you may believe that you will succeed as well. \| Verbal Persuasion \| This involves people telling you what they believe you are and are not capable of doing. Not all people will be equally persuasive. \| Imaginal Performances \| What you imagine yourself doing and how well or poorly you imagine yourself doing it. \| Affective States and Physical Sensations \| When you associate negative moods and negative physical sensations with failure, and positive moods and sensations with success. \| These five primary influencers of self-efficacy take many real-world forms that almost everyone has experienced. You may have had previous performance experiences affect your academic self-efficacy when you did well on a test and believed that you would do well on the next test. A vicarious performance may have affected your athletic self-efficacy when you saw your best friend skateboard for the first time and thought that you could skateboard well, too. Verbal persuasion could have affected your academic self-efficacy when a professor that you respect told you that you could get into the college of your choice if you worked hard at community college. It’s important to know that not all people are equally likely to influence your self-efficacy through verbal persuasion. People who you trust and respect are more likely to influence your self-efficacy than those you do not. Imaginal performances are an effective way to increase your self-efficacy. For example, imagine yourself doing well on a job interview may actually lead to more effective interviewing. Affective states and physical sensations abound when you think about the times you have given presentations in class. For example, you may have felt your heart racing while giving a presentation. If you believe your heart was racing because you had just had a lot of caffeine, it likely would not affect your performance. If you believe your heart was racing because you were doing a poor job, you might believe that you cannot give the presentation well. This is because you associate the feeling of anxiety with failure and expect to fail when you are feeling anxious. Consider academic self-efficacy in your own life. Do you think your own self-efficacy has ever affected your academic ability? Do you think you have ever studied more or less intensely because you did or did not believe in your abilities to do well? Did you skip math homework or not turn in a paper because you thought you weren't going to do well on it? Students who believe in their ability to do well academically tend to be more motivated in school (Schunk, 1991). When students attain their goals, they continue to set even more challenging goals, which can lead to better performance in school in terms of higher grades and taking more challenging classes. For example, students with high academic self-efficacies might study harder because they believe that they are able to use their abilities to study effectively. Because they studied hard, they receive an A on their next test. One question you might have about self-efficacy and academic performance is how a student’s actual academic ability interacts with self-efficacy to influence academic performance. The answer is that a student’s actual ability does play a role, but it is also influenced by self-efficacy. Students with greater ability perform better than those with lesser ability. But, among a group of students with the same exact level of academic ability, those with stronger academic self-efficacies outperform those with weaker self-efficacies. Campus Resources For Success There are many resources available at Collin College committed to helping you succeed during your time here and beyond. Being familiar with these resources, and be committed to using them when needed, is essential to your success. You may not need them right away; some you may not need at all. But you will at least find several to be vital. Be familiar with your options. Know where to find the services. Have contact information. Be prepared to visit for help. Use the following links to learn more about the services available at Collin College to support your success. Academic Advising Academic Advisors will help you select your classes, stay on track for your degree program, and make decisions about your educational and career goals. They can help you: - Review your degree progress before each registration period to ensure that you stay on track. - Explore academic programs offered at Collin College. - Learn more about transfer programs and career options. Career Center Career Services provides career guidance, resources, and programs to help students strengthen academic and career goals, establish career plans, and make successful career transitions. They can assistant with your resume, cover letter, and interview skills. Counseling Services Counselors are licensed professionals with Master's or Doctoral degrees who have been trained to provide guidance and potential solutions to emotional and psychological difficulties. They offer services and programs across the district to foster life balance, develop personal and academic growth, and help maintain a safe and healthy learning environment. ACCESS The ACCESS (Accommodations at Collin College for Equal Support Services) Office provides support to eliminate barriers. They offer a variety of services that offer equal opportunities for qualified students with a disability. Once you qualify for services, Accessibility Services staff meets with you to determine reasonable, appropriate, and effective accommodations based on the courses in which are enrolled and your disability. Veterans Resource Centers The Veterans Resource Centers coordinate college-wide services to connect military-affiliated students, with on-campus and community resources to ensure a smooth transition into college life and to foster academic success. Services range from providing information about admissions, academics, financial aid, and VA education benefits to advocacy and resource referral. Center for Academic Assistance The Anthony Peterson Center for Academic Assistance provides free learning support to students and community members. Services include subject-specific Tutoring, Writing Center, Math Lab, and Science Den. Both virtual and on campus options are available. Library Services Library Services offer a variety of support and services to students, including research assistance, study rooms, and the popular "Ask a Librarian" online option. Student Engagement The Student Engagement Office is the center for out-of-classroom activities on everyCollin College campus and throughout the District. Participating in co-curricular activities helps you gain valuable leadership skills that complement your academic work and enrich your college experience. In addition, Student Engagement issues student id's and serves as the "Lost and Found" location for each campus. Intramural Sports/Fitness Centers Intramural programming is offered in various sports. Campus fitness centers are free for students and help promote a healthier lifestyle. Practicing Academic Integrity I would prefer even to fail with honor than win by cheating. —Sophocles At most educational institutions, “academic honesty” means demonstrating and upholding the highest integrity and honesty in all the academic work that you do. In short, it means doing your own work and not cheating, and not presenting the work of others as your own. The following are some common forms of academic dishonesty prohibited by most academic institutions: Cheating Cheating can take the form of cheat sheets, looking over someone’s shoulder during an exam, or any forbidden sharing of information between students regarding an exam or exercise. Many elaborate methods of cheating have been developed over the years—storing information in graphing calculators, checking cell phones during bathroom breaks, using apps like Chegg to complete your homework or a take-home exam, using online solutions, etc. Cheating differs from most other forms of academic dishonesty, in that people can engage in it without benefiting themselves academically at all. For example, a student who illicitly telegraphed answers to a friend during a test would be cheating, even though the student’s own work is in no way affected. Deception Deception is providing false information to an instructor concerning an academic assignment. Examples of this include taking more time on a take-home test that is allowed, giving a dishonest excuse when asking for a deadline extension, or falsely claiming to have submitted work. Fabrication Fabrication is the falsification of data, information, or citations in an academic assignment. This includes making up citations to back up arguments or inventing quotations. Fabrication is most common in the natural sciences, where students sometimes falsify data to make experiments “work” or false claims are made about the research performed. Plagiarism Plagiarism, as defined in the 1995 Random House Compact Unabridged Dictionary, is the “use or close imitation of the language and thoughts of another author and the representation of them as one’s own original work.”[1] In an academic setting, it is seen as the adoption or reproduction of original intellectual creations (such as concepts, ideas, methods, pieces of information or expressions, etc.) of another author (whether an individual, group, or organization) without proper acknowledgment. This can range from borrowing a particular phrase or sentence to paraphrasing someone else’s original idea without citing it. Today, in our networked digital world, the most common form of plagiarism is copying and pasting online material without crediting the source. Common Forms of Plagiarism According to “The Reality and Solution of College Plagiarism” created by the Health Informatics department of the University of Illinois at Chicago, there are ten main forms of plagiarism that students commit: - Submitting someone else’s work as their own. - Taking passages from their own previous work without adding citations (submitting a paper you previously wrote for another class or another assignment.) - Rewriting someone’s work without properly citing sources. - Using quotations, but not citing the source. - Interweaving various sources together in the work without citing. - Citing some, but not all passages that should be cited. - Melding together cited and uncited sections of the piece. - Providing proper citations, but failing to change the structure and wording of the borrowed ideas enough. - Inaccurately citing the source. - Relying too heavily on other people’s work. Failing to bring original thought into the text. As a college student, you are now a member of a scholarly community that values other people’s ideas. In fact, you will routinely be asked to reference and discuss other people’s thoughts and writing in the course of producing your own work. That’s why it’s so important to understand what plagiarism is and the steps you can take to avoid it. Avoiding Plagiarism Below are some useful guidelines to help you avoid plagiarism and show academic honesty in your work: - Quotes: If you quote another work directly in your work, cite your source. - Paraphrase: If put someone else’s idea into your own words, you still need to cite the author. - Visual Materials: If you cite statistics, graphs, or charts from a study, cite the source. Keep in mind that if you didn’t do the original research, then you need to credit the person(s) or institution, etc. that did. The easiest way to make sure you don’t accidentally plagiarize someone else’s work is by taking careful notes as you research. If you are doing research on the Web, be sure to copy and paste the links into your notes so can keep track of the sites you’re visiting. Be sure to list all the sources you consult. There are many handy online tools to help you create and track references as you go. For example, you can try using Son of Citation Machine. Keeping careful notes will not only help you avoid inadvertent plagiarism; it will also help you if you need to return to a source later (to check or get more information). If you use citation tools like Son of Citation, be sure to check the accuracy of the citations before you submit your assignment. Lastly, if you’re in doubt about whether something constitutes plagiarism, cite the source or leave the material out. Better still, ask for help. Most colleges have a writing center, a tutoring center, and a library where students can get help with their writing. Taking the time to seek advice is better than getting in trouble for not attributing your sources. Be honest about your ideas, and give credit where it’s due. Consequences of Plagiarism In the academic world, plagiarism by students is usually considered a very serious offense that can result in punishments such as a failing grade on a particular assignment, the entire course, or even being expelled from the institution. Individual instructors and courses may have their own policies regarding academic honesty and plagiarism; statements of these can usually be found in the course syllabus or online course description. KEY TAKEAWAYS - You determine your success and everyone’s definition of success is personal. - Successful students have certain traits, characteristics, and habits, all of which can be learned and developed. - Having a Growth Mindset, believing that intelligence and skills are gained, is a key to success. - Self-efficacy, the belief that one is capable of reaching a goal, is another predictor of success. - There are several campus resources available to support your success. - Understanding and practicing Academic Integrity is a crucial component of college success. Task #1: DEVELOP YOUR PERSONAL DEFINITION OF SUCCESS For this activity, create your own definition of success. Dictionary.com defines success as “the favorable outcome of something attempted.” For many students in college, success means passing a class, earning an A, or learning something new. Beyond college, some people define success in terms of financial wealth; others measure it by the quality of their relationships with family and friends. Here is an example of a brief, philosophical definition of success: To laugh often and much; to win the respect of intelligent people and the affection of children; to earn the appreciation of honest critics and endure the betrayal of false friends; to appreciate beauty, to find the best in others; to leave the world a bit better, whether by a healthy child, a garden patch or a redeemed social condition; to know even one life has breathed easier because you have lived. This is to have succeeded. –Ralph Waldo Emerson Ultimately, before we can know if we are successful, we must first define what success means for ourselves. Directions - Write a journal entry defining what success means to you in college and beyond. To help you develop this essay, you might want to consider the following: - Find a quote (or make one up) that best summarizes your definition of success (be sure to cite the author and the source, such as the URL). - Why does this quote best represent your personal definition success? - What people do you consider to be successful and why? - What is your definition of success? - What will you do to achieve success? - What is the biggest change you need to make in order to be successful in college? - How will you know you’ve achieved success? LICENSES AND ATTRIBUTIONS LICENSES AND ATTRIBUTIONS CC LICENSED CONTENT, ORIGINAL - Set Yourself Up for Success. Authored by: Heather Syrett. Provided by: Austin Community College. License: License: CC BY-NC-SA 4.0 - Seven Keys to College Success. Authored by: Tobin Quereau. Provided by: Austin Community College. License: CC BY-NC-SA 4.0 CC LICENSED CONTENT, SPECIFIC ATTRIBUTION - Academic Honesty in EDUC 1300. Provided by: Lumen Learning. Located at: https://courses.lumenlearning.com/sanjacinto-learningframework/chapter/academic-honesty/. License: CC BY 4.0 - Carol Dweck. Provided by: Wikipedia Located at: https://en.wikipedia.org/wiki/Carol_Dweck. License: CC BY 3.0 - Defining Success in EDUC 1300. Authored by: Linda Bruce. Provided by: Lumen Learning. Located at: https://courses.lumenlearning.com/sanjacinto-learningframework/chapter/defining-success/ License: CC BY 4.0 - Fixed or Growth Mindset: Which are you? Which are your students?. Provided by: ESU 8 Wednesday Webinars Located at: https://www.youtube.com/watch?v=d2YWh10_pzo. License: CC BY-NC-SA 4.0 - Grade Point Average. Provided by: The Glossary of Education Reform. Located at: https://www.edglossary.org/grade-point-average/ License: CC BY-NC-SA 4.0 - Introduction to Success Skills in Basic Reading and Writing. Provided by: Lumen Learning. at: https://courses.lumenlearning.com/basicreadingandwriting/chapter/why-it-matters-college-success/. License: CC BY 4.0 - Motivation as self-efficacy in Educational Psychology. Authored by: By Kelvin Seifert and Rosemary Sutton. Provided by: Lumen Learning Located at: https://courses.lumenlearning.com/educationalpsychology/chapter/motivation-as-self-efficacy/ License: CC BY 4.0 - Self-Efficacy. Authored by: By James E Maddux and Evan Kleiman at George Mason University. Provided by: Noba. Located at: https://nobaproject.com/modules/self-efficacy License: CC BY-NC-SA 4.0 - Self-Fulfilling Prophecy. Provided by: Columbus State University. Located at: https://educationtrendsandissues.wikispaces.com/Self-Fulfilling+Prophecy. License: CC BY-NC-SA 4.0 - Types of Students in College Success. Authored by: Linda Bruce. Provided by: Lumen Learning. Located at: https://courses.lumenlearning.com/sanjacinto-learningframework/chapter/types-of-students/. License: CC BY 4.0 ALL RIGHTS RESERVED CONTENT - ACC Students. Provided by: Austin Community College. Located at: https://www.austincc.edu/students License: All Rights Reserved. - Developing a Growth Mindset with Carol Dweck. Provided by: Standford Alumni. Located at: https://youtu.be/hiiEeMN7vbQ. License: All Rights Reserved. License Terms: Standard YouTube License - You Can Learn Anything. Provided by: Khan Academy Located at: https://youtu.be/JC82Il2cjqA. License: All Rights Reserved. License Terms: Standard YouTube License REFERENCES - Bandura, A. (1977). Self-efficacy: Toward a unifying theory of behavioral change. Psychological Review, 84(2), 191–215. doi:10.1037/0033-295X.84.2.191 - Bandura, A. (1997). Self-efficacy: The exercise of control. New York: Worth Publishers. - Dweck, Carol S (2006). Mindset: The New Psychology of Success. New York: Random House. - Schunk, D. H. (1991). Self-efficacy and academic motivation. Educational Psychologist, 26(3–4), 207–231. doi:10.1080/00461520.1991.9653133	oercommons	2025-03-18T00:37:02.907415	Christina Friedl	{ "license": "Creative Commons - Attribution - https://creativecommons.org/licenses/by/4.0/", "url": "https://oercommons.org/courseware/lesson/85122/overview", "title": "Learning Framework: Effective Strategies for College Success, Introduction to College Success, Chapter 2: Set Yourself Up for Success", "author": "Lesson" }
https://oercommons.org/courseware/lesson/60437/overview	Chapter 1.2: The Mexican-American War, 1846–1848 Overview The Mexican-American War, 1846–1848 Learning Objectives By the end of this section, you will be able to: - Identify the causes of the Mexican-American War - Describe the outcomes of the war in 1848, especially the Mexican Cession Introduction Introduction Tensions between the United States and Mexico rapidly deteriorated in the 1840s as American expansionists eagerly eyed Mexican land to the west, including the lush northern Mexican province of California. Indeed, in 1842, a U.S. naval fleet, incorrectly believing war had broken out, seized Monterey, California, a part of Mexico. Monterey was returned the next day, but the episode only added to the uneasiness with which Mexico viewed its northern neighbor. The forces of expansion, however, could not be contained, and American voters elected James Polk in 1844 because he promised to deliver more lands. President Polk fulfilled his promise by gaining Oregon and, most spectacularly, provoking a war with Mexico that ultimately fulfilled the wildest fantasies of expansionists. By 1848, the United States encompassed much of North America, a republic that stretched from the Atlantic to the Pacific. CC LICENSED CONTENT, ORIGINAL - Revision and Adaptation. Authored by: Daniel M. Regalado. License: CC BY: Attribution James K. Polk and the Triumph of Expansion James K. Polk and the Triumph of Expansion A fervent belief in expansion gripped the United States in the 1840s. In 1845, a New York newspaper editor, John O’Sullivan, introduced the concept of “manifest destiny” to describe the popular idea of the special role of the United States in overspreading the continent—the divine right and duty of white Americans to seize and settle the American West, thus spreading Protestant, democratic values. In this climate of opinion, voters in 1844 elected James K. Polk, a slaveholder from Tennessee, because he vowed to annex Texas as a new slave state and take Oregon. Annexing Oregon was an important objective for U.S. foreign policy because it appeared to be an area rich in commercial possibilities. Northerners favored U.S. control of Oregon because ports in the Pacific Northwest would be gateways for trade with Asia. Southerners hoped that, in exchange for their support of expansion into the northwest, northerners would not oppose plans for expansion into the southwest. President Polk—whose campaign slogan in 1844 had been “Fifty-four forty or fight!”—asserted the United States’ right to gain full control of what was known as Oregon Country, from its southern border at 42° latitude (the current boundary with California) to its northern border at 54° 40′ latitude. According to an 1818 agreement, Great Britain and the United States held joint ownership of this territory, but the 1827 Treaty of Joint Occupation opened the land to settlement by both countries. Realizing that the British were not willing to cede all claims to the territory, Polk proposed the land be divided at 49° latitude (the current border between Washington and Canada). The British, however, denied U.S. claims to land north of the Columbia River (Oregon’s current northern border). Indeed, the British foreign secretary refused even to relay Polk’s proposal to London. However, reports of the difficulty Great Britain would face defending Oregon in the event of a U.S. attack, combined with concerns over affairs at home and elsewhere in its empire, quickly changed the minds of the British, and in June 1846, Queen Victoria’s government agreed to a division at the forty-ninth parallel. In contrast to the diplomatic solution with Great Britain over Oregon, when it came to Mexico, Polk and the American people proved willing to use force to wrest more land for the United States. In keeping with voters’ expectations, President Polk set his sights on the Mexican state of California. After the mistaken capture of Monterey, negotiations about purchasing the port of San Francisco from Mexico broke off until September 1845. Then, following a revolt in California that left it divided in two, Polk attempted to purchase Upper California and New Mexico as well. These efforts went nowhere. The Mexican government, angered by U.S. actions, refused to recognize the independence of Texas. Finally, after nearly a decade of public clamoring for the annexation of Texas, in December 1845 Polk officially agreed to the annexation of the former Mexican state, making the Lone Star Republic an additional slave state. Incensed that the United States had annexed Texas, however, the Mexican government refused to discuss the matter of selling land to the United States. Indeed, Mexico refused even to acknowledge Polk’s emissary, John Slidell, who had been sent to Mexico City to negotiate. Not to be deterred, Polk encouraged Thomas O. Larkin, the U.S. consul in Monterey, to assist any American settlers and any Californios, the Mexican residents of the state, who wished to proclaim their independence from Mexico. By the end of 1845, having broken diplomatic ties with the United States over Texas and having grown alarmed by American actions in California, the Mexican government warily anticipated the next move. It did not have long to wait. War with Mexico, 1846-1848 War with Mexico, 1846-1848 In 1845, when Texas joined the United States, Mexico insisted the United States had a right only to the territory northeast of the Nueces River. The United States argued in turn that it should have title to all land between the Nueces and the Rio Grande as well. Expansionistic fervor propelled the United States to war against Mexico in 1846. The United States had long argued that the Rio Grande was the border between Mexico and the United States, and at the end of the Texas war for independence Santa Anna had been pressured to agree. Mexico, however, refused to be bound by Santa Anna’s promises and insisted the border lay farther north, at the Nueces River. To set it at the Rio Grande would, in effect, allow the United States to control land it had never occupied. In Mexico’s eyes, therefore, President Polk violated its sovereign territory when he ordered U.S. troops into the disputed lands in 1846. From the Mexican perspective, it appeared the United States had invaded their nation. In January 1846, the U.S. force that was ordered to the banks of the Rio Grande to build a fort on the “American” side encountered a Mexican cavalry unit on patrol. Shots rang out, and sixteen U.S. soldiers were killed or wounded. Angrily declaring that Mexico “has invaded our territory and shed American blood upon American soil,” President Polk demanded the United States declare war on Mexico. On May 12, Congress obliged. The small but vocal antislavery faction decried the decision to go to war, arguing that Polk had deliberately provoked hostilities so the United States could annex more slave territory. Illinois representative Abraham Lincoln and other members of Congress issued the “Spot Resolutions” in which they demanded to know the precise spot on U.S. soil where American blood had been spilled. Many Whigs also denounced the war. Democrats, however, supported Polk’s decision, and volunteers for the army came forward in droves from every part of the country except New England, the seat of abolitionist activity. Enthusiasm for the war was aided by the widely held belief that Mexico was a weak, impoverished country and that the Mexican people, perceived as ignorant, lazy, and controlled by a corrupt Roman Catholic clergy, would be easy to defeat. U.S. military strategy had three main objectives: 1) Take control of northern Mexico, including New Mexico; 2) seize California; and 3) capture Mexico City. General Zachary Taylor and his Army of the Center were assigned to accomplish the first goal, and with superior weapons they soon captured the Mexican city of Monterrey. Taylor quickly became a hero in the eyes of the American people, and Polk appointed him commander of all U.S. forces. General Stephen Watts Kearny, commander of the Army of the West, accepted the surrender of Santa Fe, New Mexico, and moved on to take control of California, leaving Colonel Sterling Price in command. Despite Kearny’s assurances that New Mexicans need not fear for their lives or their property, and in fact the region’s residents rose in revolt in January 1847 in an effort to drive the Americans away. Although Price managed to put an end to the rebellion, tensions remained high. Kearny, meanwhile, arrived in California to find it already in American hands through the joint efforts of California settlers, U.S. naval commander John D. Sloat, and John C. Fremont, a former army captain and son-in-law of Missouri senator Thomas Benton. Sloat, at anchor off the coast of Mazatlan, learned that war had begun and quickly set sail for California. He seized the town of Monterey in July 1846, less than a month after a group of American settlers led by William B. Ide had taken control of Sonoma and declared California a republic. A week after the fall of Monterey, the navy took San Francisco with no resistance. Although some Californios staged a short-lived rebellion in September 1846, many others submitted to the U.S. takeover. Thus Kearny had little to do other than take command of California as its governor. Leading the Army of the South was General Winfield Scott. Both Taylor and Scott were potential competitors for the presidency, and believing—correctly—that whoever seized Mexico City would become a hero, Polk assigned Scott the campaign to avoid elevating the more popular Taylor, who was affectionately known as “Old Rough and Ready.” Scott captured Veracruz in March 1847, and moving in a northwesterly direction from there (much as Spanish conquistador Hernán Cortés had done in 1519), he slowly closed in on the capital. Every step of the way was a hard-fought victory, however, and Mexican soldiers and civilians both fought bravely to save their land from the American invaders. Mexico City’s defenders, including young military cadets, fought to the end. According to legend, cadet Juan Escutia’s last act was to save the Mexican flag, and he leapt from the city’s walls with it wrapped around his body. On September 14, 1847, Scott entered Mexico City’s central plaza; the city had fallen. While Polk and other expansionists called for “all Mexico,” the Mexican government and the United States negotiated for peace in 1848, resulting in the Treaty of Guadalupe Hidalgo. The Treaty of Guadalupe Hidalgo, signed in February 1848, was a triumph for American expansionism under which Mexico ceded nearly half its land to the United States. The Mexican Cession, as the conquest of land west of the Rio Grande was called, included the current states of California, New Mexico, Arizona, Nevada, Utah, and portions of Colorado and Wyoming. Mexico also recognized the Rio Grande as the border with the United States. Mexican citizens in the ceded territory were promised U.S. citizenship in the future when the territories they were living in became states. In exchange, the United States agreed to assume $3.35 million worth of Mexican debts owed to U.S. citizens, paid Mexico $15 million for the loss of its land, and promised to guard the residents of the Mexican Cession from Indian raids. As extensive as the Mexican Cession was, some argued the United States should not be satisfied until it had taken all of Mexico. Many who were opposed to this idea were southerners who, while desiring the annexation of more slave territory, did not want to make Mexico’s large mestizo (people of mixed Indian and European ancestry) population part of the United States. Others did not want to absorb a large group of Roman Catholics. These expansionists could not accept the idea of new U.S. territory filled with mixed-race, Catholic populations. Reading Review Questions - What happened in Monterey, California that escalated tensions between the U.S. and Mexico in 1842? - Upon what campaign promises was James Polk elected U.S. President in 1844? - What were the two arguments behind the premise of “manifest destiny”? - Describe the meaning of Polk’s campaign slogan “fifty-four forty or fight” and how this goal was ultimately attained. - Describe the impact the annexation of Texas by the U.S. had on the Mexican government. - What importance did the Nueces River and the Rio Grande have to the territorial disputes between Mexico and the U.S.? Why was there a disagreement? - What happened along the Rio Grande that caused President Polk to declare war against Mexico? - What widely held beliefs about Mexico sparked enthusiasm for the War with Mexico?	oercommons	2025-03-18T00:37:02.933951	12/06/2019	{ "license": "Creative Commons - Attribution - https://creativecommons.org/licenses/by/4.0/", "url": "https://oercommons.org/courseware/lesson/60437/overview", "title": "Texas Government 1.0, Texas History and Culture, Chapter 1.2: The Mexican-American War, 1846–1848", "author": "Annette Howard" }
https://oercommons.org/courseware/lesson/66306/overview	Assessment Overview This is a quiz for Chapter Seven. Texas Government Chapter Seven Quiz Check your knowledge of Chapter Seven by taking the quiz linked below. The quiz will open in a new browser window or tab. This is a quiz for Chapter Seven. Check your knowledge of Chapter Seven by taking the quiz linked below. The quiz will open in a new browser window or tab.	oercommons	2025-03-18T00:37:02.951619	05/05/2020	{ "license": "Creative Commons - Attribution - https://creativecommons.org/licenses/by/4.0/", "url": "https://oercommons.org/courseware/lesson/66306/overview", "title": "Texas Government 2.0, Voting and Political Participation in Texas, Assessment", "author": "Kris Seago" }
https://oercommons.org/courseware/lesson/66326/overview	How Interest Groups Influence Texas Government Overview How Interest Groups Influence Texas Government Learning Objective By the end of this section, you will be able to: - Analyze the techniques used by interest groups to influence Texas government Introduction Texas interest groups use a wide variety of techniques to attempt to influence public policy, but most fall into two primary areas: electioneering and lobbying. Electioneering Electioneering is what groups do to influence who the policymakers will be. While federal law has strict limits on the amount of money that can be raised and contributed in federal races, Texas law permits groups to form political action committees that can receive and donate unlimited amounts of money to state and local election campaigns (Note: Home rule cities in Texas can limit contributions to candidates for city positions by ordinance). The Texas Association of Realtors PAC raised nearly 2 million dollars during the 2018 election cycle, donating $1.2 million to candidates. Texans for Lawsuit Reform, a group that advocates for civil justice reform, donated $1.3 million, spread over 100 diﬀerent candidates. PACs in Texas have diﬀerent approaches to political involvement. Many interest groups follow – oﬃcially or unoﬃcially – the friendly incumbent rule. They avoid backing challengers to incumbent legislators – even when those challengers might be more in line with their group’s interests. Why? Because challengers rarely win, and many groups fear retaliation from a spurned incumbent legislator more than they value the chance – often a long shot – to replace that incumbent with a more supportive candidate. Whatever an interest group chooses to do in an election, the election is eventually over, and a winner is sworn into oﬃce whether the group supported or opposed him. That’s when electioneering gives way to lobbying. Lobbying Lobbying is simply the process of advocating for your group’s interests. Some groups hire professional lobbyists to represent them in Austin. Others rely solely on volunteers. Grassroots lobbying involves getting large numbers of constituents to contact their legislators on behalf of a particular issue. When done well, grassroots lobbying is incredibly eﬀective with legislators, who are strongly motivated to please voters who live in their districts. Less well known but also eﬀective is “grasstops” lobbying, which involves generating smaller numbers of contacts from people of special importance to legislators – possibly including their largest campaign contributors, local party oﬃcials, mayors or school superintendents. Even small numbers of highly influential people can sometimes make a significant impression. Like lawmakers, many lobbyists are lawyers, and the persons they are trying to influence have the duty of writing laws. That the disciplines of law and lobbying are intertwined could be seen in the case of a Texas lawyer, Kevin Glasheen, who had been seeking compensation for his unfairly imprisoned client. Glasheen's exonerated-prisoner client had trouble paying the legal expenses, which totaled $1,024,166.67. Glasheen then lobbied the Texas state legislature to pass a bill that increased the payout to exonerated prisoners from $50,000 per year to $80,000 per year. It succeeded, making it possible for his newly freed client to pay the lawyer's fees (the lawyer was later sued for his billing in wrongful conviction cases). Legislators frankly rely on interest groups for information. The 2019 legislature considered 10,877 individual bills and resolutions. Part-time legislators cannot possibly know how each of those proposed changes in state law might impact various industries and interests unless representatives of those groups tell them. References and Further Reading Top Ten PACs of the 2018 Texas Election Cycle. Transparency Texas. September 6, 2017. Who Are the Biggest Spenders in Texas Races? Becca Aaronson. March 1, 2016. Vertuno, J. (2019, August 23). Texas gun rights lobby pushing back on calls for new laws. AP News. Retrieved September 9, 2019. Schwartz. J. (2011, May 9). Exonerated Inmates Fight Lawyer's Lobbying Fees. The New York Times. Retrieved September 9, 2019. Licensing and Attribution LICENSED MATERIAL, ORIGINAL How Interest Groups Influence Texas Government. Authored by: Andrew Teas. License: CC BY: Attribution	oercommons	2025-03-18T00:37:02.973614	05/05/2020	{ "license": "Creative Commons - Attribution - https://creativecommons.org/licenses/by/4.0/", "url": "https://oercommons.org/courseware/lesson/66326/overview", "title": "Texas Government 2.0, Interest Groups and Lobbying in Texas, How Interest Groups Influence Texas Government", "author": "Kris Seago" }
https://oercommons.org/courseware/lesson/66325/overview	Interest Group Typologies Overview Interest Group Typologies Learning Objectives By the end of this section, you will be able to: - Identify the various interest group typologies Introduction: Types of Interest Groups As of 2019, the Texas Ethics Commission listed 1834 registered lobbyists, many of whom represent multiple clients – some interest groups, some individual companies. What are some of the types of interest groups in Texas? Texas Interest Groups Trade associations are groups of companies involved in the same business. The Texas Association of Realtors, the Texas Bankers Association and the Texas Automobile Dealers Association are three prominent examples. Professional Associations are like trade associations, but with individual – rather than company – members. The Texas Nurses Association and the Texas Society of Professional Engineers are two major Texas professional associations. The Texas Nursing Association advocates for safe nursing practices through education and licensure in the Texas Nursing Practice Act. Organized labor is another major interest group type. While union members account for less than 5 percent of wage and salary workers in Texas, unions play a prominent role in the political process. The most prominent umbrella group for labor in Texas is the AFL-CIO, but with increasing competition from SEIU Texas, which specializes in government and service workers. Historically, agriculture groups have played a more prominent role in Texas government than any other type of interest group. As Texas politics become more urban, however, groups like the Texas Farm Bureau and the Texas and Southwestern Cattle Raisers Association, while still important, don’t dominate policy in Texas as much as in the 20th Century. Racial, ethnic, and minority groups from the Texas National Association for the Advancement of Colored People (NAACP) and LULAC to Equality Texas advocate on behalf of specific groups of people based on their racial heritage, sexual orientation, or other types of minority status. Religious groups have a long history of advocacy in Texas. Groups such as the Baptist Christian Life Commission have historically held considerable influence on abortion, gambling, and alcohol issues, but are involved increasingly on social justice issues like predatory lending and human traﬃcking. One of the least-known, but most powerful classes of interest groups in Texas, are groups of local governments. The Texas Municipal League and the Texas Association of Counties have been increasingly active during state legislative sessions as legislators deal with property tax and local control issues that aﬀect their ability to serve their constituents. Finally, for every cause about which Texans are passionate, there are cause groups representing their interests. From the National Abortion Rights Action League (NARAL) to Texas Right to Life on abortion and Mothers Against Drunk Drivers (MADD) on drinking and driving laws to Bike Texas which advocates for bicyclists, cause groups lobby for their members’ views on a wide variety of policy issues. References and Further Reading Texas Board of Nursing (2017). Laws & Rules - Nursing Practice Act (NPA). United States Department of Labor - Bureau of Labor Statistics. Union Members in Texas - 2018. Licensing and Attribution CC LICENSED MATERIAL, ORIGINAL Interest Group Typologies. Authored by: Andrew Teas. License: CC BY: Attribution	oercommons	2025-03-18T00:37:02.994064	05/05/2020	{ "license": "Creative Commons - Attribution - https://creativecommons.org/licenses/by/4.0/", "url": "https://oercommons.org/courseware/lesson/66325/overview", "title": "Texas Government 2.0, Interest Groups and Lobbying in Texas, Interest Group Typologies", "author": "Kris Seago" }
https://oercommons.org/courseware/lesson/66330/overview	Introduction: Public Policy in Texas Overview Public Policy in Texas Learning Objective By the end of this chapter, you will be able to: - Discuss important public policy issues in Texas Introduction Public policy is the broad strategy government uses to do its job, the relatively stable set of purposive governmental behaviors that address matters of concern to some part of society. Most policy outcomes are the result of considerable debate, compromise, and refinement that happen over years and are finalized only after input from multiple institutions within government. Health care reform, for instance, was developed after years of analysis, reflection on existing policy, and even trial implementation at the state level. Simply put, public policy is anything the government does to achieve a particular outcome. More will be said about this in the next section; however, it is important for you to understand that public policy decisions impact our lives in many ways. As a result, we should understand how policies are formed, budgeted, implemented, and evaluated. We should also know who the policymakers are and be able to measure the eﬀectiveness of policies that have been made. This chapter explores public policy-making in Texas across a variety of leading issue areas, including public education, social welfare, Medicaid, immigration, energy, and the environment. Licensing and Attribution CC LICENSED CONTENT, ORIGINAL Revision and Adaptation. Authored by: Kris S. Seago. License: CC BY: Attribution Revision and Adaptation. Authored by: panOpen. License: CC BY: Attribution	oercommons	2025-03-18T00:37:03.010740	05/05/2020	{ "license": "Creative Commons - Attribution - https://creativecommons.org/licenses/by/4.0/", "url": "https://oercommons.org/courseware/lesson/66330/overview", "title": "Texas Government 2.0, Public Policy in Texas, Introduction: Public Policy in Texas", "author": "Kris Seago" }
https://oercommons.org/courseware/lesson/66298/overview	Glossary Overview Glossary Glossary: Local Government in Texas at-large election: an election in which officials are selected by voters of the entire geographical area, rather than from smaller districts within that area county clerks: public official who is the main record-keeper of the county county commissioner: government official (four per county) on the county commissioners' court whose main duty is the construction and maintenance of roads and bridges county commissioners' court: the main governing body of each county; has the authority to set the county tax rate and budget. county tax assessor-collector: public official who maintains the county tax records and collects taxes owed to the county district attorney: public official who prosecutes the more serious criminal cases in the district court home-rule charters: the rules under which a city operates; local governments have considerable independent governing power under these charters municipal utility district (MUD): a special district that offers services such as electricity water, sewage, and sanitation outside the city limits school district: a specific type of special district that provides public education in a designated area special district: a unit of local government that performs a single service, such as education or sanitation, within a limited geographic area Licenses and Attributions CC LICENSED CONTENT, ORIGINAL Local Government in Texas: Glossary. Authored by: Andrew Teas. License: CC BY: Attribution	oercommons	2025-03-18T00:37:03.028814	05/05/2020	{ "license": "Creative Commons - Attribution - https://creativecommons.org/licenses/by/4.0/", "url": "https://oercommons.org/courseware/lesson/66298/overview", "title": "Texas Government 2.0, Local Government in Texas, Glossary", "author": "Kris Seago" }
https://oercommons.org/courseware/lesson/87894/overview	Impact of the Transatlantic Slave Trade Overview Impact of the Transatlantic Slave Trade The Transatlantic slave trade negatively affected the peoples and societies of Western and Central Africa. Learning Objectives Evaluate the effects slavery had on economic and social life on African peoples, as well as on African states. Key Terms / Key Concepts Elmina: a fortified slave castle (feitoria) on the West African coast, now Ghana Middle Passage: the voyage across the Atlantic from Africa to the Americas, comprised the middle leg of the trans- Atlantic slave trade Bight of Biafra: the “bend” (bight) of the central West African coast in a southerly direction Whydah: West African port for exporting enslaved Africans used by the Kingdom of Dahomey in the 18th century Luanda: West African port and Portuguese colony founded in 1575 (From this port alone an estimated 1.3 million enslaved Africans were exported to the Western Hemisphere, primarily to Brazil in South America.) Jihad: according to Islamic teaching, Muslims are obligated to “struggle” (jihad), so that they will obey God’s laws (the greater jihad) and non-Muslims will obey God’s laws (the lesser jihad) Sufism: mystical teaching of Islam that seeks spiritual unity with Allah (God) Tariqa: the different schools of thought or brotherhoods into which Sufis are divided Impact of the Transatlantic Slave Trade on the Peoples of Africa The trans-Atlantic slave trade was the largest long-distance forced movement of people in recorded history. From the sixteenth to the late nineteenth centuries, over twelve million (some estimates run as high as fifteen million) African men, women, and children were enslaved, transported to the Americas, and bought and sold primarily by European and Euro-American slaveholders as chattel property used for their labor and skills. The trans-Atlantic slave trade occurred within a broader system of trade between West and Central Africa, Western Europe, and North and South America. In African ports, European traders exchanged metals, cloth, beads, guns, and ammunition for captive Africans brought to the coast from the African interior, primarily by African traders. Many captives died during the long overland journeys from the interior to the coast. European traders then held the enslaved Africans who survived in fortified slave castles before forcing them into ships for the Middle Passage across the Atlantic Ocean; some of the slave castles were Elmina in the central region (now Ghana), Goree Island (now in present day Senegal), and Bunce Island (now in present day Sierra Leone). At first, some Europeans tried to use force in acquiring slaves, but this method proved impracticable. The only workable method was acquiring slaves through trade with Africans, since they controlled all trade into the interior. Typically, Europeans were restricted to trading posts, or feitorias, along the coast. Captives were brought to the feitorias, where they were processed as cargo rather than as human beings. Slaves were kept imprisoned in small, crowded rooms, segregated by sex and age, and “fattened up” if they were deemed too small for transport. They were branded to show what merchant purchased them, that taxes had been paid, and even that they had been baptized as a Christian. The high mortality rate of the slave trade began on the forced march to the feitorias and a slave’s imprisonment within them. The mortality rate continued to climb during the second part of the journey, the Middle Passage. The Middle Passage, the voyage across the Atlantic from Africa to the Americas, comprised the middle leg of the Atlantic Triangle Trade network, which traded manufactured goods such as beads, mirrors, cloth, and firearms to Africa for slaves. Slaves were then carried to the Americas, where their labor would produce items of the last leg of the Triangle Trade, such as sugar, rum, molasses, indigo, cotton, and rice. The Middle Passage itself was a hellish experience. Slaves were segregated by sex, often stripped naked, chained together, and kept in extremely tight quarters for up to twenty-three hours a day. As many as 12 – 13 percent died during this dehumanizing experience. Although we will likely never know the exact number of people who were enslaved and brought to the Americas, the number is certainly larger than ten million. Slaves who arrived at various ports in the Americas were then sold in public auctions or smaller trading venues to plantation owners, merchants, small farmers, prosperous tradesmen, and other slave traders. These traders could then transport slaves many miles further to sell on other Caribbean islands or into the North or South American interior. Predominantly European slaveholders purchased enslaved Africans to provide labor that included domestic service and artisanal trades. The majority, however, provided agricultural labor and skills to produce plantation cash crops for national and international markets. Slaveholders used profits from these exports to expand their landholdings and purchase more enslaved Africans, perpetuating the trans-Atlantic slave trade cycle for centuries, until various European countries and new American nations officially ceased their participation in the trade in the nineteenth century (though illegal trans-Atlantic slave trading continued even after national and colonial governments issued legal bans). Overview of the impact of the Trans-Atlantic Slave Trade on Africa The trans-Atlantic slave trade impacted the societies of West and East African peoples, who were often engaged in the trafficking of slaves to European slave traders. The sheer human and environmental diversity of the African continent makes it difficult to examine the trade from Africa as a whole. The slave trade did not expand, nor, indeed, decline, in all areas of Africa at the same time. Rather, a series of marked expansions (and declines) in individual regions contributed to a more gradual composite trend for sub-Saharan Africa as a whole. Each region that exported slaves experienced a marked upswing in the amount of slaves it supplied for the trans-Atlantic trade and, from that point, the normal pattern was for a region to continue to export large numbers of slaves for a century or more. The three regions that provided the fewest slaves—Senegambia, Sierra Leone, the Windward Coast in West Africa—reached these higher levels for much shorter periods. By the third quarter of the eighteenth century, all regions had undergone an intense expansion of slave exports. A cargo of slaves could be sought at particular points along the entire Western African coast. As the Brazilian coffee and sugar boom got under way near the end of the eighteenth century, slavers rounded the Cape of Good Hope and traveled as far as southeast Africa to fill their vessels’ holds. But while the slave trade pervaded much of the African coast, its focus was no less concentrated in particular African regions than it was among European carriers. West Central Africa, the long stretch of coast south of Cape Lopez and stretching to Benguela, sent more slaves than any other part of Africa every quarter century with the exception of a fifty-year period between 1676 and 1725. From 1751 to 1850, this region supplied nearly half of the entire African labor force in the Americas; in the half century after 1800, West Central Africa sent more slaves than all the other African regions combined. Overall, the center of gravity of the volume of the trade was located in West Central Africa by 1600. It then shifted northward slowly until about 1730, before gradually returning back to its starting point by the mid-nineteenth century. Further, slaves left from relatively few ports of embarkation within each African region, even though their origins and ethnicities could be highly diverse. Although Whydah, on the Slave Coast, was once considered the busiest African slaving port on the continent, it now appears that it was surpassed by Luanda, in West Central Africa, and by Bonny, in the Bight of Biafra. These three most active ports together accounted for 2.2 million slave departures. The trade from each of these ports assumed a unique character and followed very different temporal profiles. Luanda alone dispatched some 1.3 million slaves, actively participating in the slave trade from as early as the 1570s—when the Portuguese established a foothold there—through the nineteenth century. Whydah supplied slaves over a shorter period of time and was a dominant port for only thirty years prior to 1727. Bonny, probably the second largest point of embarkation in Africa, sent four out of every five of all the slaves it ever exported in just the eighty years between 1760 and 1840. It is not surprising, therefore, that some systematic links between Africa and the Americas can be perceived. As research on the issue of trans-Atlantic connections has progressed, it has become clear that the distribution of Africans in the New World is no more random than the distribution of Europeans. Eighty percent of the slaves who went to southeast Brazil were taken from West Central Africa. Bahia traded in similar proportions with the Bight of Benin. Cuba represents the other extreme: no African region supplied more than 28 percent of the slave population in this region. Most American import regions fell between these examples, drawing on a mix of coastal regions that diversified as the trade from Africa grew to incorporate new peoples. The Kingdom of Dahomey European merchants and explorers brought many changes to West Africa. In some areas, the slave trade had the effect of breaking down societies. For instance, in the early nineteenth century the great Oyo Yoruba confederation of states began to break down due to civil wars. Conflicts escalated as participants sold slaves to acquire European weapons; these weapons were then used to acquire more slaves, thus creating a vicious cycle. Other groups grew and gained power because of their role in the slave trade, perhaps the most prominent being the West African kingdom of Dahomey. The Kingdom of Dahomey was established in the 1720s. Dahomey was built on the slave trade; kings used profits from the slave trade to acquire guns, which in turn were used to expand their kingdom by conquest and incorporation of smaller kingdoms. Most slaves were acquired either by trade with the interior or by raids into the north and west into Nigeria. Dahomey also took advantage of the civil wars among the Yoruba to gain access to a ready source of captives. European trade agents were kept isolated in the main trade port of Whydah. Only a privileged few were allowed into the interior of the kingdom to have an audience with the king; as a result, only a few contemporary sources describe the kingdom. Like his European counterparts, the king of Dahomey was an absolute monarch, possessing great power in a highly centralized state. All trade with Europeans was a royal monopoly, jealously guarded by the kings. The monarchs never allowed Europeans to deal directly with the people of the kingdom, keeping all profits for the state, and allowing this highly militarized state to grow and expand. Diverse peoples of West Africa To the northwest of the kingdom of Dahomey, a number of West African peoples were impacted by the slave trade. From the 14th through the 18th century, three smaller political states emerged in the forests along the coast of Africa, below the Songhai Empire. The uppermost groups of states were the Gonja or Volta Kingdoms, located around the Volta River and the confluence of the Niger on what was called the Windward Coast, now Sierra Leone and Liberia. Most of the people in the upper region of the Windward Coast belonged to a common language group, called Gur by linguists. They also held common religious beliefs and a common system of land ownership. They lived in decentralized societies where political power resided in associations of men and women. Below the Volta lay the Asante Empire in the southeastern geographical area of the contemporary nations of Cote d’Ivoire and Togo, as well as modern Ghana. By the 15th century the Akan peoples, who included the Baule and Twi-speaking Asante, reached dominance in the central region. Akan culture had a highly evolved political system. One hundred years or more before the rise of democracy in North America, the Asante governed themselves through a constitution and assembly. Commercially the Asante-dominated region straddled the African trade routes that carried ivory, gold, and grain. As a result, Europeans called various parts of the region the Ivory Coast, Grain Coast, and Gold Coast. The transatlantic slave trade was fed by the emergence of these Volta Kingdoms and the Asante Empire, which was a contemporary of the Dahomey Kingdom. During the 17th and early 18th centuries African people taken from these regions were predominately among those enslaved in the British North American mainland colonies. Yorubaland: Introduction The Ibo people, found around the Bight of Biafra to the southeast of Yorubaland, predominated among those enslaved in the Chesapeake region of Virginia during the late 17th and early 18th century. Yorubaland is the cultural region of the Yoruba people in West Africa. It spans the modern-day countries of Nigeria, Togo, and Benin. Yorubaland lay along the West African coast along the Bights of Benin and Biafra, where the important slave trading station of Bonny was located. Its pre-modern history is based largely on oral traditions and legends. According to Yoruba religion, Olodumare—the Supreme God—ordered Obatala to create the earth, but on Obatala’s way he found palm wine, which he drank and became intoxicated. Therefore, his younger brother Oduduwa took the three items of creation from him, climbed down from the heavens on a chain, and threw a handful of earth on the primordial ocean; he then put a baby rooster on it so that it would scatter the earth, thus creating the land on which Ile-Ife would be built. On account of his creation of the world, Oduduwa became the ancestor of the first divine king of the Yoruba, while Obatala is believed to have created the first Yoruba people out of clay. The meaning of the word “ife” in Yoruba is “expansion.” “Ile-Ife” is therefore in reference to the myth of origin, “The Land of Expansion.” Ile-Ife Evidence suggests that as of the 7th century BCE, the African peoples who lived in Yorubaland were not initially known as the Yoruba, though they shared a common ethnicity and language group. By the 8th century CE, Ile-Ife was already a powerful Yoruba kingdom, one of the earliest in Africa south of the Sahara-Sahel. Almost every Yoruba settlement traces its origin to princes of Ile-Ife. As such, Ife can be regarded as the cultural and spiritual homeland of the Yoruba nation. Archaeologically, the settlement at Ife can be dated to the 4th century BCE, with urban structures appearing in the 12th century CE. The Oòni (or king) of Ife today still claim direct descent from Oduduwa. Ile-Ife was a settlement of substantial size between the 12th and 14th centuries, with houses featuring potsherd pavements. The city is known worldwide for its ancient and naturalistic bronze—as well as stone and terracotta—sculptures, which reached their peak of artistic expression between 1200 and 1400. In the period around 1300 the artists at Ile-Ife developed a refined and naturalistic sculptural tradition in terracotta, stone, and copper alloy—copper, brass, and bronze—many of which appear to have been created under the patronage of King Obalufon II—the man who today is identified as the Yoruba patron deity of brass casting, weaving, and regalia. After this period, production declined as political and economic power shifted to the nearby kingdom of Benin, which, like the Yoruba kingdom of Oyo, developed into a major empire. The Rise of the Oyo Empire The mythical origins of the Oyo Empire lie with Oranyan (also known as Oranmiyan), the second prince of Ile-Ife, who made Oyo his new kingdom and became the first oba with the title of Alaafin of Oyo (Alaafin means “owner of the palace” in Yoruba). The oral tradition holds that he left all his treasures in Ile-Ife and allowed another king, named Adimu, to rule there. Oranyan was succeeded by Oba Ajaka, but he was deposed because he allowed his sub-chiefs too much independence. Leadership was then conferred upon Ajaka’s brother, Shango, who was later deified as the deity of thunder and lightning. Ajaka was restored after Shango’s death. His successor, Kori, managed to conquer the rest of what later historians would refer to as metropolitan Oyo. The heart of metropolitan Oyo was its capital at Oyo-Ile. Oyo had grown into a formidable inland power by the end of the 14th century, but it suffered military defeats at the hands of the Nupe led by Tsoede. Sometime around 1535, the Nupe occupied Oyo and forced its ruling dynasty to take refuge in the kingdom of Borgu. The Yoruba of Oyo went through an interregnum of eighty years as an exiled dynasty. However, they re-established Oyo to be more centralized and expansive than ever. During the 17th century, Oyo began a long stretch of growth, becoming a major empire. It never encompassed all Yoruba-speaking people, but it was the most populous kingdom in Yoruba history. The Oyo Empire rose through the outstanding organizational skills of the Yoruba, gaining wealth from trade and its powerful cavalry. It was the most politically important state in the region from the mid-17th century to the late 18th century, holding sway not only over most of the other kingdoms in Yorubaland but also over nearby African states, notably the Fon Kingdom of Dahomey in the modern Republic of Benin to the west. The Power of Oyo The key to Yoruba rebuilding Oyo was a stronger military and a more centralized government. Oba Ofinran succeeded in regaining Oyo’s original territory from the Nupe. A new capital, Oyo-Igboho, was constructed, and the original became known as Old Oyo. The next oba, Eguguojo, conquered nearly all of Yorubaland. Despite a failed attempt to seize the Benin Empire sometime between 1578 and 1608, Oyo continued to expand. The Yoruba allowed autonomy to the southeast of metropolitan Oyo, where the non-Yoruba areas could act as a buffer between Oyo and Imperial Benin. By the end of the 16th century, the Ewe and Aja states of modern Benin were paying tribute to Oyo. The reinvigorated Oyo Empire began raiding southward as early as 1682. By the end of its military expansion, its borders would reach to the coast some 200 miles southwest of its capital. At the beginning, the people were concentrated in metropolitan Oyo. With imperial expansion, Oyo reorganized to better manage its vast holdings within and outside Yorubaland; it was divided into four layers defined by relation to the core of the empire. These layers were Metropolitan Oyo, southern Yorubaland, the Egbado Corridor, and Ajaland. The Oyo Empire developed a highly sophisticated political structure to govern its territorial domains. Scholars have not determined how much of this structure existed prior to the Nupe invasion. Some of Oyo’s institutions are clearly derivative of early accomplishments in Ife. The Oyo Empire was not a hereditary monarchy, nor an absolute one. While the Alaafin of Oyo was supreme overlord of the people, he was not without checks on his power. The Oyo Mesi (seven councilors of the states) and the Yoruba Earth cult—known as Ogboni—kept the Oba’s power in check. The Oyo Mesi spoke for the politicians while the Ogboni spoke for the people, backed by the power of religion. The power of the Alaafin of Oyo in relation to the Oyo Mesi and Ogboni depended on his personal character and political shrewdness. Oyo became the southern emporium of the trans-Saharan trade. Exchanges were made in salt, leather, horses, kola nuts, ivory, cloth, and slaves. The Yoruba of metropolitan Oyo were also highly skilled in craft making and iron work. Aside from taxes on trade products coming in and out of the empire, Oyo also became wealthy off the taxes imposed on its tributaries. Oyo’s imperial success made Yoruba a lingua franca almost to the shores of the Volta. Toward the end of the 18th century, the empire acted as a go-between for both the trans-Saharan and trans-Atlantic slave trade. By 1680, the Oyo Empire spanned over 150,000 square kilometers. Decline In the second half of the 18th century, dynastic intrigues, palace coups, and failed military campaigns began to weaken the Oyo Empire. Recurrent power struggles and resulting periods without a reigning king created a vacuum, in which the power of regional commanders rose. As Oyo tore itself apart via political intrigue, its vassals began taking advantage of the situation to press for independence. Some of them succeeded, and Oyo never regained its prominence in the region. It became a protectorate of Great Britain in 1888 before further fragmenting into warring factions. The Oyo state ceased to exist as any sort of power in 1896. Sokoto Caliphate North of the Oyo state in West Africa, the Sokoto Caliphate arose as a sovereign Sunni Muslim caliphate in West Africa that was founded during the jihad of the Fulani War in 1804 by Usman dan Fodio. It was dissolved when the British conquered the area in 1903 and annexed it into the newly established Northern Nigeria Protectorate. Developed in the context of multiple independent Hausa Kingdoms, at its height the caliphate linked over 30 different emirates and over 10 million people in the most powerful state in the region and one of the most significant empires in Africa in the nineteenth century. Bringing decades of economic growth throughout the region, the caliphate was a loose confederation of emirates that recognized the Amir al-Mu'minin, the Sultan of Sokoto as their overlord. An estimated 1 million to 2.5 million non-Muslim slaves were captured during the Fulani War. Slaves provided labor for plantations and were provided an opportunity to become Muslims. Rise of the Sokoto Caliphate The major power in the region in the 17th and 18th centuries had been the Bornu Empire. However, revolutions and the rise of new forces decreased the power of the Bornu empire, and by 1759 its rulers had lost control over the oasis town of Bilma and access to the Trans-Saharan trade. Vassal cities of the empire gradually became autonomous, and the result by 1780 was a political array of independent states in the region. The fall of the Songhai Empire in 1591 to Morocco had freed much of central Africa, and a number of Hausa sultanates led by different Hausa aristocracies had grown to fill the void. Three of the most significant to develop were the sultanates of Gobir, Kebbi (both in the Rima River valley), and Zamfara, all in present-day Nigeria. These kingdoms engaged in regular warfare against each other, especially in conducting slave raids. To pay for the constant warfare, they imposed high taxation on their citizens. The region between the Niger River and Lake Chad was largely populated with the Hausa, the Fulani, and other ethnic groups that had immigrated to the area, such as the Tuareg. Much of the Hausa population had settled in the cities throughout the region and became urbanized. The Fulani, in contrast, had largely remained a pastoral community, herding cattle, goats, and sheep; they populated grasslands between the towns throughout the region. With increasing trade, a good number of Fulani settled in towns, forming a distinct minority. Much of the population had converted to Islam in the centuries before; however, local pagan beliefs persisted in many areas, especially in the aristocracy. At the end of the 1700s, an increase in Islamic preaching occurred throughout the Hausa kingdoms. A number of the preachers were linked in a shared school of Islamic study. Scholars were invited or traveled to the Hausa lands from Muslim North Africa and joined the courts of some sultanates, such as in Kano. These scholars preached a return to adherence to Islamic tradition. Usman dan Fodio, an Islamic scholar and an urbanized Fulani, had been actively educating and preaching in the city of Gobir with the approval and support of the Hausa leadership of the city. However, when Yunfa, a former student of dan Fodio, became the sultan of Gobir, he restricted dan Fodio's activities, eventually forcing him into exile in Gudu. A large number of people left Gobir to join dan Fodio, who also began to gather new supporters from other regions. Feeling threatened by his former teacher, Yunfa declared war on dan Fodio on February 21, 1804. Usman dan Fodio was elected "Commander of the Faithful" (Amir al-Mu'minin) by his followers, marking the beginning of the Sokoto state. Usman dan Fodio then created a number of flag bearers amongst those following him, creating an early political structure of the empire. Declaring a jihad against the Hausa kings, dan Fodio rallied his primarily Fulani “warrior-scholars” against Gobir. Despite early losses at the Battle of Tsuntua and elsewhere, the forces of dan Fodio began taking over some key cities starting in 1805. The Fulani used guerrilla warfare to turn the conflict in their favor and gathered support from the civilian population, which had come to resent the despotic rule and high taxes of the Hausa kings. Even some non-Muslim Fulani started to support dan Fodio. The war lasted from 1804 until 1808, and it resulted in thousands of deaths. The forces of dan Fodio were able to capture the states of Katsina and Daura, the important kingdom of Kano in 1807, and finally Gobir in 1809. In the same year, Muhammed Bello, the son of dan Fodio, founded the city of Sokoto, which became the capital of the Sokoto state. The jihad had created a new slaving frontier on the basis of rejuvenated Islam. By 1900 the Sokoto state had at least 1 million and perhaps as many as 2.5 million slaves, second in size only to the United States (which had 4 million in 1860), among all modern slave societies. However, there was far less of a distinction between slaves and their masters in the Sokoto state. Expansion of the Sokoto State From 1808 until the mid-1830s, the Sokoto state expanded, gradually annexing the plains to the west and key parts of Yorubaland. It became one of the largest states in Africa, stretching from modern-day Burkina Faso to Cameroon and including most of northern Nigeria and southern Niger. At its height, the Sokoto state included over 30 different emirates under its political structure. The political structure of the state was organized with the sultan of Sokoto ruling from the city of Sokoto (and for a brief period under Muhammad Bello from Wurno). The leader of each emirate was appointed by the sultan as the flag bearer for that city but was given wide independence and autonomy. Much of the growth of the state occurred through the establishment of an extensive system of ribats as part of the consolidation policy of Muhammed Bello—the second Sultan. Ribats were established, founding a number of new cities with walled fortresses, schools, markets, and other buildings. These proved crucial in expansion through developing new cities, settling the pastoral Fulani people, and supporting the growth of plantations which were vital to the economy. By 1837, the Sokoto state had a population of around 10 million people. Administrative Structure The Sokoto state was largely organized around a number of mostly independent emirates pledging allegiance to the sultan of Sokoto. The administration was initially built to follow the teachings of the prophet Muhammad as well as the theories of Al-Mawardi found in “The Ordinances of Government.” The Hausa kingdoms prior to Usman dan Fodio had been run largely through hereditary succession. The early rulers of Sokoto, dan Fodio and Bello, abolished systems of hereditary succession, preferring leaders to be appointed by virtue of their Islamic scholarship and moral standing. Emirs were appointed by the sultan; they traveled yearly to pledge allegiance and deliver taxes in the form of crops, cowry shells, and slaves. When a sultan died or retired from the office, an appointment council made up of the emirs would select a replacement. Direct lines of succession were largely not followed, although each sultan claimed direct descent from dan Fodio. Major administrative authority in the empire was divided between Sokoto and the Gwandu Emirates. In 1815, Usman dan Fodio retired from the administrative business of the state and divided the area taken over during the Fulani War. He appointed his brother Abdullahi dan Fodio to rule in the west in the Gwandu Emirate and appointed his son Muhammed Bello to govern the Sokoto Sultanate. The Emir at Gwandu retained allegiance to the Sokoto Sultanate and spiritual guidance from the sultan, but the emir managed the separate emirates under his supervision independently from the sultan. The administrative structure of loose allegiances of the emirates to the sultan did not always function smoothly. There was a series of revolutions by the Hausa aristocracy in 1816 – 1817 during the reign of Muhammed Bello, but the sultan ended these by granting the leaders titles to land. There were multiple crises that arose during the 19th century between the Sokoto Sultanate and many of the subservient emirates: notably, the Adamawa Emirate and the Kano Emirate. A serious revolt occurred in 1836 in the city-state of Gobir, which was crushed by Muhammed Bello at the Battle of Gawakuke. The Sufi community throughout the region proved crucial in the administration of the state. The Tariqa brotherhoods, most notably the Qadiriyya, to which every successive sultan of Sokoto was an adherent, provided a group linking the distinct emirates to the authority of the sultan. Scholars claim that this Islamic scholarship community provided an “embryonic bureaucracy” that linked the cities throughout the Sokoto state. Economy After the establishment of the Caliphate, there were decades of economic growth throughout the region, particularly after a wave of revolts in 1816 – 1817. The Sokoto Caliphate established significant trade over the trans-Saharan routes. After the Fulani War, all land in the empire was declared waqf—owned by the entire community. However, the Sultan allocated land to individuals or families, as could an emir. Such land could be inherited by family members but could not be sold. Exchange was based largely on slaves, cowries, or gold. Major crops produced included cotton, indigo, kola and shea nuts, grain, rice, tobacco, and onion. Slavery remained a large part of the economy, although its operation changed with the end of the Atlantic slave trade in the early 19th century. Slaves were gained through raiding and via markets, just as they had earlier been in West Africa. The founder of the Caliphate allowed slavery only for non-Muslims; this was viewed as a regulation that would bring non-Muslims into the Muslim community. However, the expansion of agricultural plantations under the Caliphate was dependent on slave labor, and around half of the Caliphate's population was enslaved in the 19th century. The plantations were established around the ribats, and large areas of agricultural production took place around the cities of the empire. The institution of slavery was mediated by the lack of a racial barrier among the peoples, and by a complex and varying set of relations between owners and slaves, which included the right to accumulate property by working on their own plots, manumission, and the potential for slaves to convert and become members of the Islamic community. There are historical records of slaves reaching high levels of government and administration in the Sokoto Caliphate. Its commercial prosperity was also based on Islamic traditions, market integration, internal peace, and an extensive export-trade network. Kingdom of Kongo The Kongdom of Kongo is significant in exploring the historic contexts of African American heritage because the majority of all Africans enslaved in the Southern English colonies were from West Central Africa. The history and culture of West Central African peoples is thus important to the understanding of African American people in the present because of their high representation among enslaved peoples. It has been estimated that 69% of all African people transported in the Transatlantic Slave Trade between 1517 – 1700 CE were from West Central Africa and, between 1701 – 1800, people from West Central Africa comprised about 38% of all Africans brought to the West to be enslaved. In South Carolina, by 1730, the number of Africans or “salt-water negroes,” mostly from West Central Africa, and “native-born” African Americans, many descended from West Central Africans, exceeded the white population. However, slave traders trnasported the majority of enslaved Africans from this region to Brazil. To the south of the Bights of Biafra and Benin in West Central Africa, the Portuguese under the leadership of Paulo Dias de Novais established a protectorate over the Kingdom of Kongo and founded a colony at Luanda in 1575, in the modern nation of Angola. The city of Luanda became one of the main ports for the export of enslaved Africans across the Atlantic. In the century before Portuguese exploration of West Africa, the Kongo was another kingdom that developed in West Central Africa. In the three hundred years from the date Ne Lukeni Kia Nzinga founded the kingdom until the Portuguese destroyed it in 1665, Kongo was an organized, stable, and politically centralized society based on a subsistence economy. The Bakongo (the Kongo people), today several million strong, live in the modern Democratic Republic of the Congo, Congo-Brazzaville, neighboring Cabinda, and Angola. The present division of their territory into modern political entities masks the fact that the area was once united under the suzerainty of the ancient Kingdom of Kongo—one of the most important civilizations ever to emerge in Africa. The Kings of the Kongo ruled over an area stretching from the Kwilu-Nyari River, just north of the port of Loango, to the river Loje in northern Angola, and from the Atlantic to the inland valley of the Kwango. The Kongo encompassed an area roughly equaling the miles between New York City and Richmond, Virginia, in terms of coastal distance and between Baltimore and Eire, Pennsylvania, in terms of inland breadth. By 1600, after a century of overseas contact with the Portuguese, the complex Kongo kingdom dominated a region more than half the size of England which stretched from the Atlantic to the Kwango. The Bakongo shared a common culture with the people of eight adjoining regions, all of whom were either part of the Kongo Kingdom during the transatlantic slave trade or were part of the kingdoms formed by peoples fleeing from the advancing armies of Kongo chiefdoms. In their records slave traders called the Bakongo, as well as the people from the adjoining regions “Congos” and “Angolas,” although they may have been Mbembe, Mbanda, Nsundi, Mpangu, Mbata, Mbamba or Loango. Ki-Kongo-speaking groups inhabited the West Central African region then known as the Loango Coast—the term used to describe a historically significant area of West Central Africa extending from Cape Lopez or Cape Catherine in Gabon to Luanda in Angola. Within this region, Loango has been the name of a kingdom, a province, and a port. Once linked to the powerful Kongo Kingdom, the Loango Kingdom was dominated by the Villi—a Kongo people who migrated to the coastal region during the 1300s. Loango became an independent state probably in the late 1300s or early 1400s. Along with two other Kongo-related kingdoms, Kakongo, and Ngoyo (present day Cabinda), it became one of the most important trading states north of the Congo River. A common social structure was shared by people in the coastal kingdoms of Loango, Kakongo, Ngoyo, Vungu, and the Yombe chiefdoms, as well as the Teke federation in the east and the Nsundi societies on either side of the Zaire River from the Matadi/Vungu area in the west to Mapumbu of Malebo pool in the east. The provincial regions, districts, and villages each had chiefs and a hierarchical system through which tribute flowed upward to the King of the Kongo and rewards flowed downward. Each regional clan or group had a profession or craft, such as weaving, basket making, potting, and iron working. Tribute and trade consisted of natural resources, agricultural products, textiles, other material cultural artifacts, and cowries shells. The “Kongos” and “Angolas” shared a “ lingua franca ” or trade language that allowed them to communicate. They also shared other cultural characteristics, such as matrilineal social organization and a cosmology or world view expressed in their religious beliefs and practices. Woman-and-child figures are visual metaphors for both individual and societal fertility among Kongo Peoples; these images reflect their matrilineal social organization—the tracing of kinship through the mother’s side of the family. The mother and child was a common theme representing a woman who has saved her family line from extinction. Matrilineal social organization and certain cosmological beliefs expressed in religious ceremonies and funerary practices continue to be evident in the culture of rural South Carolina and Florida African Americans, who are descendants of enslaved Africans. Before the 1920s, male and female figures carved in stone served as Kongo funerary monuments commemorating the accomplishments of the deceased. Kongo mortuary figures are noted for their seated postures, expressive gestures and details of jewelry and headwear that indicate the deceased’s status. The leopard claw hat is worn by male rulers and women acting as regents. European slave trade led to internal wars, enslavement of multitudes, introduction of major political upheavals, migrations, and power shifts from greater to lesser-centralized authority of Kongo and other African societies. Most notably the slave trade destroyed old lineages and kinship ties upon which the basis of social order and organization was maintained in African societies. Christianity in the Kingdom of Kongo The conversion of Kongo to Christianity was one of the more remarkable accomplishments of the early modern Catholic church. Within a few years of contact with the Portuguese, following a brief exchange of people, King Nzinga a Nkuwu of Kongo was baptized in 1491 as João I. His son Afonso (1509 – 1542) then established the church in the kingdom and created an educational network that trained the local nobility in Christian religious concepts, financing its operations and keeping it firmly under his control. During his reign, locally educated Kongolese elites carried the faith to literally every corner of his domains, so that when he died in 1542 it could rightfully be said that Kongo was a Christian country. Missionaries from Portugal played a remarkably small role in the propagation of Christianity, primarily being valued for their capacity to administer the sacraments, as this could only be done by ordained priests. Afonso expected even this dependency upon a foreign clergy to end, and Rome cooperated with him by elevating his son, Henrique, to the status of bishop. However, this did not produce a long-lasting tradition of local ordination. In 1534, the Portuguese crown claimed the right to appoint bishops for Kongo, and subsequently kept the numbers of priests low, while failing to promote significant numbers of Kongolese to holy orders. Thus, Kongo was in the interesting position for most of its history as a Christian kingdom of hosting foreign priests primarily to administer the sacraments while keeping lay people in charge of Christian education throughout the realm. The Jesuits became involved in Kongo shortly after Afonso’s death, with a mission that began in 1548. Afonso’s successor Diogo I (1545 – 61) sent a Kongolese man of whole or partial Portuguese descent named Diogo Gomes, educated in Kongo’s school system, as an ambassador to Portugal to request missionaries. Gomes contacted the Jesuits, accompanied them to Kongo, and then joined the order himself, taking the name Cornélio Gomes. He was probably responsible for the linguistic content of the first Kikongo catechism (a summary of church teachings), published in 1556 (but no longer extant). The catechism likely included the linguistic equations between Christianity and local religion that would characterize Kongo’s own interpretation of the faith. The mission ran into political difficulties with Diogo over matters of precedence and some local customs. It lasted only a few years. When they came with the colonial mission of Paulo Dias de Novais in 1575, the Jesuits played a key role in the evangelization of the Portuguese colony of Angola and its surrounding Kimbundu-speaking neighbors. Their experience is an example of evangelization in a colonial setting in Africa, and it contrasts with Jesuit approaches to conversion in the neighboring and independent Kingdom of Kongo. They drew heavily on previous experiences in the Kingdom of Kongo, which had itself become Christian a century earlier and pioneered a marriage between African religion and Christian spirituality. When Jesuits came to Kongo in 1548 they found an existing established church and added relatively little to it before they left following political disputes. When Dias de Novais came to found Angola, he initially was militarily dependent on Kongo’s assistance and the Jesuits, too, were dependent on the Kongolese version of Christianity, which is clear in their choice of vocabulary in the Kimbundu catechism that they sponsored and oversaw in 1628. However, the colonial situation in Angola made the Jesuits more willing to accept the idea of conversion by the sword, and they were notably less tolerant of African religious inclusions in Angola than in Kongo. It was from contact with Kongo’s southern neighbor of Ndongo that the Jesuits would come both as missionaries to non-Christians and as part of the Portuguese conquest, but their engagement was always tempered by contact with Kongo. Engagement with Ndongo began in 1560 when Portugal dispatched Paulo Dias de Novais and four Jesuits to the kingdom in response to King Ngola Kiluanje’s request for missionaries. The mission did not make much progress and Dias de Novais soon returned to Portugal, leaving only the Jesuit Francisco de Gouveia to labor on in Ndongo, where he made some converts and established a small community of Christians. While Gouveia enjoyed considerable influence, he never managed to convert the king. When Dias de Novais returned to Angola in 1575, it was with an army, more Jesuits, and a charter to subjugate and to conquer the Kingdom of Angola. Kongo would play an important role in the initial conquest of Angola, for Dias de Novais’s mission had begun largely because Kongo’s king Álvaro I (1568 – 87) agreed to allow Portugal to use his territory at Luanda as a base in compensation for the help Portugal had given him in quelling an uprising by a mysterious group of people called “Jagas.” In addition to relying on Kongo for a base, Novais offered services to Kiluanje kia Ndambi, King of Ndongo, as mercenaries and assisted him in putting down rebellions of his own. But in 1579, upon hearing of Dias de Novais’s charter and commission to conquer Angola, Ndongo’s king expelled the Portuguese from his lands. In the aftermath of this disaster, the Portuguese fell back on their alliance with Kongo, but Kongo then retracted its official support of the Portuguese colony following the defeat of the Kongolese army by Ndongo in 1580. However, Kongo continued to play an important role for some time both in Portuguese politics in Angola and in the way in which Christianity developed there. Even without official support from the king, many Kongolese noblemen privately helped the Portuguese. According to one report of 1588, some 4,000 Kongolese were serving in the Portuguese forces, and Andrew Battell, a captive Englishman serving in Portuguese forces around 1600, noted that it was a regular practice to bring a Kongolese nobleman to come with a troop of soldiers and to serve as an organizer for the new Christian community, as well as to be an intermediary between the surrendered Mbundu lord and the Portuguese assigned to collect tribute from him. In addition to receiving assistance from these noble allies, Dias de Novais also built support by taking in disgruntled local rulers from the fringe areas of Ndongo’s control along the Kwanza and Bengo Rivers. The Jesuits successfully converted some of these local rulers to Christianity. Conversion was considered a step toward their becoming Portuguese vassals, a change of status that was required by Portugal both for the allied and the conquered in the region. Baltazar Barreira, one of the leading Jesuits of the mission, described the baptism in 1581 of the first of these allied nobles, named Songa, as occurring in a large ceremony that was conducted by the Jesuits with great pomp and which included a number of Kongolese participants. In addition to an installation ceremony, there was also a ritualistic burning of country “idols.” These ceremonious conversions, which were made quickly and with considerable political expediency, characterized the advance of Portuguese rule in Angola. If military aid from Kongo was important, the country played an even more substantial role in the Christian evangelization of Angola. The dependency of the Angola mission on Kongo was symbolically marked in 1596 when Rome elevated Kongo’s capital of São Salvador as the seat of the bishop of Kongo and Angola, placing the nascent Angolan church under the nominal control of Kongo, where the bishop’s cathedral was located. Kongo’s ascendancy in religious matters was more symbolic than real, and Portugal claimed the right to appoint bishops of this new see. This joint alliance of the Jesuits with both the Kongo church and Kongo’s military was sharply challenged in the early seventeenth century. Thanks to some key alliances, Portugal was able to recover the military initiative and made major conquests in Ndongo, driving the king from the capital and forcing him to come to terms. But in the process they also made incursions into Kongo and in 1622 launched a major, but unsuccessful, invasion. From that point onward, Kongo became the sworn enemy of Portugal and formal ecclesiastical relations were strained to a breaking point. The new estrangement between Kongo and Angola meant that the Angolan church would not benefit from Kongo’s long-established network of schools and schoolmasters who led theological instruction in every corner of the country, just at the time when the Portuguese were conquering territory that was far from the area around Kongo’s coastal land of Luanda. The Jesuits, along with Portuguese secular priests, were thus responsible for building a network themselves in Angola, and they never won the sort of general adherence to Christianity found in Kongo. Despite the substantial differences in their political situations, missionaries both in Kongo and the Kimbundu-speaking areas of Angola developed Christian theologies that essentially incorporated large components of indigenous spirituality. These two syncretic systems could then potentially have been translated into other African religious systems and carried across the Atlantic, where so many Central Africans served as catechists. The role of Kongolese clergy and lay catechists in developing a syncretic form of Christianity in conquered Angola may just as well have served the same purpose in the America of the slaves. The conversion of Angolans had its reflection in the religion of slaves in Brazil. The same wave of Portuguese conquest and colonization that had led to the formation of Kimbundu Christianity also brought thousands of slaves to Brazil; there, in the most successful of the sixteenth-century captaincies of Bahia and Pernambuco, the Jesuits took the lead not only in converting the indigenous Brazilians but also the African slaves who came among them. In this, they employed the language of their early catechisms. Jesuits in Pernambuco, for example, studied Kimbundu and learned to read and even to compose in the language, as sixteenth-century sources reveal. Both Christian and traditional religious ideas and practices crossed the Atlantic with these slaves. Queen Ana Nzinga African peoples fiercely resisted Portuguese expansion under the leadership of the Queen Ana Nzinga. In 1624, she inherited the throne of Ndongo, just to the east of the Portuguese colony of Luanda. To put a stop to slave raids in her kingdom and attacks by rival African states on her kingdom, she agreed to an alliance with the Portuguese and to become baptized as a Christian in 1626. When the slave raids continued and the Portuguese reneged on this alliance, Ana Nzinga and her supporters migrated into the African interior away from Portuguese control and formed the new kingdom of Matamba. The new kingdom waged war on the Portuguese and became a haven for runaway slaves. In 1641, the queen even formed an alliance with the Dutch, whose forces conquered and briefly occupied Luanda before the Portuguese were able to recover and retake the colony. Ironically by the time of her death in 1663, the queen was rebaptized as a Christian, while her kingdom, Matamba became a major supplier of slaves to the Portuguese by securing slaves from outlying regions. Ana Nzinga’s life story illustrates that indigenous Africans were not simply passive agents in the African slave trade. Kingdoms of Madagascar On the island of Madagascar off the east coast of Africa, a number of states emerged that were heavily involved in the slave trade. Among the many fragmented communities that populated Madagascar, the Sakalava, Merina, and Betsimisaraka seized the opportunity to unite disparate groups and establish powerful kingdoms under their rule. Diverse Populations and the Rise of Great Kingdoms Over the past 2,000 years, Madagascar has received waves of settlers of diverse origins, including Austronesian, Bantu, Arab, South Asian, Chinese, and European populations. Centuries of intermarriages created the Malagasy people, who primarily speak Malagasy, an Austronesian language with Bantu, Malay, Arabic, French, and English influences. Most of the genetic makeup of the average Malagasy, however, reflects an almost equal blend of Austronesian and Bantu influences, especially in coastal regions. Other populations often intermixed with the existent population to a more limited degree or have sought to preserve a separate community from the majority Malagasy. By the European Middle Ages c 1200 CE, over a dozen predominant ethnic identities had emerged on the island, typified by rule under a local chieftain. Leaders of some communities, such as the Sakalava, Merina, and Betsimisaraka, seized the opportunity to unite these disparate groups and establish powerful kingdoms under their rule. The kingdoms increased their wealth and power through exchanges with European, Arab, and other seafaring traders, whether they were legitimate vessels or pirates. Sakalava Madagascar’s western clan chiefs began to extend their power through trade with their Indian Ocean neighbors: first with Arab, Persian, and Somali traders who connected Madagascar with East Africa, the Middle East, and India; later with European slave traders. The wealth created in Madagascar through trade produced a state system ruled by powerful regional monarchs known as the Maroserana. These monarchs adopted the cultural traditions of subjects in their territories and, thereby, expanded their kingdoms. They took on divine status, and new nobility and artisan classes were created. Madagascar functioned as a contact port for the other Swahili seaport city-states, such as Sofala, Kilwa, Mombasa, and Zanzibar. By c. 1200 CE, large chiefdoms began to dominate considerable areas of the island. Among these were the Betsimisaraka alliance of the eastern coast and the Sakalava chiefdoms of the Menabe (centered in what is now the town of Morondava) and of the Boina (centered in what is now the provincial capital of Mahajanga). The influence of the Sakalava extended across the area that is now the provinces of Antsiranana, Mahajanga, and Toliara. According to local tradition, the founders of the Sakalava kingdom were Maroseraña—or Maroseranana, “those who owned many ports”—princes from the Fiherenana (now Toliara). They quickly subdued the neighboring princes, starting with the southern ones, in the Mahafaly area. The true founder of Sakalava dominance was Andriamisara. His son Andriandahifotsy (c. 1610 – 1658) extended his authority northwards, past the Mangoky River. His two sons, Andriamanetiarivo and Andriamandisoarivo, extended gains further up to the Tsongay region (now Mahajanga). At about that time, the empire started to split, resulting in a southern kingdom (Menabe) and a northern kingdom (Boina). Further splits followed, despite continued extension of the Boina princes’ reach into the extreme north, in Antankarana country. Betsmiraka Like the Sakalava to the west, today’s Betsimisaraka are composed of numerous ethnic sub-groups that formed a confederation in the early 18th century. Through the late 17th century, the various clans of the eastern seaboard were governed by chieftains who typically ruled over one or two villages. Around 1700, the Tsikoa clans began uniting around a series of powerful leaders. Ramanano, the chief of Vatomandry, was elected in 1710 as the leader of the Tsikoa—“those who are steadfast”—and initiated invasions of the northern ports. A northern Betsimisaraka zana-malata (a person of mixed native and European origin) named Ratsimilaho led a resistance to these invasions and successfully united his compatriots around this cause. In 1712, he forced the Tsikoa to flee, and was elected king of all the Betsimisaraka and, at his capital at Foulpointe, was given a new name: Ramaromanompo—“Lord Served by Many.” He established alliances with the southern Betsimisaraka and the neighboring Bezanozano, extending his authority over these areas by allowing local chiefs to maintain their power while offering tributes of rice, cattle, and slaves. By 1730, he was one of the most powerful kings of Madagascar. By the time of his death in 1754, his moderate and stabilizing rule had provided nearly forty years of unity among the diverse clans within the Betsimisaraka political union. He also allied the Betsimisaraka with the other most powerful kingdom of the time, the Sakalava of the west coast, through marriage with Matave, the only daughter of Iboina king Andrianbaba. Ratsimilaho’s successors gradually weakened the union, leaving it vulnerable to the growing influence and presence of European and particularly French settlers, slave traders, missionaries, and merchants. The fractured Betsimisaraka kingdom was easily colonized in 1817 by Radama I, king of Merina. The subjugation of the Betsimisaraka in the 19th century left the population relatively impoverished. Merina The Merina emerged as the politically dominant group over the course of the 17th and 18th centuries. Oral history traces the emergence of a united kingdom in the central highlands of Madagascar—a region called Imerina—back to early 16th century king Andriamanelo. By 1824, sovereigns in his line had conquered nearly all of Madagascar, particularly through the military strategy and ambitious political policies of Andrianampoinimerina (c. 1785 – 1810) and his son Radama I (1792 – 1828). The kingdom’s contact with British and later French powers led local leaders to build schools and a modern army based on European models. The Merina oral histories mention several attacks by Sakalava raiders against their villages as early as the 17th century and during the entire 18th century. However, it seems that the term was used generically to design all the nomadic peoples in the sparsely settled territories between the Merina country and the western coast of the island. The Merina king Radama I’s wars with the western coast of the island ended in a fragile peace sealed through his marriage with the daughter of a king of Menabe. Though the Merina were never to annex the two last Sakalava strongholds of Menabe and Boina (Mahajanga), the Sakalava never again posed a threat to the central plateau, which remained under Merina control until the French colonization of the island in 1896. The Merina kingdom reached the peak of its power in the early 19th century. In a number of military expeditions, large numbers of non-Merina were captured and used for slave labor. By the 1850s, these slaves were replaced by imported slaves from East Africa, mostly of Makoa ethnicity. Until the 1820s, the imported slave labor benefited all classes of Merina society, but in the period of 1825 to 1861 a general impoverishment of small farmers led to the concentration of slave ownership in the hands of the ruling elite. The slave-based economy led to a constant danger of a slave revolt, and for a period in the 1820s all non-Merina males captured in military expeditions were killed rather than enslaved for fear of an armed uprising. There was a brief period of increased prosperity in the late 1870s, as slave imports began to pick up again, but it was cut short with the abolishment of slavery under French administration in 1896. Due to the influence of British missionaries, the Merina upper classes converted entirely to Protestantism in the mid-19th century, following the example of their queen, Ranavalona II. Primary Sources The African Slave Trade The three following primary sources offer insights on the experiences of enslaved African peoples when the Transatlantic slave trade was in operation. John Barbot John Barbot, an agent for the French Royal African Company, made at least two voyages to the West Coast of Africa, in 1678 and 1682. "PREPOSSESSED OF THE OPINION...THAT EUROPEANS ARE FOND OF THEIR FLESH" By John Barbot Those sold by the Blacks are for the most part prisoners of war, taken either in fight, or pursuit, or in the incursions they make into their enemies territories; others stolen away by their own countrymen; and some there are, who will sell their own children, kindred, or neighbours. This has been often seen, and to compass it, they desire the person they intend to sell, to help them in carrying something to the factory by way of trade, and when there, the person so deluded, not understanding the language, is old and deliver'd up as a slave, notwithstanding all his resistance, and exclaiming against the treachery.... The kings are so absolute, that upon any slight pretense of offences committed by their subjects, they order them to be sold for slaves, without regard to rank, or possession.... Abundance of little Blacks of both sexes are also stolen away by their neighbours, when found abroad on the roads, or in the woods; or else in the Cougans, or corn- fields, at the time of the year, when their parents keep them there all day, to scare away the devouring small birds, that come to feed on the millet, in swarms, as has been said above. In times of dearth and famine, abundance of those people will sell themselves, for a maintenance, and to prevent starving. When I first arriv'd at Goerree, in December, 1681, I could have bought a great number, at very easy rates, if I could have found provisions to subsist them; so great was the dearth then, in that part of Nigritia. To conclude, some slaves are also brought to these Blacks, from very remote inland countries, by way of trade, and sold for things of very inconsiderable value; but these slaves are generally poor and weak, by reason of the barbarous usage they have had in traveling so far, being continually beaten, and almost famish'd; so inhuman are the Blacks to one another.... The trade of slaves is in a more peculiar manner the business of kings, rich men, and prime merchants, exclusive of the inferior sort of Blacks. These slaves are severely and barbarously treated by their masters, who subsist them poorly, and beat them inhumanly, as may be seen by the scabs and wounds on the bodies of many of them when sold to us. They scarce allow them the least rag to cover their nakedness, which they also take off from them when sold to Europeans; and they always go bare- headed. The wives and children of slaves, are also slaves to the master under whom they are married; and when dead, they never bury them, but cast out the bodies into some by place, to be devoured by birds, or beasts of prey. This barbarous usage of those unfortunate wretches, makes it appear, that the fate of such as are bought and transported from the coast to America, or other parts of the world, by Europeans, is less deplorable, than that of those who end their days in their native country; for aboard ships all possible care is taken to preserve and subsist them for the interest of the owners, and when sold in America, the same motive ought to prevail with their masters to use them well, that they may live the longer, and do them more service. Not to mention the inestimable advantage they may reap, of becoming christians, and saving their souls, if they make a true use of their condition.... Many of those slaves we transport from Guinea to America are prepossessed with the opinion, that they are carried like sheep to the slaughter, and that the Europeans are fond of their flesh; which notion so far prevails with some, as to make them fall into a deep melancholy and despair, and to refuse all sustenance, tho' never so much compelled and even beaten to oblige them to take some nourishment: notwithstanding all which, they will starve to death; whereof I have had several instances in my own slaves both aboard and at Guadalupe. And tho' I must say I am naturally compassionate, yet have I been necessitated sometimes to cause the teeth of those wretches to be broken, because they would not open their mouths, or be prevailed upon by any entreaties to feed themselves; and thus have forced some sustenance into their throats.... As the slaves come down to Fida from the inland country, they are put into a booth, or prison, built for that purpose, near the beach, all of them together; and when the Europeans are to receive them, every part of every one of them, to the smallest member, men and women being all stark naked. Such as are allowed good and sound, are set on one side, and the others by themselves; which slaves so rejected are there called Mackrons, being above thirty five years of age, or defective in their limbs, eyes or teeth; or grown grey, or that have the venereal disease, or any other imperfection. These being set aside, each of the others, which have passed as good, is marked on the breast, with a red- hot iron, imprinting the mark of the French, English, or Dutch companies, that so each nation may distinguish their own, and to prevent their being chang'd by the natives for worse, as they are apt enough to do. In this particular, care is taken that the women, as tenderest, be not burnt too hard. The branded slaves, after this, are returned to their former booth, where the factor is to subsist them at his own charge, which amounts to about two- pence a day for each of them, with bread and water, which is all their allowance. There they continue sometimes ten or fifteen days, till the sea is still enough to send them aboard; for very often it continues too boisterous for so long a time, unless in January, February and March, which is commonly the calmest season: and when it is so, the slaves are carried off by parcels, in bar- canoes, and put aboard the ships in the road. Before they enter the canoes, or come out of the booth, their former Black masters strip them of every rag they have, without distinction of men or women; to supply which, in orderly ships, each of them as they come aboard is allowed a piece of canvas, to wrap around their waist, which is very acceptable to those poor wretches.... If there happens to be no stock of slaves at Fida, the factor must trust the Blacks with his goods, to the value of a hundred and fifty, or two hundred slaves; which goods they carry up into the inland, to buy slaves, at all the markets, for above two hundred leagues up the country, where they are kept like cattle in Europe; the slaves sold there being generally prisoners of war, taken from their enemies, like other booty, and perhaps some few sold by their own countrymen, in extreme want, or upon a famine; as also some as a punishment of heinous crimes: tho' many Europeans believe that parents sell their own children, men their wives and relations, which, if it ever happens, is so seldom, that it cannot justly be charged upon a whole nation, as a custom and common practice.... One thing is to be taken notice of by sea- faring men, that this Fida and Ardra slaves are of all the others, the most apt to revolt aboard ships, by a conspiracy carried on amongst themselves; especially such as are brought down to Fida, from very remote inland countries, who easily draw others into their plot: for being used to see mens flesh eaten in their own country, and publick markets held for the purpose, they are very full of the notion, that we buy and transport them to the same purpose; and will therefore watch all opportunities to deliver themselves, by assaulting a ship's crew, and murdering them all, if possible: whereof, we have almost every year some instances, in one European ship or other, that is filled with slaves. Source: John Barbot, "A Description of the Coasts of North and South Guinea," in Thomas Astley and John Churchill, eds., Collection of Voyages and Travels (London, 1732). Olaudah Equiano (Gustavus Vassa) Olaudah Equiano also known as Gustavus Vassa vividly recounts the shock and isolation that he felt during the Middle Passage to Barbados and his fear that the European slavers would eat him. "A MULTITUDE OF BLACK PEOPLE...CHAINED TOGETHER" Their complexions, differing so much from ours, their long hair and the language they spoke, which was different from any I had ever heard, united to confirm me in this belief. Indeed, such were the horrors of my views and fears at the moment, that if ten thousand worlds had been my own, I would have freely parted with them all to have exchanged my condition with that of the meanest slave of my own country. When I looked around the ship and saw a large furnace of copper boiling, and a multitude of black people of every description chained together, every one of their countenances expressing dejection and sorrow, I no longer doubted my fate. Quite overpowered with horror and anguish, I fell motionless on the deck and fainted. When I recovered a little, I found some black people about me, and I believe some were those who had brought me on board and had been receiving their pay. They talked to me in order to cheer me up, but all in vain. I asked them if we were not to be eaten by those white men with horrible looks, red faces and long hair. They told me I was not. I took a little down my palate, which, instead of reviving me as they thought it would, threw me into the greatest consternation at the strange feeling it produced, having never tasted such liquor before. Soon after this, the blacks who had brought me on board went off and left me abandoned to despair. I now saw myself deprived of all chance of returning to my native country or even the least glimpse of hope of gaining the shore, which I now considered as friendly. I even wished for my former slavery in preference to my present situation, which was filled with horrors of every kind. There I received such a salutation in my nostrils as I had never experienced in my life. With the loathesomeness of the stench and the crying together, I became so sick and low that I was not able to eat, nor had I the least desire to taste anything. I now wished for the last friend, Death, to relieve me. Soon, to my grief, two of the white men offered me eatables and on my refusing to eat, one of them held me fast by the hands and laid me across the windlass and tied my feet while the other flogged me severely. I had never experienced anything of this kind before. If I could have gotten over the nettings, I would have jumped over the side, but I could not. The crew used to watch very closely those of us who were not chained down to the decks, lest we should leap into the water. I have seen some of these poor African prisoners most severely cut for attempting to do so, and hourly whipped for not eating. This indeed was often the case with myself. I inquired of these what was to be done with us. They gave me to understand we were to be carried to these white people's country to work for them. I then was a little revived, and thought if it were no worse than working, my situation was not so desperate. But still I feared that I should be put to death, the white people looked and acted in so savage a manner. I have never seen among my people such instances of brutal cruelty, and this not only shown towards us blacks, but also to some of the whites themselves. One white man in particular I saw, when we were permitted to be on deck, flogged so unmercifully with a large rope near the foremast that he died in consequence of it, and they tossed him over the side as they would have done a brute. This made me fear these people the more, and I expected nothing less than to be treated in the same manner. I asked them if these people had no country, but lived in this hollow place? They told me they did not but came from a distant land. "Then," said I, "how comes it that in all our country we never heard of them?" They told me because they lived so far off. I then asked where were their women? Had they any like themselves? I was told they had. "And why do we not see them" I asked. They answered, "Because they were left behind." I asked how the vessel would go? They told me they could not tell, but there was cloth put upon the masts by the help of the ropes I saw, and then vessels went on, and the white men had some spell or magic they put in the water when they liked in order to stop the vessel when they liked. I was exceedingly amazed at this account, and really thought they were spirits. I therefore wished much to be from amongst them, for I expected they would sacrifice me. But my wishes were in vain- - for we were so quartered that it was impossible for us to make our escape. At last, when the ship we were in had got in all her cargo, they made ready with many fearful noises, and we were all put under deck, so that we could not see how they managed the vessel. The stench of the hold while we were on the coast was so intolerably loathsome, that it was dangerous to remain there for any time...some of us had been permitted to stay on the deck for the fresh air. But now that the whole ship's cargo were confined together, it became absolutely pestilential. The closeness of the place and the heat of the climate, added to the number of the ship, which was so crowded that each had scarcely room to turn himself, almost suffocated us. This produced copious perspirations so that the air became unfit for respiration from a variety of loathsome smells, and brought on a sickness among the slaves, of which many died- - thus falling victims of the improvident avarice, as I may call it, of their purchasers. This wretched situation was again aggravated by the galling of the chains, which now became insupportable, and the filth of the necessary tubs [toilets] into which the children often fell and were almost suffocated. The shrieks of the women and the groans of the dying rendered the whole a scene of horror almost inconceivable. Happily perhaps for myself, I was soon reduced so low that it was necessary to keep me almost always on deck and from my extreme youth I was not put into fetters. In this situation I expected every hour to share the fate of my companions, some of whom were almost daily brought upon the deck at the point of death, which I began to hope would soon put an end to my miseries. Often did I think many of the inhabitants of the deep much more happy than myself. I envied them the freedom they enjoyed, and as often wished I could change my condition for theirs. Every circumstance I met with, served only to render my state more painful and heightened my apprehensions and my opinion of the cruelty of the whites. One day, when we had a smooth sea and moderate wind, two of my wearied countrymen who were chained together (I was near them at the time), preferring death to such a life of misery, somehow made through the nettings and jumped into the sea. Immediately another quite dejected fellow, who on account of his illness was suffered to be out of irons, followed their example. I believe many more would very soon have done the same if they had not been prevented by the ship's crew, who were instantly alarmed. Those of us that were the most active were in a moment put down under the deck, and there was such a noise and confusion among the people of the ship as I never heard before to stop her and get the boat out to go after the slaves. However, two of the wretches were drowned, but they got the other and afterwards flogged him unmercifully for thus attempting to prefer death to slavery. I can now relate hardships which are inseparable from this accursed trade. Many a time we were near suffocation from the want of fresh air, which we were often without for whole days together. This, and the stench of the necessary tubs, carried off many. Source: The Interesting Narrative of the Life of Olaudah Equiano or Gustavus Vassa the African (London, 1789). Alexander Falconbridge Alexander Falconbridge, a surgeon aboard slave ships and later the governor of a British colony for freed slaves in Sierra Leone, offers a vivid account of Middle Passage "THE MEN NEGROES...ARE...FASTENED TOGETHER...BY HANDCUFFS" From the time of the arrival of the ships to their departure, which is usually about three months, scarce a day passes without some Negroes being purchased and carried on board; sometimes in small and sometimes in large numbers. The whole number taken on board depends on circumstances. In a voyage I once made, our stock of merchandise was exhausted in the purchase of about 380 Negroes, which was expected to have procured 500... The unhappy wretches thus disposed of are bought by the black traders at fairs, which are held for that purpose, at the distance of upwards of two hundred miles from the sea coast; and these fairs are said to be supplied from an interior part of the country. Many Negroes, upon being questioned relative to the places of their nativity, have asserted that they have travelled during the revolution of several moons (their usual method of calculating time) before they have reached the places where they were purchased by the black traders. At these fairs, which are held at uncertain periods, but generally every six weeks, several thousands are frequently exposed to sale who had been collected from all parts of the country for a very considerable distance around....During one of my voyages, the black traders brought down, in different canoes, from twelve to fifteen hundred Negroes who had been purchased at one fair. They consisted chiefly of men and boys, the women seldom exceeding a third of the whole number. From forty to two hundred Negroes are generally purchased at a time by the black traders, according to the opulence of the buyer, and consist of all ages, from a month to sixty years and upwards. Scarcely any age or situation is deemed an exception, the price being proportionable. Women sometimes form a part of them, who happen to be so far advanced in their pregnancy as to be delivered during their journey from the fairs to the coast; and I have frequently seen instances of deliveries on board ship.... When the Negroes, whom the black traders have to dispose of, are shown to the European purchasers, they first examine them relative to their age. They then minutely inspect their persons and inquire into the state of their health; if they are inflicted with any disease or are deformed or have bad eyes or teeth; if they are lame or weak in the joints or distorted in the back or of a slender make or narrow in the chest; in short, if they have been ill or are afflicted in any manner so as to render them incapable of much labor. If any of the foregoing defects are discovered in them they are rejected. But if approved of, they are generally taken on board the ship the same evening. The purchaser has liberty to return on the following morning, but not afterwards, such as upon re- examination are found exceptionable.... Near the mainmast a partition is constructed of boards which reaches athwart the ship. This division is called a barricado. It is about eight feet in height and is made to project about two feet over the sides of the ship. In this barricado there is a door at which a sentinel is placed during the time the Negroes are permitted to come upon the deck. It serves to keep the different sexes apart; and as there are small holes in it, where blunderbusses are fixed and sometimes a cannon, it is found very convenient for quelling the insurrections that now and then happen.... The men Negroes, on being brought aboard the ship, are immediately fastened together, two and two, by handcuffs on their wrists and by irons riveted on their legs. They are then sent down between the decks and placed in an apartment partitioned off for that purpose. The women also are placed in a separate apartment between the decks, but without being ironed. An adjoining room on the same deck is appointed for the boys. Thus they are all placed in different apartments. But at the same time, however, they are frequently stowed so close, as to admit of no other position than lying on their sides. Nor with the height between decks, unless directly under the grating, permit the indulgence of an erect posture; especially where there are platforms, which is generally the case. These platforms are a kind of shelf, about eight or nine feet in breadth, extending from the side of the ship toward the centre. They are placed nearly midway between the decks, at the distance of two or three feet from each deck. Upon these the Negroes are stowed in the same manner as they are on the deck underneath. In each of the apartments are placed three or four large buckets, of a conical form, nearly two feet in diameter at the bottom and only one foot at the top and in depth of about twenty- eight inches, to which, when necessary, the Negroes have recourse. It often happens that those who are placed at a distance from the buckets, in endeavoring to get to them, tumble over their companions, in consequence of their being shackled. These accidents, although unavoidable, are productive of continual quarrels in which some of them are always bruised. In this distressed situation, unable to proceed and prevented from getting to the tubs, they desist from the attempt; and as the necessities of nature are not to be resisted, ease themselves as they lie. This becomes a fresh source of boils and disturbances and tends to render the condition of the poor captive wretches still more uncomfortable. The nuisance arising from these circumstances is not infrequently increased by the tubs being too small for the purpose intended and their being emptied but once every day. The rule for doing so, however, varies in different ships according to the attention paid to the health and convenience of the slaves by the captain. About eight o'clock in the morning the Negroes are generally brought upon deck. Their irons being examined, a long chain, which is locked to a ring- bolt fixed in the deck, is run through the rings of the shackles of the men and then locked to another ring- bolt fixed also in the deck. By this means fifty or sixty and sometimes more are fastened to one chain in order to prevent them from rising or endeavoring to escape. If the weather proves favorable they are permitted to remain in that situation till four or five in the afternoon when they are disengaged from the chain and sent below. The diet of the Negroes while on board, consists chiefly of horse beans boiled to the consistency of a pulp; of boiled yams and rice and sometimes a small quantity of beef or pork. The latter are frequently taken from the provisions laid in for the sailors. They sometimes make use of a sauce composed of palm- oil mixed with flour, water and pepper, which the sailors call slabber- sauce. Yams are the favorite food of the Eboe [Ibo] or Bight Negroes, and rice or corn of those from the Gold or Windward Coast; each preferring the produce of their native soil.... They are commonly fed twice a day; about eight o'clock in the morning and four in the afternoon. In most ships they are only fed with their own food once a day. Their food is served up to them in tubs about the size of a small water bucket. They are placed round these tubs, in companies of ten to each tub, out of which they feed themselves with wooden spoons. These they soon lose and when they are not allowed others they feed themselves with their hands. In favorable weather they are fed upon deck but in bad weather their food is given them below. Numberless quarrels take place among them during their meals; more especially when they are put upon short allowance, which frequently happens if the passage form the coast of Guinea to the West Indies islands proves of unusual length. In that case, the weak are obliged to be content with a very scanty portion. Their allowance of water is about half a pint each at every meal. It is handed round in a bucket and given to each Negro in a pannekin, a small utensil with a straight handle, somewhat similar to a sauce- boat. However, when the ships approach the islands with a favourable breeze, the slaves are no longer restricted. Upon the Negroes refusing to take sustenance, I have seen coals of fire, glowing hot, put on a shovel and placed so near their lips as to scorch and burn them. And this has been accompanied with threats of forcing them to swallow the coals if they any longer persisted in refusing to eat. These means have generally had the desired effect. I have also been credibly informed that a certain captain in the slave- trade, poured melted lead on such of his Negroes as obstinately refused their food. Exercise being deemed necessary for the preservation of their health they are sometimes obliged to dance when the weather will permit their coming on deck. If they go about it reluctantly or do not move with agility, they are flogged; a person standing by them all the time with a cat- o'- nine- tails in his hands for the purpose. Their music, upon these occasions, consists of a drum, sometimes with only one head; and when that is worn out they make use of the bottom of one of the tubs before described. The poor wretches are frequently compelled to sing also; but when they do so, their songs are generally, as may naturally be expected, melancholy lamentations of their exile from their native country. The women are furnished with beads for the purpose of affording them some diversion. But this end is generally defeated by the squabbles which are occasioned in consequence of their stealing from each other. On board some ships the common sailors are allowed to have intercourse with such of the black women whose consent they can procure. And some of them have been known to take the inconstancy of their paramours so much to heart as to leap overboard and drown themselves. The officers are permitted to indulge their passions among them at pleasure and sometimes are guilty of such excesses as disgrace human nature.... The hardships and inconveniences suffered by the Negroes during the passage are scarcely to be enumerated or conceived. They are far more violently affected by seasickness than Europeans. It frequently terminates in death, especially among the women. But the exclusion of fresh air is among the most intolerable. For the purpose of admitting this needful refreshment, most of the ships in the slave trade are provided, between the decks, with five or sick air- ports on each side of the ship of about five inches in length and four in breadth. In addition, some ships, but not one in twenty, have what they denominate wind- sails. But whenever the sea is rough and the rain heavy is becomes necessary to shut these and every other conveyance by which the air is admitted. The fresh air being thus excluded, the Negroes' rooms soon grow intolerable hot. The confined air, rendered noxious by the effluvia exhaled from their bodies and being repeatedly breathed, soon produces fevers and fluxes which generally carries of great numbers of them. During the voyages I made, I was frequently witness to the fatal effects of this exclusion of fresh air. I will give one instance, as it serves to convey some idea, though a very faint one, of their terrible sufferings....Some wet and blowing weather having occasioned the port- holes to be shut and the grating to be covered, fluxes and fevers among the Negroes ensued. While they were in this situation, I frequently went down among them till at length their room became so extremely hot as to be only bearable for a very short time. But the excessive heat was not the only thing that rendered their situation intolerable. The deck, that is the floor of their rooms, was so covered with the blood and mucus which had proceeded from them in consequence of the flux, that it resembled a slaughter- house. It is not in the power of the human imagination to picture a situation more dreadful or disgusting. Numbers of the slaves having fainted, they were carried upon deck where several of them died and the rest with great difficulty were restored.... As very few of the Negroes can so far brook the loss of their liberty and the hardships they endure, they are ever on the watch to take advantage of the least negligence in their oppressors. Insurrections are frequently the consequence; which are seldom expressed without much bloodshed. Sometimes these are successful and the whole ship's company is cut off. They are likewise always ready to seize every opportunity for committing some acts of desperation to free themselves from their miserable state and notwithstanding the restraints which are laid, they often succeed. Source: Alexander Falconbridge, An Account of the Slave Trade on the Coast of Africa (London, 1788). Attributions Title Image Title page of The Interesting Narrative of the Life of Olaudah Equiano, or Gustavus Vassa, the African (New York: W. Durrell, 1791) - Library Company of Philadelphia, No restrictions, via Wikimedia Commons Adapted from: https://courses.lumenlearning.com/atd-tcc-worldciv2/chapter/the-transatlantic-slave-trade-2/ https://creativecommons.org/licenses/by-nc-nd/4.0/ https://courses.lumenlearning.com/atd-tcc-worldciv2/chapter/the-transatlantic-slave-trade/ https://creativecommons.org/licenses/by-sa/4.0/ http://www.vgskole.net/prosjekt/slavrute/6.htm Public Domain compiled by Steven Mintz https://guides.hostos.cuny.edu/lac118/3-1 http://creativecommons.org/licenses/by-nc/4.0/ http://creativecommons.org/licenses/by-nc-sa/3.0/us/ https://courses.lumenlearning.com/boundless-worldhistory/chapter/west-african-empires/ https://creativecommons.org/licenses/by-sa/4.0/ https://callipedia.miraheze.org/wiki/Sokoto_Caliphate https://creativecommons.org/licenses/by-sa/4.0/ https://brill.com/view/journals/jjs/1/2/article-p245_6.xml?language=en http://creativecommons.org/licenses/by-nc/4.0 https://courses.lumenlearning.com/boundless-worldhistory/chapter/southern-african-states/ https://creativecommons.org/licenses/by-sa/4.0/ Alexander Ives Bortolot, "Women Leaders in African History: Ana Nzinga, Queen of Ndongo" https://www.metmuseum.org/toah/hd/pwmn_2/hd_pwmn_2.htm	oercommons	2025-03-18T00:37:03.103915	Neil Greenwood	{ "license": "Creative Commons - Attribution - https://creativecommons.org/licenses/by/4.0/", "url": "https://oercommons.org/courseware/lesson/87894/overview", "title": "Statewide Dual Credit World History, The Making of Early Modern World 1450-1700 CE, Chapter 6: Exploration, Impact of the Transatlantic Slave Trade", "author": "Anna McCollum" }
https://oercommons.org/courseware/lesson/87872/overview	The Peace of Westphalia Overview The Peace of Westphalia The Peace of Westphalia was a series of peace treaties signed between May and October 1648. It was signed by warring parties in the Westphalian cities of Osnabrück and Münster. The collection of treaties ended the Thirty Years’ War. Learning Objective - Evaluate the impact of the Treaty of Westphalia on Europe. Key Terms / Key Concepts Peace of Westphalia: a collection of peace treaties that ended the Thirty Years’ War The Peace of Westphalia Over a four-year period, the warring nations of the Thirty Years’ War (the Holy Roman Empire, France, and Sweden) were actively negotiating at Osnabrück and Münster in Westphalia (present-day northwest Germany). The peace negotiations involved a total of 109 delegations representing European powers, including Holy Roman Emperor Ferdinand III, Philip IV of Spain, the Kingdom of France, the Swedish Empire, the Dutch Republic, the princes of the Holy Roman Empire, and sovereigns of the free imperial cities. The end of the war was not brought about by one treaty, but instead by a group of treaties, collectively named the Peace of Westphalia. The three treaties involved were the Peace of Münster (between the Dutch Republic and the Kingdom of Spain), the Treaty of Münster (between the Holy Roman Emperor and France and their respective allies), and the Treaty of Osnabrück (between the Holy Roman Empire and Sweden and their respective allies). These treaties ended both the Thirty Years’ War (1618 – 1648) in the Holy Roman Empire and the Eighty Years’ War (1568 – 1648) between Spain and the Dutch Republic, with Spain formally recognizing the independence of the Dutch Republic. Terms of the Treaties Along with ending open warfare between the belligerents, the Peace of Westphalia established several important tenets and agreements, including: - All parties would recognize the Peace of Augsburg of 1555, in which each prince would have the right to determine the religion of his own state. This affirmed the principle of cuius regio, eius religio (Whose realm, his religion). And the options at the time were Catholicism, Lutheranism, and Calvinism. - Christians living in principalities where their denomination was not the established church were guaranteed the right to practice their faith in public during allotted hours and in private at their will. There were also several territorial adjustments brought about by the peace settlements. The independence of Switzerland from the empire was formally recognized. Sweden received Western Pomerania, Wismar, and the Prince-Bishoprics of Bremen and Verden as hereditary fiefs, thus gaining a seat and vote in the Imperial Diet of the Holy Roman Empire. Barriers to trade and commerce erected during the war were also abolished, and a degree of free navigation was guaranteed on the Rhine. And France came out of the war in a far better position than any of the other participants. France retained the control of the Bishoprics of Metz, Toul, and Verdun near Lorraine, received the cities of the Décapole in Alsace and the city of Pignerol near the Spanish Duchy of Milan. The Impact of the Peace of Westphalia The Peace of Westphalia did not entirely end conflicts arising out of the Thirty Years’ War. Fighting continued between France and Spain until the Treaty of the Pyrenees in 1659. Nevertheless, it did settle many outstanding European issues of the time. Some of the principles developed at Westphalia, especially those relating to respecting the boundaries of sovereign states and non-interference in their domestic affairs, became central to the world order that developed over the following centuries, and remain in effect today. Many of the imperial territories established in the Peace of Westphalia later became the sovereign nation-states of modern Europe. The Peace of Westphalia established the precedent of having peace treaties negotiated and created by a diplomatic congress, as well as a new system of political order in central Europe based upon the concept of co-existing sovereign states. Inter-state aggression was to be held in check by a balance of power. A norm was established against interference in another state’s domestic affairs. As European influence spread across the globe, these Westphalian principles, especially the concept of sovereign states, became central to international law and to the prevailing world order. Attributions Images courtesy of Wikimedia Commons. Boundless World History "The Thirty Years War" https://courses.lumenlearning.com/boundless-worldhistory/chapter/the-thirty-years-war/	oercommons	2025-03-18T00:37:03.131047	Neil Greenwood	{ "license": "Creative Commons - Attribution - https://creativecommons.org/licenses/by/4.0/", "url": "https://oercommons.org/courseware/lesson/87872/overview", "title": "Statewide Dual Credit World History, The Making of Early Modern World 1450-1700 CE, Chapter 5: Europe, The Peace of Westphalia", "author": "Anna McCollum" }
https://oercommons.org/courseware/lesson/87933/overview	Social Consequences of Industrial Revolution in Europe Overview Overview of the Social Consequences of the Industrial Revolution The social consequences of the Industrial Revolution grew out of a myriad of technological and organizational changes. These social consequences involved various waves of migration and demographic dislocations, changes in class structures, new forms of interaction among members of different classes, and the emergence of a new set of consumer cultures fed by the mass production of the Industrial Revolution. The Industrial Revolution generated a number of new economic, political, and social developments and trends that dramatically changed the industrialized world beginning in the mid-nineteenth century. These new developments and trends manifested themselves in various social consequences, including new issues discussed and debated, urbanization, the working classes, poverty, and the cult of domesticity. And these consequences helped affect the world in which we live today. Learning Objectives - Analyze the human and environmental consequences of Industrialization and the factory system in England. - Compare the lives of factory owners and workers in England during Industrialization. - Compare the new political and labor organizations with governmental responses to worker unrest. - Identify, explain, and assess the historic significance and impact of the new developments and trends in the aftermath of the Industrial Revolution. Key Terms / Key Concepts The Condition of the Working Class in England: 1844 sociological study of industrializing and urbanizing England from the perspectives of the industrial working class Friedrich Engels: sociologist and author of The Condition of the Working Class in England factory system: a method of manufacturing that employs machinery and division of labor, which was first adopted in Britain at the beginning of the Industrial Revolution (late 18th century) and later spread around the world, reducing the required skill level of workers and increasing output per worker One of the best-known accounts of factory workers’ living conditions during the Industrial Revolution is Friedrich Engels’s The Condition of the Working Class in England in 1844. In it, Engels described backstreet sections of Manchester and other mill towns where people lived in crude shanties and shacks, some not completely enclosed, some with dirt floors. These shanty towns had narrow walkways between irregularly shaped lots and dwellings. There were no sanitary facilities. The population density was extremely high. Eight to ten unrelated mill workers often shared a room with no furniture and slept on a pile of straw or sawdust. Disease spread through a contaminated water supply. By the late 1880s, Engels noted that the extreme poverty and lack of sanitation he wrote about in 1844 had largely disappeared. Since then, the historical debate on the question of the living conditions of factory workers has been very controversial. While some have pointed out that living conditions of the poor workers were tragic everywhere and industrialization, in fact, slowly improved the living standards of a steadily increasing number of workers, others have concluded that living standards for the majority of the population did not grow meaningfully until the late 19th and 20th centuries and that in many ways workers’ living standards declined under early capitalism. Industrialization and Urbanization Industrialization and emergence of the factory system triggered rural-to-urban migration and thus led to a rapid growth of cities, where during the Industrial Revolution workers faced the challenge of dire conditions and developed new ways of living. Although initially inefficient, the arrival of steam power signified the beginning of the mechanization that would enhance the burgeoning textile industries in Manchester into the world’s first center of mass production. As textile manufacture switched from the home to factories, Manchester and towns in south and east Lancashire became the largest and most productive cotton spinning center in the world in 1871, with 32% of global cotton production. Industrialization led to the creation of the factory and the factory system contributed to the growth of urban areas, as large numbers of workers migrated into the cities in search of work in the factories. Nowhere was this better illustrated than in Manchester, the world’s first industrial city, nicknamed Cottonopolis because of its mills and associated industries that made it the global center of the textile industry. Manchester experienced a six-fold increase in its population between 1771 and 1831; it had a population of 10,000 in 1717, but by 1911 it had burgeoned to 2.3 million. Bradford grew by 50% every ten years between 1811 and 1851, and by 1851 only 50% of the population of Bradford was actually born there. In England and Wales, the proportion of the population living in cities jumped from 17% in 1801 to 72% in 1891. Poverty and the Working Classes in the Aftermath of the Industrial Revolution Industrialization changed living and working standards dramatically, reducing many to poverty. People in the working classes had new opportunities for employment and faced new challenges. A new culture of consumption grew out of the mass production of a growing number of inexpensive consumer goods. Members of the working classes enjoyed only limited access to these goods, along with only crowded, substandard, even unhealthy, housing in the growing industrial cities of England, Europe, and the United States. Such conditions effectively consigned many in the industrial working classes to an effective state of poverty. These conditions and the responses of people in these working classes to these conditions changed the economic, political, and social landscapes of the industrializing world. Conditions improved over the course of the 19th century due to new public health acts that regulated things like sewage, hygiene, and home construction. In the introduction of his 1892 edition, Engels notes that most of the conditions he wrote about in 1844 had been greatly improved. Working-Class Women Over time, more men than women would find industrial employment, and industrial wages provided a higher level of material security than agricultural employment. Consequently, women, who were traditionally involved in all agricultural labor, would be left behind in less-profitable agriculture. By the late 1860s, very low wages in agricultural work turned women to industrial employment. In industrialized areas, women could find employment on assembly lines, providing industrial laundry services, and in the textile mills that sprang up during the Industrial Revolution, in such cities as Manchester, Leeds, and Birmingham. Spinning and winding wool, silk, and other types of piecework were a common way of earning income by working from home, but wages were very low and hours long. Often 14 hours per day were needed to earn enough to survive. Needlework was the single highest-paid occupation for women working from home, but the work paid little and women often had to rent sewing machines that they could not afford to buy. These home manufacturing industries became known as “sweated industries” (think of today’s sweat shops). The Select Committee of the British House of Commons defined sweated industries in 1890 as “work carried on for inadequate wages and for excessive hours in unsanitary conditions.” By 1906, such workers earned about a penny an hour. Women were never paid the same wage as a man for the same work, despite the fact that they were as likely as men to be married and supporting children. Organizational Changes and Developments generated by the Industrial Revolution The Industrial Revolution gave rise to a wide range of organizational changes and developments. These changes and developments were part of the larger rationalization of industrializing societies. Such changes and developments include new manufacturing structures, new ways of organizing workers, and new organizations representing the new groups which emerged with the Industrial Revolution. These organizational changes and developments were part of industrial societies becoming more systematic, more compartmentalized, and more professionalized. Learning Objectives - Analyze the human and environmental consequences of Industrialization and the factory system in England. - Compare the lives of factory owners and workers in England during Industrialization. - Identify, explain, and assess the historic significance and impact of the new developments and trends in the aftermath of the Industrial Revolution. Key Terms / Key Concepts factory system: a method of manufacturing that employs machinery and division of labor, which was first adopted in Britain at the beginning of the Industrial Revolution (late 18th century) and later spread around the world, reducing the required skill level of workers and increasing output per worker Luddites: organized, English textile workers who often protested labor conditions by destroying machinery The Factory System The factory system, fueled by technological progress, made production much faster, cheaper, and more uniform, but it also disconnected the workers from the means of production and placed them under the control of powerful industrialists. Consequently, their roles in manufacturing and their status in their countries changed. They went from being artisans to wage workers who mind machines, to members of a new industrial working class. Between 1820 and 1850, mechanized factories supplanted traditional artisan shops as the predominant form of manufacturing institution, because the larger-scale factories enjoyed a significant technological advantage over the small artisan shops. The earliest factories under this system developed in the cotton and wool textiles industry. Later generations of factories included mechanized shoe production and manufacturing of machinery, including machine tools. Factories that supplied the railroad industry included rolling mills, foundries, and locomotive works. Agricultural-equipment factories produced cast-steel plows and reapers. Bicycles were mass-produced beginning in the 1880s. The factory system was a new way of organizing labor made necessary by the development of machines, which were too large to house in a worker’s cottage. Working hours were as long as they had been for the farmer: from dawn to dusk, six days per week. Factories also essentially reduced skilled and unskilled workers to replaceable commodities. At the farm or in the cottage industry, each family member and worker was indispensable to a given operation and workers had to possess knowledge and often advanced skills that resulted from years of learning through practice. Conversely, under the factory system, workers were easily replaceable as skills required to operate machines could be acquired very quickly. Factory workers typically lived within walking distance to work until the introduction of bicycles and electric street railways in the 1890s. Thus, the factory system was largely responsible for the rise of urban living, as large numbers of workers migrated into the towns in search of employment in the factories. Many mills had to provide dormitories for workers, especially for girls and women. Opposition to the Industrialization of Manufacturing Much manufacturing in the 18th century had been carried out in homes under the domestic or putting-out system, especially the weaving of cloth and spinning of thread and yarn, which was often done with just a single loom or spinning wheel. As these devices were mechanized, machine-made goods were able to underprice the cottagers, leaving them unable to earn enough to make their efforts worthwhile. The transition to industrialization was not without difficulty. For example, a group of English textile workers known as Luddites protested against industrialization and sometimes sabotaged factories. They continued an already established tradition of workers opposing labor-saving machinery. Numerous inventors in the textile industry suffered harassment when developing their machines or devices. However, in many industries the transition to factory production was not so divisive. Machine-breaking was criminalized by the Parliament of the United Kingdom as early as 1721. Parliament subsequently made “machine breaking” (i.e. industrial sabotage) a capital crime with the Frame Breaking Act of 1812 and the Malicious Damage Act of 1861. Lord Byron—the famous British Romantic poet—opposed this legislation, becoming one of the few prominent defenders of the Luddites. Debate arose concerning the morality of the factory system, as workers complained about unfair working conditions. One of the problems concerned women’s labor; women were always paid less than men and, in many cases, as little as a quarter of what men made. Child labor was also a major part of the system; in the early 19th century, education was not compulsory and, in working families, children’s wages were seen as a necessary contribution to the family budget. Additionally, there were major concerns about the number of hours employees were forced to work, as well as the dangerous or unhealthy conditions of factories themselves. Some of the unfair working conditions seemed to be addressed with inherent changes in society and the development of technology. For instance, automation in the late 19th century is credited with ending child labor and according to many historians, it was more effective than gradually changing child labor laws. Additionally, years of schooling began to increase sharply from the end of the 19th century, when elementary state-provided education for all became a viable concept (with the Prussian and Austrian empires as pioneers of obligatory education laws), which led to the assumption that children should be in school (although not for as many years as is currently required). Some industrialists themselves tried to improve factory and living conditions for their workers. One of the earliest such reformers was Robert Owen, known for his pioneering efforts in improving conditions for workers at the New Lanark mills and often regarded as one of the key thinkers of the early socialist movement. Early Reform Efforts A number of new problems grew out of industrialization, including exploitive and abusive child labor practices, unsafe working conditions, overcrowding, among other unsanitary living conditions, and the centralization of economic and political power in new elites. These problems quickly spawned reforms to correct them. These early reforms marked the beginning of a new age of industrial and urban reform. Learning Objectives - Analyze the human and environmental consequences of Industrialization and the factory system in England. - Compare the lives of factory owners and workers in England during Industrialization. - Identify, explain, and assess the historic significance and impact of the new developments and trends in the aftermath of the Industrial Revolution. Key Terms / Key Concepts factory acts - reform legislation enacted by the British Parliament during the nineteenth century toward the end of improving working conditions in new industrial factors Charles Dickens - English author who chronicled the impact of industrialization on England during the first half of the nineteenth century During the nineteenth century various European legislatures, U.S. state legislatures, and the Japanese legislature enacted a number or reform laws to improve working conditions in the new manufacturing factories. The British Parliament passed a series of factory acts as part of these efforts. The first legislation in response to the abuses experienced by child laborers did not even attempt to ban child labor but merely to improve working conditions for some child workers. The Health and Morals of Apprentices Act 1802, sometimes known as the Factory Act 1802, was designed to improve conditions for apprentices working in cotton mills. The Act was introduced by Sir Robert Peel, who became concerned after a 1784 outbreak of a “malignant fever” at one of his cotton mills, which he later blamed on “gross mismanagement” by his subordinates. The Act required that cotton mills and factories be properly ventilated and basic requirements on cleanliness be met. Apprentices in these premises were to be given a basic education and attend a religious service at least once a month. They were to be provided with clothing and their working hours were limited to no more than twelve hours a day (excluding meal breaks). They were not to work at night. Despite its modest provisions, the 1802 Act was not effectively enforced and did not address the working conditions of free children, who were not apprentices and who rapidly came to heavily outnumber the apprentices in mills. Regulating the way masters treated their apprentices was a recognized responsibility of Parliament and hence the Act itself was non-contentious, but coming between employer and employee to specify on what terms a person might sell their labor (or that of their children) was highly contentious. Hence it was not until 1819 that an Act to limit the hours of work (and set a minimum age) for free children working in cotton mills was piloted through Parliament by Peel and his son Robert (the future Prime Minister). Strictly speaking, Peel’s Cotton Mills and Factories Act of 1819 paved the way for subsequent Factory Acts and set up effective means of industry regulation. These 1802 and 1819 Acts were largely ineffective. For instance, in 1824 Charles Dickens, British author of Oliver Twist, was a child-laborer, forced to work in a blacking factory at the age of twelve in order to help pay off his father’s growing debts; as many note, his bad experiences as a child-laborer colored his future compositions. After radical agitation by child labor opponents, a Royal Commission recommended in 1833 that children aged 11 – 18 should work a maximum of 12 hours per day, children aged 9 – 11 a maximum of eight hours, and children under the age of nine were no longer permitted to work. This act, however, only applied to the textile industry, and further agitation led to another act in 1847 limiting both adults and children to 10-hour working days. In 1841, about 216,000 people were employed in the mines. Women and children worked underground for 11 or 12 hours a day for smaller wages than men. The public became aware of conditions in the country’s collieries in 1838 after an accident at Huskar Colliery in Silkstone, near Barnsley. A stream overflowed into the ventilation drift after violent thunderstorms causing the death of 26 children, 11 girls ages 8 to 16 and 15 boys between 9 and 12 years of age. The disaster came to the attention of Queen Victoria, who ordered an inquiry. Lord Ashley headed the royal commission of inquiry that investigated the conditions of workers, especially children, in the coal mines in 1840. Commissioners visited collieries and mining communities gathering information, sometimes against the mine owners’ wishes. The report, illustrated by engraved illustrations and the personal accounts of mine workers, was published in 1842. Victorian society was shocked to discover that children as young as five or six worked as trappers, opening and shutting ventilation doors down the mine before becoming hurriers, pushing and pulling coal tubs and corfs. As a result, the Mines and Collieries Act 1842, commonly known as the Mines Act of 1842, was passed. It prohibited all girls and boys under ten years old from working underground in coal mines. The Factories Act 1844 banned women and young adults from working more than 12-hour days and children from the ages 9 to 13 from working 9-hour days. The Factories Act 1847, also known as the Ten Hours Act, made it illegal for women and young people (13 – 18) to work more than 10 hours and a maximum 63 hours a week in textile mills. The last two major factory acts of the Industrial Revolution were introduced in 1850 and 1856. Factories could no longer dictate work hours for women and children, who were to work from 6 a.m. to 6 p.m. in the summer and 7 a.m. to 7 p.m. in the winter. These acts deprived the manufacturers of a significant amount of power and authority, which was deemed a necessity so as to ensure more ethical working conditions. They also constituted the beginning of a new period of reform. Changes in Family Structure In the laboring class at the end of the 18th and beginning of the 19th centuries, women traditionally married men of the same social status (e.g., a shoemaker’s daughter would marry a shoemaker’s son). Marriage outside this norm was not common. During the Industrial Revolution, marriage shifted from this tradition to a more sociable union between wife and husband in the laboring class. Women and men tended to marry someone from the same job, geographical location, or social group. Miners remained an exception to this trend and a coal miner’s daughter still tended to marry a coal miner’s son. Learning Objectives - Analyze the human and environmental consequences of Industrialization and the factory system in England. - Compare the lives of factory owners and workers in England during Industrialization. - Identify, explain, and assess the historic significance and impact of the new developments and trends in the aftermath of the Industrial Revolution. The rural pre-industrial work sphere was usually shaped by the father, who controlled the pace of work for his family. However, factories and mills undermined the old patriarchal authority to a certain extent. Factories put husbands, wives, and children under the same conditions and authority of the manufacturer masters. In the latter half of the Industrial Revolution, women could find employment on assembly lines, providing industrial laundry services, and in the textile mills that sprang up during the Industrial Revolution in such cities as Manchester, Leeds, and Birmingham. Spinning and winding wool, silk, and other types of piecework were a common way of earning income by working from home, but wages were very low and hours long. Often 14 hours per day were needed to earn enough to survive. Needlework was the single highest-paid occupation for women working from home, but the work paid little and women often had to rent sewing machines that they could not afford to buy. These home manufacturing industries became known as “sweated industries” (think of today’s sweat shops). The Select Committee of the House of Commons defined sweated industries in 1890 as “work carried on for inadequate wages and for excessive hours in unsanitary conditions.” By 1906, such workers earned about a penny an hour. Women were never paid the same wage as a man for the same work, despite the fact that they were as likely as men to be married and supporting children. Industrialization and Labor Organization The concentration of workers in factories, mines, and mills inspired the development of labor unions during the Industrial Revolution. After the initial decades of political hostility towards organized labor, skilled male workers emerged as the early beneficiaries of the labor movement. The rapid expansion of industrial society during the Industrial Revolution drew women, children, rural workers, and immigrants into the industrial work force in large numbers and in new roles. This pool of unskilled and semi-skilled labor spontaneously organized in fits and starts throughout the early phases of industrialization and would later provide an important arena for the development of trade unions. Trade unions have sometimes been seen as successors to the guilds of medieval Europe, although the relationship between the two is disputed as the masters of the guilds employed workers (apprentices and journeymen) who were not allowed to organize. The concentration of labor in mills, factories, and mines facilitated the organization of workers to help advance the interests of working people. A union could demand better terms by withdrawing all labor and causing a consequent cessation of production. Employers had to decide between giving in to the union demands at a cost to themselves or suffering the cost of the lost production. Skilled workers were hard to replace, and these were the first groups to successfully advance their conditions through this kind of bargaining. Learning Objectives - Analyze the human and environmental consequences of Industrialization and the factory system in England. - Compare the lives of factory owners and workers in England during Industrialization. - Identify, explain, and assess the historic significance and impact of the new developments and trends in the aftermath of the Industrial Revolution. Trade unions and collective bargaining were outlawed from no later than the middle of the 14th century when the Ordinance of Laborers was enacted in the Kingdom of England. As collective bargaining and early worker unions grew with the onset of the Industrial Revolution, the government began to clamp down on what it saw as the danger of popular unrest at the time of the Napoleonic Wars. In 1799, the Combination Act was passed, which banned trade unions and collective bargaining by British workers. Although the unions were subject to often severe repression until 1824, they were already widespread in some cities. Workplace militancy manifested itself in many different ways. For example, Luddites were a group of English textile workers and self-employed weavers who in the 19th century destroyed weaving machinery as a form of protest. The group was protesting the use of machinery to get around standard labor practices, fearing that the years they had spent learning the craft would go to waste and unskilled machine operators would rob them of their livelihoods. One of the first mass work strikes emerged in 1820 in Scotland, an event known today as the Radical War. 60,000 workers went on a general strike. Their demands went far beyond labor regulations and included a general call for reforms. The strike was quickly crushed by soldiers and police. Early Trade Unions By the 1810s, the first labor organizations to bring together workers of divergent occupations were formed. Possibly the first such union was the General Union of Trades, also known as the Philanthropic Society, founded in 1818 in Manchester. The latter name was to hide the organization’s real purpose in a time when trade unions were still illegal. Under the pressure of both workers and the middle- and upper-class activists sympathetic of the workers’ repeal, the law banning unions was repealed in 1824. However, the Combinations of Workmen Act 1825 severely restricted their activity. It prohibited trade unions from attempting to collectively bargain for better terms and conditions at work and suppressed the right to strike. That did not stop the fledgling labor movements and unions began forming rapidly. The first attempts at setting up a national general union were made in the 1820s and 1830s. The National Association for the Protection of Labor was established in 1830 by John Doherty, after an apparently unsuccessful attempt to create a similar national presence with the National Union of Cotton Spinners. The Association quickly enrolled approximately 150 unions, consisting mostly of textile workers, but also including mechanics, blacksmiths, and various others. Membership rose to between 10,000 and 20,000 individuals spread across the five counties of Lancashire, Cheshire, Derbyshire, Nottinghamshire, and Leicestershire within a year. To establish awareness and legitimacy, the union started the weekly Voice of the People publication, with the declared intention “to unite the productive classes of the community in one common bond of union.” In England, the members of the Friendly Society of Agricultural laborers became popular heroes, and 800,000 signatures were collected for their release. Their supporters organized a political march, one of the first successful marches in the UK, and all were pardoned on condition of good conduct in 1836. In 1834, Welsh socialist Robert Owen established the Grand National Consolidated Trades Union. The organization attracted a range of socialists from Owenites to revolutionaries and played a part in the protests after the Tolpuddle Martyrs’ case. In 1833, six men from Tolpuddle in Dorset founded the Friendly Society of Agricultural Laborers to protest against the gradual lowering of agricultural wages. The Tolpuddle laborers refused to work for less than 10 shillings a week; by this time wages had been reduced to seven shillings and would be further reduced to six. In 1834, James Frampton, a local landowner and magistrate, wrote to Home Secretary Lord Melbourne to complain about the union. As a result of obscure law that prohibited the swearing of secret oaths, six men were arrested, tried, found guilty, and transported to Australia—which treated as a penal colony. Owen’s union collapsed shortly afterwards. Early Political Developments Industrialization also contributed to political democratization in the industrializing West. This political democratization had begun in the West with the Enlightenment, with roots going back to the Scientific Revolution and the Protestant Reformation. Britain led the way with a succession of reforms which incrementally increased the number of men during the nineteenth century and women in the early twentieth century. Other industrial Western nations closely followed the British examples. Notably and remarkably the dominant European American political and economic elites in the United States denied the vote, among other rights of citizenship to African Americans to the late nineteenth century. Learning Objectives - Analyze the human and environmental consequences of Industrialization and the factory system in England. - Identify, explain, and assess the historic significance and impact of the new developments and trends in the aftermath of the Industrial Revolution. - Compare the new political and labor organizations with governmental responses to worker unrest. Key Terms / Key Concepts Chartism - organized movement led by English workers who advocated for improved labor conditions during the Industrial Revolution First, Second, and Third Reform Acts - a succession of British parliamentary electoral reforms during the nineteenth century that incrementally increased the number of men in England who were allowed to vote Cult of Domesticity - term for nineteenth-century system of gender subordination imposed on women, mostly in the middle and upper classes, in industrializing nations Chartism In the later 1830s and 1840s, trade unionism was overshadowed by political activity. Of particular importance was Chartism—a working-class movement for political reform in Britain that existed from 1838 to 1858. It took its name from the People’s Charter of 1838 and was a national protest movement, with particular strongholds of support in Northern England, the East Midlands, the Staffordshire Potteries, the Black Country, and the South Wales Valleys. Support for the movement was at its highest in 1839, 1842, and 1848, when petitions signed by millions of working people were presented to Parliament. The strategy used the scale of support demonstrated these petitions and the accompanying mass meetings to put pressure on politicians to concede manhood suffrage. Chartism thus relied on constitutional methods to secure its aims, although there were some who became involved in radical activities, notably in south Wales and Yorkshire. The government did not yield to any of the demands and suffrage had to wait another two decades. Chartism was popular among some trade unions, especially London’s tailors, shoemakers, carpenters, and masons. One reason was the fear of the influx of unskilled labor, especially in tailoring and shoe making. In Manchester and Glasgow, engineers were deeply involved in Chartist activities. Many trade unions were active in the general strike of 1842, which spread to 15 counties in England and Wales and eight in Scotland. Chartism taught techniques and political skills that inspired trade union leadership. Chartists saw themselves fighting against political corruption and for democracy in an industrial society, but they attracted support beyond the radical political groups for economic reasons, such as opposing wage cuts and unemployment. The First, Second, and Third Reform Acts The British Parliament led the way in industrial political democratization with three acts which progressively the number of men who could vote in British elections. The first act, passed in 1832, extended the vote to men in the middle classes and redistributed parliamentary seats on the basis of population changes that had occurred with industrial urbanization. The second act, passed in 1867, granted the vote to men in the urban working classes. These acts also gave rise to modern political parties in Britain which actively sought the support of voters by tayloring their policies and priorities to these voters. The third act, passed in 1884, extended the vote to men in the rural working classes. Other Western industrial nations similarly proceeded with political democratization. The United States, as a notable exception, denied the vote to African Americans in the U.S. until the late twentieth century, through statute and violence. The 1861-5 Confederate Rebellion in the southern states of the U.S. from Texas through Virginia sought to construct a new nation on the foundation of the chattel enslavement of African Americans. Connection to Women’s Rights Movements Women's rights advocates of the late 18th and early 19th centuries—such as Mary Wollstonecraft, Frances Wright, and Harriet Martineau in Britain—were widely accused of disrupting the natural order of things and condemned as unfeminine. “They are only semi-women, mental hermaphrodites,” wrote Henry F. Harrington in the Ladies' Companion. However, after the Jacksonian era (1812 to 1850) saw the expansion of voting rights to virtually all white males in the United States, many women believed it was their opportunity for increased civil liberties. Early feminist opposition to many of the values promoted by the Cult of Domesticity (especially concerning women's suffrage, political activism, and legal independence) culminated in the Seneca Falls Convention in 1848. This convention was the first national effort in the U.S. and one of the early national efforts in the West to contest the discrimination that underlay the Cult of Domesticity. The slow progress that women have had to endure in their efforts to end gender discrimination and repudiate the Cult of Domesticity since the Industrial Revolution illustrate the resilience of both. Attributions The 1851 image of the Crystal Palace in London is a lithograph produced by J. McNeven. Images courtesy of Wikipedia Commons Title Image - 1851 Crystal Palace interior print Attribution: J. McNeven, Public domain, via Wikimedia Commons. Provided by: Wikipedia. Location: https://commons.wikimedia.org/wiki/File:Crystal_Palace_-_interior.jpg. License: CC BY-SA: Attribution-ShareAlike Boundless World History "Social Change" Adapted from https://courses.lumenlearning.com/boundless-worldhistory/chapter/social-change/ CC licensed content, Shared previously - Curation and Revision. Provided by: Boundless.com. License: CC BY-SA: Attribution-ShareAlike CC licensed content, Specific attribution - Factory system. Provided by: Wikipedia. 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License: Public Domain: No Known Copyright	oercommons	2025-03-18T00:37:03.181065	Neil Greenwood	{ "license": "Creative Commons - Attribution - https://creativecommons.org/licenses/by/4.0/", "url": "https://oercommons.org/courseware/lesson/87933/overview", "title": "Statewide Dual Credit World History, European Imperialism and Crises 1871-1919 CE, Chapter 10: Enlightenment and Colonization, Social Consequences of Industrial Revolution in Europe", "author": "Anna McCollum" }
https://oercommons.org/courseware/lesson/87893/overview	The Development of the African Transatlantic Slave Trade Overview The Development of the African Transatlantic Slave Trade The advance of a world-wide market economy and capitalism provided a framework for the development of Transatlantic trade and the slave trade. Learning Objectives - Describe the factors that led to the development of the African Slave Trade in Europe, Americas, and Africa. Key Terms / Key Concepts - Mercantilism: an economic system consisting of a royal government controlling colonies abroad and overseeing trade and land-holdings at home. (The ultimate example of this system was the biggest owner of colonies that produced bullion: Spain.) - Triangle Trade: a trading system between Africa, the Americas, and Europe (Slaves from Africa were shipped to the New World to work on plantations. Raw goods—e.g. sugar, tobacco, cotton, coffee—were processed and shipped to Europe. Finished and manufactured goods were then shipped to Africa to exchange for slaves.) - Indentured Servants: Europeans who worked as slaves in the New World under contact for 4-7 years typically in exchange for passage across the Atlantic - Asiento System: direct slave trading contracts between the Spanish government and European merchants to sell slaves within the Spanish Empire in Latin America (This system broke up the Portuguese slave trade monopoly after 1580. The Dutch took advantage of these contracts to compete with the Portuguese and Spanish for direct access to African slave trading, and the British and French eventually followed.) Prelude to Trade Empires and Early Capitalism European society underwent a major change during the early modern period with regards to its outlook on wealth and property. Along with that change came the growth of a new kind of state and society, one not only defined by the growth of bureaucracy seen in absolutism but also in the power of the moneyed classes whose wealth was not predicated on owning land. The rise of that class to prominence in certain societies, especially those of the Netherlands and England, accompanied the birth of the most distinctly modern form of economics: capitalism. In the Middle Ages, wealth, land, and power were intimately connected. Nobles were defined by their ownership of land and by their participation in armed conflict. That changed by the early modern period, especially as it became increasingly common for monarchs to sell noble titles to generate money for the state. By the seventeenth century the European nobility were split between “nobles of the sword”—who inherited their titles from their warlike ancestors— and “nobles of the robe”—who had either been appointed by kings or purchased titles. Both categories of nobility were far more likely to be owners of land who exploited peasants than to be warriors. Among almost all of them, there was considerable contempt for merchants, who were often seen as parasites who undermined good Christian morality and the proper order of society. Even nobles of the robe, who had only joined the nobility within the last generation, tended to cultivate a practiced loathing for mere merchants, who they felt were socially inferior. In addition, the economic theory of the medieval period posited that there was a finite, limited amount of wealth in the world, and that the only thing that could be done to become wealthier was to get and hold on to more of it. In the medieval and even Renaissance-era mindset, the only forms of wealth were land and bullion (precious metals), and since there is only so much land and so much gold and silver out there, if one society grew richer, by definition every other society grew poorer. According to this finite resource mindset, kingdoms could only increase their wealth by seizing more territory, especially territory that would somehow increase the flow of precious metals into royal coffers. Trade was only important insofar as trade surpluses with other states could be maintained, thereby ensuring that more bullion was flowing into the economy than was flowing out. Colonies abroad provided raw materials and bullion itself. As a whole, this concept was called mercantilism: an economic system consisting of a royal government controlling colonies abroad and overseeing landholdings at home. The ultimate example of this system was the biggest owner of colonies that produced bullion: Spain. Mercantilism worked well enough, but commerce fit awkwardly into its paradigm. Trade was not thought to generate new wealth, since it did not directly dig up more silver or gold, nor did it seize wealth from other countries. Trade did not "make" anything according to the mercantilist outlook. Of all classes of society, bankers in particular were despised by traditional elites since they not only did not produce anything themselves but also profited off of the wealth of others. These attitudes started undergoing significant changes in the sixteenth and seventeenth centuries, mostly as a result of the incredible success of overseas corporations—groups that generated enormous wealth outside of the auspices of mercantilist theory. Many of the beneficiaries of the new wealth of the sixteenth and seventeenth centuries were not noblemen; they were instead wealthy merchant townsfolk, especially in places like the Dutch Republic and, later, England. These were men who amassed huge fortunes but did not fit neatly into the existing power structure of landholding nobles, the church, and the common people. These changes inspired an increasingly spirited battle over the rights of property, spurring the idea that not just land but wealth itself was something that the state should protect and encourage to grow. Early Capitalism The growth of commercial wealth was closely tied to the growth of overseas empires. The initial wave of European colonization (mostly in the Americas) had been driven by a search for gold and a desire to convert foreigners to Christianity. However, European powers came to pursue colonies and trade routes in the name of commodities and the wealth they generated by the seventeenth century. In this period of empire-building, European states sought additional territory and power overseas primarily for economic reasons. Because of the enormous wealth to be generated from not only gold and silver but also from commodities like sugar, tobacco, and coffee (as well as luxury commodities like spices that had always been important), the states of Europe were willing to war constantly among themselves as well as to perpetrate one of the greatest crimes in history: the Atlantic Slave Trade. In short, the seventeenth and eighteenth centuries the first phase of a system that would later be called capitalism arises— an economic system in which the exchange of commodities for profit generated wealth to be reinvested in the name of still greater profits. In turn, capitalism is dependent on governments that enforce legal systems that protect property and, historically, by wars with rivals that tried to carve out bigger chunks of the global market. To reiterate, capitalism was (and remains) a combination of two major economic and political phenomena: enterprises run explicitly for profit and a legal framework to protect and encourage the generation of profit. The pursuit of profit was nothing new, historically, but the political power enjoyed by merchants, the political focus on overseas expansion for profit, and the laws enacted to encourage these processes were new. Overseas Expansion in the Seventeenth and Eighteenth Centuries The development of early capitalism was intimately connected with overseas expansion. Europe was an important center of a truly global economy by the seventeenth century, and it was that economy that fueled the development of capitalistic, commercial societies in places like the Netherlands and England. While the original impulse behind overseas expansion during this period was primarily commercial—focusing on the search for commodities and profit, it was also a major political focus of all of the European powers by the eighteenth century. In other words, European elites actively sought not just to trade with overseas territories but also to conquer and control, both for profit and for their own political "glory" and aggrandizement. The result was a dramatic expansion of European influence or direct control in areas of the globe in which Europe had never before had an influence. In result, by 1800 roughly 35% of the globe was directly or indirectly controlled by European powers. Military technology and organization were key factors in this European global expansion. The early-modern military revolution (i.e. the evolution of gunpowder warfare during and after the Renaissance period) resulted in highly-trained soldiers with the most advanced military technology in the world by the late seventeenth centuries. As European powers expanded, they built fortresses in the modern style and defended them with cannons, muskets, and warships that often outmatched the military forces and technology they encountered. In the case of China, Japan, and the Philippines, for instance, local rulers learned that the easiest way to deal with European piracy was not to try to fight European ships, but instead to cut off trade with European merchants until restitution had been paid. European states also benefited from the relative political fragmentation of parts of the non-European world. There were powerful kingdoms and empires in Africa, the Middle East, and Asia that defied European attempts at hegemony, but much of the world was controlled by smaller states. A prime example is India. This region had become divided into dozens of small kingdoms, along with a few larger ones due to the decline of the Mughal Empire by the early eighteenth century. When the British and French began taking control of Indian territory, it was against the resistance of small Indian kingdoms, not some kind of (nonexistent) overall Indian state. An important note regarding European colonial power: this period saw the consolidation of European holdings in the New World and the beginning of empires in places like India, but it did not include major landholdings in Africa, the Middle East, or East Asia. In places with powerful states—China, the Ottoman Empire, and Japan—even the relative superiority of European arms was not sufficient to seize territory. Likewise, not only were African states able to successfully fight off Europeans as well, but African diseases made it impossible for large numbers of Europeans to colonize or occupy much African territory. As the Slave Trade burgeoned, Europeans did launch slave raids, but most slaves had been captured by African slavers who enjoyed enormous profits from the exchange. Likewise, European states and the corporations they supported worked diligently to establish monopolies on trade with various parts of the world. However, "monopolies" in this case only meant monopolies in trade going to and from Europe. There were enormous, established, and powerful networks of trade between Africa, India, South Asia, Southeast Asia, China, Japan, and the Pacific, all of which were dominated by non-European merchants. To cite one example, the Indian Ocean had served as an oceanic crossroads of trade between Africa and Asia for thousands of years. Europeans broke into those markets primarily by securing control of goods that made their way back to Europe rather than seizing control of intra-Asian or African trade routes, although they did try to dominate those routes when they could, and Europeans were able to seize at least some territories directly in the process. The Netherlands The Dutch were at the forefront of these changes. During their rebellion against Spain in the late sixteenth century, the Dutch began to look to revenue generated from trade as an economic lifeline. They served both as the middlemen in European commerce, shipping and selling things like timber from Russia, textiles from England, and wine from Germany. They also increasingly served as Europe’s bankers. The Dutch invented both formalized currency exchange and the stock market, both of which led to huge fortunes for Dutch merchants. A simple way to characterize the growth of Dutch commercial power was that the Netherlands replaced northern Italy as the heart of European trade after the Renaissance. In 1602, Dutch merchants, with the support of the state, created the world's first corporation: the Dutch East India Company (VOC in its Dutch acronym). It was created to serve as the republic's official trading company—a company with a legal monopoly to trade within a certain region: India and Southeast Asia. The VOC proved phenomenally successful in pushing out other European merchants in the Indies, through a combination of brute force and the careful deployment of legal strategies. A common approach was to offer “protection” from the supposedly more rapacious European powers, like Portugal, in return for trade monopolies from spice-producing regions. In many cases, the VOC simply used the promise of protection as a smokescreen for seizing complete control of a given area, especially in Indonesia which eventually became a Dutch colony. In other areas local rulers remained in political control but lost power over their own spice production and trade. For the better part of the seventeenth century, the Dutch controlled an enormous amount of the hugely profitable trade in luxury goods and spices from the East Indies as a result. The profits for Dutch merchants and investors were concomitantly high. As an example, above and beyond direct profits by individual members of the company, all stockholders in the VOC received dividends of 30% on their investments within the first ten years, in addition to a dramatic boost in value of the stocks themselves. The other states of Europe were both aghast at Dutch success and grudgingly admiring of it. In 1601, there were 100 more Dutch ships in the port of London at any given time than there were English ships, and by 1620 about half of all European merchant vessels were Dutch. In 1652, the Dutch seized control of the Cape of Good Hope at the southern tip of Africa, allowing them to control shipping going around Africa in route to Asia. They also exerted additional military force in the Indies to force native merchants to trade only with them and not other Europeans. The Dutch takeover of the Cape of Good Hope was the historical origin of the modern nation of South Africa; they were the first permanent European settlers. The Dutch were also the only European power allowed to keep a small trading colony in Japan, which was otherwise completely cut off to westerners after 1641 (thanks to a failed Portuguese-sponsored Christian uprising against the Japanese shogun). The iconic moment in the history of the Dutch golden age of early capitalism was the tulip craze of the 1620s – 1630s. Tulips grow well in the Netherlands and had long been cultivated for European elites. A tulip fad among Dutch elites in the 1620s drove up the price of tulip bulbs dramatically. Soon, enterprising merchants started buying and selling bulbs with no intention of planting them or even selling them to someone who would; they simply traded the bulbs as a valuable commodity unto themselves. In 1625, one bulb was sold for 5,000 guilders, about half the cost of a mansion in Amsterdam. However, the real height of the craze was the winter of 1636 – 1637, when individual bulbs sometimes changed hands ten times in a day for increasing profits. This was the equivalent of “flipping” bulbs; it had nothing to do with the actual tulips any longer. The element to emphasize is not just the seemingly irrational nature of the boom, but of the mindset: the Dutch moneyed classes were already embracing speculative market economies, in which the value of a given commodity has almost nothing to do with what it does, but instead from what people are willing to spend on it. In capitalist economies this phenomenon often leads to "bubbles" of rising values that then eventually collapse. In this case, the tulip craze did indeed come crashing down in the winter of 1637 – 1638, but in the meantime, it presaged the emergence of commodity speculation for centuries to come. The development of this early form of capitalism unquestionably originated in the Netherlands, but it spread from there. One by one, the other major states of Europe started to adopt Dutch methods of managing finances: sophisticated accounting, carefully organized tax policy, and an emphasis on hands-on knowledge of finances up to the highest levels of royal government. For example, Louis XIV insisted that his son study political economy and Colbert, Louis’ head of finance, wrote detailed instructions on how a king should oversee state finances. This was a significant change, since until the mid-seventeenth century at the earliest, to be a king was to refuse to dirty one’s hands with commerce. It was because of the incredible success of the Dutch that kings and nobles throughout Europe began to change their outlooks and values. Ultimately, at least among some kings and nobles in Western Europe, humanistic education and the traditional martial values of the nobility were combined with practical knowledge, or at least appreciation of mercantile techniques. Ultimately, the Dutch Golden Age was the seventeenth century. When the Netherlands was dragged into the wars initiated by Louis XIV toward the end of the seventeenth century, it spelled the beginning of the end for their dominance. The other states of Europe began to focus their own efforts on trade and were able to surpass Dutch efforts, although not their prosperity as the Netherlands has remained a resolutely prosperous country ever since. During that period, however, the Dutch had created a global trade network, proved that commercial dominance would play a crucial factor in political power in the future, and overseen a cultural blossoming of art and architecture. Britain and the Slave Trade Of the other European states, the British were the most successful at imitating the Dutch. In 1667 the British king Charles II officially designated the royal treasury as the coordinating body of British state finances and made sure it was overseen by officials trained in the Dutch style of political economy. The British parliament grew increasingly savvy with financial issues as well, having numerous debates about the best and most profitable use of state funds. In 1651, both to try to seize trade from the Dutch and to fend off Britain's traditional enemies—France and Spain, parliament passed the English Navigation Acts, which reserved commerce with English colonies for English ships. This, in turn, led to extensive piracy and conflict between the powers of Europe in their colonial territories, as they tried to seize profitable lands and enforce their respective monopolies. Ultimately, the British fought three wars with the Dutch, defeating them each time and, among other things, seizing the Dutch port of New Amsterdam in North America (which the English promptly renamed New York). Britain also fought Spain in both the seventeenth and eighteenth centuries, ultimately acquiring Jamaica and Florida as colonies. In terms of trade, the major prize, at least initially, was the Caribbean, due to its suitability for growing sugar. Sugar quickly became the colonial product, hugely valuable in Europe and relatively easy to cultivate compared to exotic products like spices, which were only available from Asian sources. And it was ultimately the profits of sugar that helped bankroll the British growth in power in the seventeenth and, especially, the eighteenth centuries. During this period, sugar consumption in Europe doubled every 25 years. The only efficient way to grow sugar was through proto-industrialized plantations with rendering facilities built to extract the raw sugar from sugar cane. That, in turn, required an enormous amount of back-breaking, dangerous labor. Most Native American slaves quickly died off or escaped and hence the Atlantic Slave Trade between Africa and the New World began in earnest by the early seventeenth century. The Slave Trade between Africa and the New World was, quite simply, one of the worst injustices of human history. Millions of people were ripped from their homeland, transported to a foreign continent in atrocious conditions, and either worked to death or murdered by their owners in the name of "discipline.” The contemporary North American perception of the life of slaves—that of incredibly difficult but not always lethal conditions of work—is largely inaccurate because only a small minority of slaves were ever sent to North America. The immense majority of slaves were instead sent to the Caribbean or Brazil, both areas in which working conditions were far worse than the (still abysmal) working conditions present in North America. Sugar was the major crop of the Caribbean and one of the major crops of Brazil. And the average life of a slave once introduced to sugar cultivation was seven years before he or she died from exhaustion or injury. In sum, most slaves were sent to be worked to death on sugar plantations. The slave trade was part of what historians have described as the “triangle trade” between Africa, the Americas, and Europe. Slaves from Africa were shipped to the New World to work on plantations. Raw goods—e.g. sugar, tobacco, cotton, coffee—were processed and shipped to Europe. Finished and manufactured goods were then shipped to Africa to exchange for slaves. This cycle of exchange grew decade-by-decade over the course of the seventeenth and eighteenth centuries. The leg of the triangle trade that connected Africa and the Americas was known as the Middle Passage because slave ships went directly across the middle of the Atlantic, most traveling to Brazil or the Caribbean, as noted above. Slaves on board ships were packed in so tightly they could not move for most of the voyage, with slave ship captains calculating into their profit margins the fact that a significant percentage of their human cargo would die in route. Over a million slaves died in the seventeenth and eighteenth centuries as a result of the Middle Passage. In turn, over 90% of the millions of slaves that were sent to the Caribbean or Brazil perished from exhaustion or injury while cultivating sugar and coffee, well as while mining in Brazil. This resulted in a demand for constant slave replacements. The Atlantic Slave Trade was the first time in history that slavery was specifically racial in character. Because it was Africans who were enslaved to work in the Americas under the control of Europeans, Europeans developed a range of racist theories to excuse the practice from its obvious immorality. In fact, the whole idea of human "race" is largely derived from the Slave Trade. Biologically, "race" is nothing more than a handful of unimportant cosmetic differences between people, but thanks to the history of the enslavement of Africans, Europeans in the early modern period led the charge in describing "race" as some kind of fundamental human category, with some races supposedly enjoying "natural" superiority. That conceit would obviously cast a perverse shadow on the present. The Enslavement of Africans The transatlantic slave trade was the largest long-distance coerced movement of people in history and, prior to the mid-nineteenth century, formed the major demographic well-spring for the re-peopling of the Americas following the collapse of the Amerindian population. Cumulatively, as late as 1820, nearly four Africans had crossed the Atlantic for every European, and, given the differences in the sex ratios between European and African migrant streams, about four out of every five females that traversed the Atlantic were from Africa. The Atlantic Ocean was once a formidable barrier that prevented regular interaction between those peoples inhabiting the four continents it touched; beginning in the late fifteenth century, it became a commercial highway that integrated the histories of Africa, Europe, and the Americas for the first time. As the above figures suggest, slavery and the slave trade were the linchpins of this process. With the decline of the Amerindian population, labor from Africa formed the basis for the exploitation of the gold and agricultural resources from the Americas, with sugar plantations absorbing well over two thirds of slaves carried across the Atlantic by the major European and Euro-American powers. For several centuries slaves were the most important reason for contact between Europeans and Africans. European expansion to the Americas mainly affected tropical and semi-tropical areas. Several products that were either previously unknown to Europeans (like tobacco) or previously had been a luxury for Europeans (like gold or sugar) could be now obtained by Europeans in abundant amounts. But while Europeans could control the production of such exotic goods, it became apparent in the first two centuries after 1500 that they chose not to supply the labor that would make such output possible. Free European migrants and indentured servants never traveled across the Atlantic in sufficient numbers to meet the labor needs of expanding plantations. Convicts and prisoners—the only Europeans who were ever forced to migrate—were too few in number. Slavery or some form of coerced labor was the only possible option if European consumers were to gain access to more tropical produce and precious metals. Europeans came rely on Africans as slaves due to the different values of societies around the Atlantic and, more particularly, the way groups of people involved in creating a trans-Atlantic community saw themselves in relation to others. In short, how they defined their identity. Ocean-going technology brought Europeans into large-scale face-to-face contact with peoples who were culturally and physically more different from themselves than any others with whom they had interacted in the previous millennium. In neither Africa nor Asia could Europeans initially threaten territorial control, with the single and limited exception of western Angola. African capacity to resist Europeans ensured that sugar plantations were established in the Americas rather than in Africa. But if Africans, aided by tropical pathogens, were able to resist the potential European invaders, some Africans were prepared to sell slaves to Europeans for use in the Americas. As this suggests, European domination of Amerindians was complete. Indeed, from the European perspective it was much too complete. The epidemic diseases of the Old World destroyed not only native American societies, but also a potential labor supply. Every society in history before 1900 provided at least an unthinking answer to the question of which groups are to be considered eligible for enslavement, and normally they did not recruit heavily from their own community. A revolution in ocean-going technology gave Europeans the ability to get continuous access to remote peoples and move them against their will over very long distances. Strikingly, it was much cheaper to obtain slaves in Europe than to send a vessel to the coast of Africa without proper harbors and remote from European political, financial, and military power. That this option was never seriously considered suggests a European inability to enslave other Europeans. Except for a few social deviants, neither Africans nor Europeans would enslave members of their own societies, but in the early modern period, Africans had a somewhat narrower conception of who was eligible for enslavement than Europeans had. It was this difference in definitions of eligibility for enslavement which explains the dramatic rise of the trans-Atlantic slave trade. Slavery, which had disappeared from northwest Europe long before this point, exploded into a far greater significance and intensity than it had possessed at any point in human history. The major cause was a dissonance in African and European ideas of eligibility for enslavement at the root of which lies culture or societal norms, not easily tied to economics. Without this dissonance, there would have been no African slavery in the Americas. Europeans shared a common Christian identity that discouraged them from enslaving fellow European believers, whereas African peoples were divided into diverse religions and cultures, who were willing to enslave peoples of opposing cultures. The slave trade was thus a product of differing constructions of social identity and the ocean-going technology that brought Atlantic societies into sudden contact with each other. The trans-Atlantic slave trade grew from a strong, initially European, demand for labor in the Americas, driven by consumers of plantation produce and precious metals. Because Amerindians died in large numbers, and insufficient numbers of Europeans were prepared to cross the Atlantic, the form that this demand took was shaped by conceptions of social identity on four continents, which ensured that the labor would comprise mainly slaves from Africa. But the central question of which peoples from Africa went to a given region of the Americas, and which group of Europeans or their descendants organized such a movement, cannot be answered without an understanding of the wind and ocean currents of the North and South Atlantic. There are two systems of wind and ocean currents in the North and South Atlantic that follow the pattern of giant wheels—one lies north of the equator turns clockwise, while its counterpart to the south turns counterclockwise. The northern wheel largely shaped the north European slave trade and was dominated by the English. The southern wheel shaped the huge traffic to Brazil, which for three centuries was almost the almost exclusive preserve of the largest slave traders of all, the Portuguese. Despite their use of the Portuguese flag, slave traders using the southern wheel ran their business from ports in Brazil, not in Portugal. Winds and currents thus ensured two major slave trades: the first rooted in Europe, the second in Brazil. Winds and currents also ensured that Africans carried to Brazil came overwhelmingly from Angola, with south-east Africa and the Bight of Benin playing smaller roles. Africans carried to North America, including the Caribbean, left from mainly West Africa, with the Bights of Biafra and Benin and the Gold Coast predominating. Just as Brazil overlapped on the northern system by drawing on the Bight of Benin, some slaves from northern Angola were carried into the Caribbean by the English, French, and Dutch. Early Slaving Voyages The first Africans forced to work in the New World left from Europe at the beginning of the sixteenth century, not from Africa. There were few vessels that carried only slaves on this early route, so that most would have crossed the Atlantic in smaller groups on vessels carrying many other commodities, rather than dedicated slave ships. Such a slave route was possible because an extensive traffic in African slaves from Africa to Europe and the Atlantic islands had existed for half a century before Columbian contact, such that ten percent of the population of Lisbon was black in 1455, and black slaves were common on large estates in the Portuguese Algarve. The first slave voyage direct from Africa to the Americas probably sailed in 1526. Before mid-century, all transatlantic slave ships sold their slaves in the Spanish Caribbean, with the gold mines in Cibao on Hispaniola emerging as a major purchaser. Cartagena, in modern Columbia, appears as the first mainland Spanish American destination for a slave vessel, which landed in the year 1549. On the African side, the great majority of people entering the early slave trade came from the Upper Guinea coast, and moved through Portuguese factories initially in Arguim, and later the Cape Verde islands. Nevertheless, the 1526 voyage set out from the other major Portuguese factory in West Africa—Sao Tome in the Bight of Biafra—though the slaves almost certainly originated in the Congo. The slave traffic to Brazil, eventually accounting for about forty percent of the trade, got underway around 1560. Sugar drove this traffic, as Africans gradually replaced the Amerindian labor force on which the early sugar mills (called engenhos) had depended from 1560 to 1620. By the time the Dutch invaded Brazil in 1630, Pernambuco, Bahia, and Rio de Janeiro were supplying almost all of the sugar consumed in Europe, and almost all the slaves producing it were African. Consistent with the earlier discussion of Atlantic wind and ocean currents, there were two major branches of the trans-Atlantic slave trade operating by 1640: one to Brazil, and the other to the mainland Spanish Americas. Together they accounted for less than 7,500 departures a year from the whole of sub-Saharan Africa, almost all of them by 1600 from west-central Africa. The sugar complex spread to the eastern Caribbean from the beginning of the 1640s. Sugar consumption steadily increased in Europe, and the slave system began two centuries of westward expansion across tropical and sub-tropical North America. At the end of the seventeenth century, gold discoveries in first Minas Gerais, and later in Goias and other parts of Brazil, began a transformation of the slave trade which triggered further expansion of the business. In Africa, the Bights of Benin and Biafra became major sources of supply, in addition to Angola, and were joined later by the more marginal provenance zones of Sierra Leone, the Windward Coast, and South-east Africa. The volume of slaves carried off reached thirty thousand per annum in the 1690s and eighty-five thousand a century later. More than eight out of ten Africans pulled into the traffic in the era of the slave trade made their journeys in the century and a half after 1700. Establishing the Trade In the fifteenth century, Portugal became the first European nation to take significant part in African slave trading. The Portuguese primarily acquired slaves for labor on Atlantic African island plantations, and later for plantations in Brazil and the Caribbean, though they also sent a small number to Europe. Initially, Portuguese explorers attempted to acquire African labor through direct raids along the coast, but they found that these attacks were costly and often ineffective against West and Central African military strategies. For example, in 1444, Portuguese marauders arrived in Senegal ready to assault and capture Africans using armor, swords, and deep-sea vessels. But the Portuguese discovered that the Senegalese outmaneuvered their ships using light, shallow water vessels better suited to the estuaries of the Senegalese coast. In addition, the Senegalese fought with poison arrows that slipped through their armor and decimated the Portuguese soldiers. Subsequently, Portuguese traders generally abandoned direct combat and established commercial relations with West and Central African leaders, who agreed to sell slaves taken from various African wars or domestic trading, as well as gold and other commodities, in exchange for European and North African goods. Over time, the Portuguese developed additional slave trade partnerships with African leaders along the West and Central African coast and claimed a monopoly over these relationships, which initially limited access to the trade for other western European competitors. Despite Portuguese claims, African leaders enforced their own local laws and customs in negotiating trade relations. Many welcomed additional trade with Europeans from other nations. The Portuguese developed a trading relationship with the Kingdom of Kongo, which existed from the fourteenth to the nineteenth centuries in what is now Angola and the Democratic Republic of Congo. Civil War within Kongo during the trans-Atlantic slave trade would lead to many of its subjects becoming captives traded to the Portuguese. When Portuguese, and later their European competitors, found that peaceful commercial relations alone did not generate enough enslaved Africans to fill the growing demands of the trans-Atlantic slave trade, they formed military alliances with certain African groups against their enemies. This encouraged more extensive warfare to produce captives for trading. While European-backed Africans had their own political or economic reasons for fighting with other African enemies, the end result for European traders in these military alliances was greater access to enslaved war captives. To a lesser extent, Europeans also pursued African colonization to secure access to slaves and other goods. For example, the Portuguese colonized portions of Angola in 1571 with the help of military alliances from Kongo, but were pushed out in 1591 by their former allies. Throughout this early period, African leaders and European competitors ultimately prevented these attempts at African colonization from becoming as extensive as in the Americas. The Portuguese dominated the early trans-Atlantic slave trade on the African coast in the sixteenth century. As a result, other European nations first gained access to enslaved Africans through privateering during wars with the Portuguese, rather than through direct trade. When English, Dutch, or French privateers captured Portuguese ships during Atlantic maritime conflicts, they often found enslaved Africans on these ships, as well as Atlantic trade goods, and they sent these captives to work in their own colonies. In this way, privateering generated a market interest in the trans-Atlantic slave trade across European colonies in the Americas. After Portugal temporarily united with Spain in 1580, the Spanish broke up the Portuguese slave trade monopoly by offering direct slave trading contracts to other European merchants. Known as the Asiento system, the Dutch took advantage of these contracts to compete with the Portuguese and Spanish for direct access to African slave trading, and the British and French eventually followed. By the eighteenth century, when the trans-Atlantic slave trade reached its trafficking peak, the British (followed by the French and Portuguese) had become the largest carriers of enslaved Africans across the Atlantic. The overwhelming majority of enslaved Africans went to plantations in Brazil and the Caribbean, and a smaller percentage went to North America and other parts of South and Central America. Empire and Slavery In the second half of the eighteenth century six imperial systems straddled the Atlantic, each one sustained by a slave trade. The English, French, Portuguese, Spanish, Dutch, and Danish all operated behind trade barriers (termed mercantilistic restrictions) and produced a range of plantation produce: sugar, rice, indigo, coffee, tobacco, alcohol, and some precious metals, with sugar usually being the most valuable. It is extraordinary that consumers’ pursuit of this limited range of exotic consumer goods, which collectively added so little to human welfare, could have generated the horrors and misery of the Middle Passage and plantation slavery for so long. Given the dominance of Portuguese and British slave traders, it is not surprising that Brazil and the British Americas received the most Africans, though both nations became adept at supplying foreign slave systems as well. Throughout the slave trade, more than seven out of every ten slaves went to these regions. The French Americas imported about half the slaves that the British did, with the majority going to Saint-Domingue. The Spanish flag, which dominated in the earliest phase of the trade before retreating in the face of competition, began to expand again in the late nineteenth century with the growth of the Cuban sugar economy. By the next century—between 1750 and 1850—every one of these empires had either disappeared or become severely truncated. A massive shift to freer trade meant that, instead of six plantation empires controlled from Europe, there were now only three plantation complexes: two of which—Brazil and the United States—were independent, and the third, Cuba, was far wealthier and more dynamic than its European owner. Extreme specialization led to the United States producing most of the world’s cotton, Cuba most of the world’s sugar, and Brazil with a similar dominance in coffee. Slaves thus might disembark in six separate jurisdictions in the Americas in the eighteenth century. But by 1850 they went overwhelmingly to only two areas: Brazil and Cuba. American cotton planters drew on Africa for almost none of their labor needs, relying instead on natural population growth and a domestic slave trade. Indeed, overall the United States absorbed only 5 percent of the slaves arriving in the Americas. This massive reorganization of the traffic and the rapid natural growth of the US slave population had little immediate impact on the size of the slave trade. The British, Americans, Danish, and Dutch dropped out of the slave trade, but the decade 1821 to 1830 still saw over 80,000 people a year leaving Africa in slave ships. Well over a million more—one tenth of the volume carried off in the slave trade era—followed in the next twenty years. The Transatlantic Slave Trade The African Slave Trade involved interaction of different peoples fron Europe, Africa, and the Americas. Learning Objectives - Describe the factors that led to the delevlopment of the African Slave Trade in Europe, Americas, and Africa Key Terms / Key Concepts Yemasee War: A conflict between English colonists and the indigenous Yemasee people (1715 -1717) that arose due to the enslavement of the Yemasee by colonial slave traders. Dahomey: An African kingdom in West Africa that grew wealthy on the Transatlantic slave trade in the 18th century. Black Caribs: Peoples on the island of St. Vincent in the Caribbean where Africans intermarried and adopted the culture of the indigenous Carib people. The Transatlantic Slave Trade The emergence of Trans-Atlantic Slave trade overlaps with other important historical developments of the Early Modern World: the growth of capitalism and the Age of Exploration. Due to the demand in European markets for luxury goods from distant lands, merchants desired to obtain these commodities such as tobacco and sugar, which were cultivated in the newly discovered lands of the Western Hemisphere. However, epidemic diseases, introduced by the Columbian Exchange that accompanied the Age of Exploration, had decimated the indigenous population. There was thus a severe shortage of labor across the Western Hemisphere. To meet the demand for labor, slave traders exported African slaves across the Atlantic to the colonies of the New World in large numbers beginning in the 16th century. In the English colonies of Barbados, Virginia, Carolina, and Maryland in North America in the 17th century, European indentured servants and enslaved natives at first served primarily as the labor force. However, the enslavement of natives resulted in costly wars between native tribes and the colonists (Yemassee War -1715-1717) and indentured servants had to be set free after an contractually agreed period (usually 4 -7 years). Consequently, by the early 18th century African slaves had become the primary labor force in these colonies as well. What was the Trans-Atlantic Slave Trade? The Trans-Atlantic slave trade was a flourishing business in world trade from the 16th through the 19th century. Although the term ‘African’ can refer to any native of the African continent, the African peoples enslaved and exported across the Atlantic largely inhabited west central and east central Africa in what is the modern nations of Nigeria, Angola and Mozambique. The enslavement and sale of slaves was a business operation that required the cooperation of European and African agents. Africans did not hesitate to sell other Africans into slavery. For example, the kingdom of Dahomey in West Africa in the 18th century conducted raids and wars against neighboring peoples to secure a steady supply of slaves to sell to European slave traders. Likewise, Scandinavian Vikings in the 9th century CE had no qualms about enslaving European Slavs in what is today Russia and selling them to Muslim slave traders. African Muslims did object to enslaving African Muslims, but the Muslim Fulani people (modern northern Nigeria) would enslave the non-Muslim Igbo and Yoruba peoples (modern southern Nigeria) into slavery. Likewise, European slave traders justified their actions because the enslaved Africans were not Christians. The Transatlantic slave trade was also a risky venture. Slave traders in crossing the Atlantic, limited the number of adult males in their cargoes and transported a majority of woman and children since they feared slave uprisings on their ships. Once successfully transported and sold in the Western Hemisphere, African slaves escaped and formed new independent communities in areas where the control of colonial authorities was weak or non-existent, such as the Black Caribs of St Vincent in the Caribbean, the Maroons in the interior highlands of Jamaica, the Quillombos of Brazil, and the Angola community in Spanish Florida. Enslaved Africans also rose up violently in open rebellion against their owners, such as the Stono Rebellion in South Carolina (1739), the Nat Turner Rebellion in Virginia (1831), and the so-called “Baptist War” in Jamaica (1831). The massive slave rebellion on the French colony of Saint-Domingue (1791) resulted ultimately in the creation of the independent republic of Haiti in 1804. The experience of enslaved Africans in the Western Hemisphere also varied from region to region. Across much of Latin America and the Caribbean, slave owners often freed their African slaves or their children after the Roman Catholic Church baptized these slaves as Christians. Consequently, slave traders constantly imported new slaves from Africa into these regions. Children born from the unions of slave owners and slave women were also free. In the English North American colonies and later the United States, however, slave owners rarely freed their slaves even when these slaves converted to the Christian faith, and children born from enslaved women largely remained slaves even if their fathers were slave owners. Consequently, the slave population continued to expand in the United States even after the United States banned the import of African slaves in 1807. Even though the sale and ownership of slaves was a risky and dangerous business investment, the enslavement and transportation of an estimated 12 million Africans to the Western Hemisphere over three centuries is a testament to the power of the profit motive in a capitalist system. Attributions Title Image Illustration in anti-slavery book by Blake, William, 1860 - Internet Archive Book Images, No restrictions, via Wikimedia Commons Adapted from: http://creativecommons.org/licenses/by-nc-sa/3.0/us/ https://guides.hostos.cuny.edu/lac118/3-1 http://creativecommons.org/licenses/by-nc/4.0/ https://courses.lumenlearning.com/atd-tcc-worldciv2/chapter/the-transatlantic-slave-trade-2/ https://creativecommons.org/licenses/by-nc-nd/4.0/	oercommons	2025-03-18T00:37:03.229698	Neil Greenwood	{ "license": "Creative Commons - Attribution - https://creativecommons.org/licenses/by/4.0/", "url": "https://oercommons.org/courseware/lesson/87893/overview", "title": "Statewide Dual Credit World History, The Making of Early Modern World 1450-1700 CE, Chapter 6: Exploration, The Development of the African Transatlantic Slave Trade", "author": "Anna McCollum" }
https://oercommons.org/courseware/lesson/87915/overview	The American Revolution Overview The American Revolution The American Revolution can be seen as a succession of misunderstandings exacerbated by stubbornness on both sides. The 1763 Treaty of Paris, which ended the French and Indian War, set the stage for the Revolution by leaving the British empire with a large national debt, the price for obtaining New France and half of Louisiana, the French colonies in North America. Parliament proceeded to impose taxes indirectly on residents of British North America in order to reduce the debts from the British war effort. Many members of the Parliament saw these taxes as a reasonable recompence from the North American colonists for protection from the French by the British Army and Navy. The colonists came to see these taxes as violations of their rights as English subjects, specifically the right to not be taxed unless represented in Parliament. The Revolution inspired a succession of dissatisfied populations across the world through the twentieth century to initiate their own revolutions. Learning Objective - Analyze the causes, main events, and results of the American Revolution. Key Terms / Key Concepts 1763 Treaty of Paris: treaty that ended the French and Indian War and paved the way for the disputes at the heart of the American Revolution Stamp Act: indirect tax imposed on Thirteen Colonies, which helped to ignite the Revolution Boston Massacre - 5 March 1770 confrontation between British soldiers and Bostonians, in which five Bostonians were killed, exacerbating tensions between the British government and colonists Battles of Lexington and Concord - first battles of the Revolutionary War George Washington - commander of the Continental Army Common Sense - essay published in early 1776 arguing for the national independence of the Thirteen Colonies Thomas Jefferson - author of the Declaration of Independence Declaration of Independence: official declaration by the Second Continental Congress of the independence from the British empire of the thirteen colonies In 1763 – 4 Parliament set the stage for the Revolution by enacting a series of taxes and regulations on the British North American colonists. The British government saw these taxes as necessary to reduce the British imperial debt, which included the cost of protecting the colonies. These acts angered a number of colonists. The Stamp Act, which imposed an indirect tax on the colonists, provoked the greatest rage. And this rage manifested itself in protests, attacks on British officials in the colonies, and economic boycotts. Parliament responded to the protests and attacks by sending more troops to restore order in the colonies, as well as to the economic boycotts by repealing the Stamp Act. Parliament’s repeal of the Stamp Act was a response to the pleas of British merchants, who were losing money as a result of the colonial boycotts. Many colonists who protested the Stamp Act mistakenly concluded that they had forced Parliament to repeal this act, which reinforced their belief that violence was the way to force Parliament to act. One group in particular, the Sons of Liberty, felt violence was the preferred reaction to British taxes and restrictions. They believed they could compel Parliament to bend to their collective will. However, violence by the Sons of Liberty, among other groups and individuals, hardened the resolve of many in Parliament to restore order in the colonies. In 1767 Parliament imposed new indirect taxes on the colonists that would be collected outside of the colonies instead of in the colonies, thus not leaving British officials vulnerable to colonists’ attacks. Colonists renewed their protests, including more violence. The violence prompted the British government to send more troops to the Thirteen Colonies, which further enflamed the situation between the British Government and colonists angry about British government restrictions and taxes. The presence of British troops in the colonies, there to preserve or restore order, provoked numerous incidents of violence between colonists and British soldiers. The most famous incident was the 5 March 1770 Boston Massacre, in which British soldiers fired into a group of Bostonians who had attacked the soldiers. This incident raised related issues, including where and how the soldiers involved in crimes against citizens should be tried. The results of the trials involving the British soldiers indicted for killing five Bostonians raised questions in the minds of many of colonists about being able to get justice in the British imperial court systems. After several years of relative quiet another incident in Boston, the Boston Tea Party, ignited several events that eventually led to the outbreak of the Revolutionary War and then the Second Continental Congress’ declaration of independence for the Thirteen Colonies. Parliament responded to this protest of the 1773 Tea Act by imposing new restrictions on Massachusetts and Boston. These restrictions prompted colonial leaders to convene the First Continental Congress—the first intercolonial assembly to address the situation with the British government. Colonists protested British actions in a variety of ways and through a variety of groups with no centralized leadership until 1774. In response to what they saw as British violations of their rights as English subjects colonists started organizing local militias and collecting arms in community arms depots. In April 1775 British troops from Boston marched on Concord, Massachusetts to confiscate the arms at a colonial arms depot; this led to fighting with Massachusetts colonial militia at Lexington and Concord, west of Boston. These Battles of Lexington and Concord mark the beginning of the Revolutionary War. Ironically, the Revolutionary War prompted many colonists to consider national independence as the only way to protect their rights as English subjects. Support for national independence grew over the rest of 1775 and the first half of 1776, reinforced by the June 1775 Battle of Bunker Hill. The Second Continental Congress, the successor to the First Continental Congress, had convened in May 1775. Over the rest of 1775 this body created a Continental Army, named George Washington as its commander, and created a Continental Navy, before creating the U.S. The British Army’s employment of Hessian soldiers and the early 1776 publication of Common Sense by Thomas Paine attracted more colonists to the goal of national independence. In the spring of 1776, the Second Continental Congress commissioned a committee to write the Declaration of Independence. Thomas Jefferson agreed to write it. Jefferson wrote the Declaration of Independence as a synthesis of Enlightenment ideas and English political traditions, in which he asserted the right of a people to declare independence from a government that did not serve them well. In it, he listed colonists’ complaints against the British government, embodied in the person of King George III. The Declaration of Independence is a declaration of national independence for the Thirteen Colonies. Although it subsequently inspired a succession of movements to abolish various forms of racial, ethnic, religious, and gender discrimination, it only explicitly addressed national sovereignty. Ironically, French government assistance to the U.S. in pursuit of French imperial and strategic interests, including retaking territory lost to Britain and Spain in the French and Indian War, gained the French empire nothing and exposed people in France to revolutionary ideas that contributed to the revolution that brought down the French monarchy a little over a decade later. The ancien regime monarchy of France had hoped to regain territory lost to Britain and Spain in the 1763 Treaty of Paris that ended the French and Indian War, the British name for the North American counterpart to the Seven Years. Instead the commitment of resources, men, and ships to the U.S. cause by the French government, much more like the British government than the republican government of the U.S., exacerbated the French debt, setting off a chain of events that led to the French Revolution and, eventually, the overthrow of the French monarchy. Ultimately, the 1763 Treaty of Paris that ended the French and Indian War was the catalyst for the American and the French Revolutions, and, by extension, subsequent revolutions in the Americas, Eurasia, and Africa, among numerous other movements to eliminate various forms of discrimination all the way to the present. The American Revolution occurred in the context of new ideas about sovereignty articulated as part of the Enlightenment. The Declaration of Independence became a model for subsequent struggles for national independence in the Americas and for personal sovereignty and constitutional government in Europe into the twentieth century. The United States’ successful achievement of national independence inspired a succession of revolutions, both successful and unsuccessful, that continue to the present time. Ironically, the Declaration of Independence was written by a slaveholder and affirmed by the Second Continental Congress, the majority of whose members were also slaveholders. Primary Sources: Declaration of Independence Declaration of Independence, July 4, 1776 When in the course of human events, it becomes necessary for one people to dissolve the political bands which have connected them with another, and to assume among the powers of the earth, the separate and equal station to which the laws of nature and of nature's God entitle them, a decent respect to the opinions of mankind requires that they should declare the causes which impel them to the separation. We hold these truths to be self-evident: That all men are created equal; that they are endowed by their Creator with certain unalienable rights; that among these are life, liberty, and the pursuit of happiness; that, to secure these rights, governments are instituted among men, deriving their just powers from the consent of the governed; that whenever any form of government becomes destructive of these ends, it is the right of the people to alter or to abolish it, and to institute new government, laying its foundation on such principles, and organizing its powers in such form, as to them shall seem most likely to effect their safety and happiness. Prudence, indeed, will dictate that governments long established should not be changed for light and transient causes; and accordingly all experience hath shown that mankind are more disposed to suffer, while evils are sufferable than to right themselves by abolishing the forms to which they are accustomed. But when a long train of abuses and usurpations, pursuing invariably the same object, evinces a design to reduce them under absolute despotism, it is their right, it is their duty, to throw off such government, and to provide new guards for their future security. Such has been the patient sufferance of these colonies; and such is now the necessity which constrains them to alter their former systems of government. The history of the present King of Great Britain is a history of repeated injuries and usurpations, all having in direct object the establishment of an absolute tyranny over these states. To prove this, let facts be submitted to a candid world. He has refused his assent to laws, the most wholesome and necessary for the public good. He has forbidden his governors to pass laws of immediate and pressing importance, unless suspended in their operation till his assent should be obtained; and, when so suspended, he has utterly neglected to attend to them. He has refused to pass other laws for the accommodation of large districts of people, unless those people would relinquish the right of representation in the legislature, a right inestimable to them, and formidable to tyrants only. He has called together legislative bodies at places unusual uncomfortable, and distant from the depository of their public records, for the sole purpose of fatiguing them into compliance with his measures. He has dissolved representative houses repeatedly, for opposing, with manly firmness, his invasions on the rights of the people. He has refused for a long time, after such dissolutions, to cause others to be elected; whereby the legislative powers, incapable of annihilation, have returned to the people at large for their exercise; the state remaining, in the mean time, exposed to all the dangers of invasions from without and convulsions within. He has endeavored to prevent the population of these states; for that purpose obstructing the laws for naturalization of foreigners; refusing to pass others to encourage their migration hither, and raising the conditions of new appropriations of lands. He has obstructed the administration of justice, by refusing his assent to laws for establishing judiciary powers. He has made judges dependent on his will alone, for the tenure of their offices, and the amount and payment of their salaries. He has erected a multitude of new offices, and sent hither swarms of officers to harass our people and eat out their substance. He has kept among us, in times of peace, standing armies, without the consent of our legislatures. He has affected to render the military independent of, and superior to, the civil power. He has combined with others to subject us to a jurisdiction foreign to our Constitution and unacknowledged by our laws, giving his assent to their acts of pretended legislation: For quartering large bodies of armed troops among us; For protecting them, by a mock trial, from punishment for any murders which they should commit on the inhabitants of these states; For cutting off our trade with all parts of the world; For imposing taxes on us without our consent; For depriving us, in many cases, of the benefits of trial by jury; For transporting us beyond seas, to be tried for pretended offenses; For abolishing the free system of English laws in a neighboring province, establishing therein an arbitrary government, and enlarging its boundaries, so as to render it at once an example and fit instrument for introducing the same absolute rule into these colonies; For taking away our charters, abolishing our most valuable laws, and altering fundamentally the forms of our governments; For suspending our own legislatures, and declaring themselves invested with power to legislate for us in all cases whatsoever. He has abdicated government here, by declaring us out of his protection and waging war against us. He has plundered our seas, ravaged our coasts, burned our towns, and destroyed the lives of our people. He is at this time transporting large armies of foreign mercenaries to complete the works of death, desolation, and tyranny already begun with circumstances of cruelty and perfidy scarcely paralleled in the most barbarous ages, and totally unworthy the head of a civilized nation. He has constrained our fellow-citizens, taken captive on the high seas, to bear arms against their country, to become the executioners of their friends and brethren, or to fall themselves by their hands. He has excited domestic insurrection among us, and has endeavored to bring on the inhabitants of our frontiers the merciless Indian savages, whose known rule of warfare is an undistinguished destruction of all ages, sexes, and conditions. In every stage of these oppressions we have petitioned for redress in the most humble terms; our repeated petitions have been answered only by repeated injury. A prince, whose character is thus marked by every act which may define a tyrant, is unfit to be the ruler of a free people. Nor have we been wanting in our attentions to our British brethren. We have warned them, from time to time, of attempts by their legislature to extend an unwarrantable jurisdiction over us. We have reminded them of the circumstances of our emigration and settlement here. We have appealed to their native justice and magnanimity; and we have conjured them, by the ties of our common kindred, to disavow these usurpations which would inevitably interrupt our connections and correspondence. They too, have been deaf to the voice of justice and of consanguinity. We must, therefore, acquiesce in the necessity which denounces our separation, and hold them as we hold the rest of mankind, enemies in war, in peace friends. We, therefore, the representatives of the United States of America, in General Congress assembled, appealing to the Supreme Judge of the world for the rectitude of our intentions, do, in the name and by the authority of the good people of these colonies solemnly publish and declare, That these United Colonies are, and of right ought to be, FREE AND INDEPENDENT STATES; that they are absolved from all allegiance to the British crown and that all political connection between them and the state of Great Britain is, and ought to be, totally dissolved; and that, as free and independent states, they have full power to levy war, conclude peace, contract alliances, establish commerce, and do all other acts and things which independent states may of right do. And for the support of this declaration, with a firm reliance on the protection of Divine Providence, we mutually pledge to each other our lives, our fortunes, and our sacred honor. [Signed by] JOHN HANCOCK [President] New Hampshire JOSIAH BARTLETT, WM. WHIPPLE, MATTHEW THORNTON. Massachusetts Bay SAML. ADAMS, JOHN ADAMS, ROBT. TREAT PAINE, ELBRIDGE GERRY Rhode Island STEP. HOPKINS, WILLIAM ELLERY. Connecticut ROGER SHERMAN, SAM'EL HUNTINGTON, WM. WILLIAMS, OLIVER WOLCOTT. New York WM. FLOYD, PHIL. LIVINGSTON, FRANS. LEWIS, LEWIS MORRIS. New Jersey RICHD. STOCKTON, JNO. WITHERSPOON, FRAS. HOPKINSON, JOHN HART, ABRA. CLARK. Pennsylvania ROBT. MORRIS BENJAMIN RUSH, BENJA. FRANKLIN, JOHN MORTON, GEO. CLYMER, JAS. SMITH, GEO. TAYLOR, JAMES WILSON, GEO. ROSS. Delaware CAESAR RODNEY, GEO. READ, THO. M'KEAN. Maryland SAMUEL CHASE, WM. PACA, THOS. STONE, CHARLES CARROLL of Carrollton. Virginia GEORGE WYTHE, RICHARD HENRY LEE, TH. JEFFERSON, BENJA. HARRISON, THS. NELSON, JR., FRANCIS LIGHTFOOT LEE, CARTER BRAXTON. North Carolina WM. HOOPER, JOSEPH HEWES, JOHN PENN. South Carolina EDWARD RUTLEDGE, THOS. HAYWARD, JUNR., THOMAS LYNCH, JUNR., ARTHUR MIDDLETON. Georgia BUTTON GWINNETT, LYMAN HALL, GEO. WALTON. NOTE.-Mr. Ferdinand Jefferson, Keeper of the Rolls in the Department of State, at Washington, says: " The names of the signers are spelt above as in the facsimile of the original, but the punctuation of them is not always the same; neither do the names of the States appear in the facsimile of the original. The names of the signers of each State are grouped together in the facsimile of the original, except the name of Matthew Thornton, which follows that of Oliver Wolcott."-Revised Statutes of the United States, 2d edition, 1878, p. 6. Source: From Yale Law School Lillian Goldman Law Library: The Avalon Project \| Attributions Images courtesy of Wikipedia Commons Title Image - 1819 painting of the signing of the Declaration of Independence by John Trumbull. Attribution: John Trumbull, Public Domain, via Wikipedia Commons. Provided by: Wikipedia. Location: https://en.wikipedia.org/wiki/File:Declaration_of_Independence_(1819),_by_John_Trumbull.jpg#filehistory. License: CC BY-SA: Attribution-ShareAlike Adapted from Boundless World History. "North America" https://www.coursehero.com/study-guides/boundless-worldhistory/north-america/	oercommons	2025-03-18T00:37:03.262743	Neil Greenwood	{ "license": "Creative Commons - Attribution - https://creativecommons.org/licenses/by/4.0/", "url": "https://oercommons.org/courseware/lesson/87915/overview", "title": "Statewide Dual Credit World History, The Period of Revolution 1650-1871 CE, Chapter 9: Revolution, The American Revolution", "author": "Anna McCollum" }
https://oercommons.org/courseware/lesson/87945/overview	Imperial Russia in the First Half of the 19th Century Overview On the Cusp of a New World: Russia from Alexander I to Alexander II Napoleon Bonaparte’s greatest adversary was a man who he, and much of Europe, greatly underestimated—Tsar Alexander I, the grandson of Catherine the Great of Russia. Alexander proved not only an excellent military strategist but also carried on the enlightened, domestic policies of his grandmother. He was a supreme autocrat, and truly acted as the “tsar of all the Russias,” as his title claimed. However, not all of the succeeding Romanov tsars would prove as capable a leader as Alexander I. Increasingly, a deep rift emerged between Russia’s outdated system of autocracy, and the growing desires of the people, who saw Western Europeans gaining rights and independence in ways that were impossible in Russia. As Russian territory expanded, so too did the discontent of its people. Learning Objectives - Evaluate the political, social, and economic challenges of Russia during the early-mid 1800s. - Analyze the growing differences between Russia in the 1800s, and Western Europe. Key Terms / Key Concepts Alexander I: Tsar of Russia in the early 1800s who defeated Napoleon and also continued enlightened, domestic reforms Alexander II: progressive tsar who liberated the Russian serfs Crimean War: war for the possession of Crimea between Russia, and an allied group of forces including England, France, and the Ottoman Empire Decembrist Uprising: event where part of the Russian military revolted against the ascension of the new tsar, Nicholas I Emancipation Reform of 1861: Russian document that liberated the serfs under Tsar Alexander II January Uprising: Polish revolt to reclaim independence that resulted in decades of Russian reprisals Kingdom of Poland: semi-independent Polish state with a constitution, but ruled by Russia monarchs Nicholas I: tsar of Russia during the Decembrist Uprising and the Crimean War November Uprising: Polish revolt against Russian violations of their constitution in 1830 – 31 Russo-Polish War: war that arose out of the November Uprising and resulted in the loss of Polish independence Alexander I and the Serfs Alexander I wanted to resolve a crucial issue in Russia—the status of the serfs. He acknowledged that serfdom was a feudal concept that Western Europe had dissolved centuries before in favor of more democratic and capitalist systems of labor. The fact remained, though, that Alexander was an autocrat. He ruled supremely in Russia. Entirely dissolving serfdom stood in direct contrast with his principles as tsar. During the reign of Alexander I only about 7,300 male peasants (with families) or about 0.5% of serfs were freed. While Alexander could not be so liberal in his thinking as to emancipate the serfs, he was still an enlightened tsar who believed in slow, progressive reform. He introduced new laws that allowed all classes except the serfs to own land, even small-time farmers; this was a privilege previously confined to the nobility. Alexander I and Poland After Napoleon’s final defeat and exile, Alexander I had two main goals: to gain control of Poland and promote the peaceful coexistence of European nations. For the Poles, Alexander created the “Congress Poland” (formerly the Duchy of Warsaw), and granted the state a constitution. Though officially known as the Kingdom of Poland, the state had considerable political autonomy guaranteed by a liberal constitution, its rulers, the Russian Emperors, generally disregarded any restrictions on their power. Effectively it was little more than a puppet state of the Russian Empire. Thus, Alexander I became the constitutional monarch of Poland while remaining the autocratic tsar of Russia. He was also the monarch of Finland, which had been annexed in 1809 and awarded autonomous status. The Congress finalized Russian control of Finland. Alexander's Final Years Despite the liberal, romantic inclinations of his youth, later in his rule Alexander I grew steadily more conservative, isolated from the day-to-day affairs of the state, and inclined to religious mysticism. Once a supporter of limited liberalism, at the end of 1818 Alexander’s views began to change. A revolutionary conspiracy among the officers of the guard and a foolish plot to kidnap him are said to have shaken the foundations of his liberalism. It was the increasing discontent in France, Germany, and among his own people, that completed Alexander’s conversion. The lofty hopes that the tsar had once held for his country were frustrated by its immense size and backwardness. While vacationing in 1825, Alexander fell ill with typhus and died at only 47. Mysteriously, stories circulated soon afterward that the tsar had not died but had merely faked his death. The rumors bespoke of a monk in Siberia who was unusually tall (like Alexander) whom no one seemed to know. The monk, Feodor Kuzmich, also had unusual mannerisms and a social awkwardness that people described as someone hiding from a previous life. Adding to the rumors were the fact that much later, Kuzmich would receive a visit from the tsarevich (crown prince), Alexander III. His grave would also be visited by Tsar Nicholas II. While historians overwhelmingly dismiss the theory of Alexander I as nothing but popular legend, it is a legend with many twists and curiosities that has had popularity since the mid-1800s. The Decembrist Revolt When Alexander I died, he did not have a legitimate, direct heir. The imperial throne instead fell to one of his younger brothers—Nicholas or Constantine. Neither wanted the throne, or the responsibility of being the tsar. In secret, Constantine, Alexander’s heir apparent, had already renounced the throne. Fatefully, Nicholas, the youngest of the brothers, would become tsar. Although a capable man, Nicholas I was more conservative than Alexander. This, combined with the secret renunciation of the throne by Constantine, would set the new, young tsar on a collision course with his people. The Decembrist Revolt took place in Imperial Russia on December 26, 1825. It was largely an aristocratic movement whose chief actors were army officers. A group of officers commanding about 3,000 men refused to swear allegiance to Nicholas, proclaiming instead their loyalty to the idea of a Russia that had a constitution. They realized, however, that they were soon outnumbered and outgunned. The majority of the tsar’s troops remained loyal. Skirmishes erupted between the two sides. At one point, Nicholas I sent out his personal messenger to call for an end to the fight. The messenger was killed, and the Decembrists were quickly overrun. The surviving rebels were exiled to Siberia. Nicholas I defeated the Decembrists easily. Still, their discontent represented major, growing disparity between the government of Russia and its people. While most of Europe was enjoying increased rights and voices in government, Russia remained two-hundred-years behind the times. This point would haunt the Russian tsars, who intellectually understood the peoples’ frustration but still refused to give the people much power. This disparity would increase to such an extent that it would lead to the complete destruction of the tsarist government in 1917 and usher in communism. Tsar Nicholas I Nicholas I was the Emperor of Russia from 1825 until 1855, as well as King of Poland and Grand Duke of Finland. He is best-known as a political conservative whose reign was marked by geographical expansion, repression of dissent, economic stagnation, poor administrative policies, a corrupt bureaucracy, and frequent wars that culminated in Russia’s disastrous defeat in the Crimean War of 1853 – 56. Nicholas was successful against Russia’s neighboring southern rivals. Through successfully ending the Russo-Persian War (1826 – 28), he seized the last territories in the Caucasus held by Persia (land comprising modern day Armenia and Azerbaijan). After gaining what is now Dagestan, Georgia, Azerbaijan, and Armenia from Persia, the clear geopolitical and territorial upper hand in the Caucasus was Russia’s. He ended the Russo-Turkish War (1828 – 29) successfully as well. Later, however, he led Russia into the Crimean War (1853 – 56) with disastrous results. Historians emphasize that his micromanagement of the armies hindered his generals, as did his misguided strategy. Fuller notes that historians have frequently concluded that “the reign of Nicholas I was a catastrophic failure in both domestic and foreign policy.” On the eve of his death, the Russian Empire reached its geographical zenith, spanning over 7.7 million square miles but in desperate need of reform. The November Uprising Even though Alexander I had given the Kingdom of Poland a constitution, the Russian tsars and their inner circle violated the constitution by increasingly ignoring or stripping away Polish freedoms. By the late 1820s, the Kingdom of Poland was little more than a puppet state of the Russian empire. In response to the violations of their liberties, Poles grew increasingly frustrated. In November 1830, a group of young men from the Warsaw Officer’s School attacked the Belweder Palace in Warsaw, where the tsar’s brother was living. Although he escaped, the Polish state rallied behind the movement. Soon, much of Warsaw, and Poland, was behind the movement to evict the Russian presence and establish independence. Across the Kingdom of Poland, Poles argued that they were a people entirely independent from the Russians. Their languages, though similar, were different. Poles were largely Catholic Christians, whereas Russians were Orthodox. Customs and traditions also differed. In short, the Poles argued they were their own people and worthy of complete independence. Russia disagreed, most likely because Poland was a country of enormous agricultural and natural resources. The Uprising continued to gain support in Poland as the Russians sent reinforcements to end the rebellion. By February 1831, the November Uprising had transformed into a war. The Russo-Polish War In February 1831, war enveloped much of the Kingdom of Poland. Early in the conflict, the Poles won small victories. But their overall strategy and defense remained poorly organized. Russian troops were well-trained, whereas Polish troops were inexperienced and undisciplined. Outnumbered and outgunned, the Poles were forced to surrender to the Russians in October 1831 as the Russians encircled Warsaw. For the time being, the Russians had defeated the Poles. Warsaw was stripped of its university and reduced in status to a military town. Poland lost its constitution and its autonomy. It would be a key component of the Russian empire for the next eighty years. Still, the Poles would prove that although they had been defeated in the Russo-Polish War, they had not lost the will to fight. The Crimean War For much of Nicholas’s reign, Russia was seen as a major military power with considerable strength. The Crimean War at the end of his reign demonstrated to the world what no one had previously realized: Russia was militarily weak, technologically backward, and administratively incompetent. Despite his grand ambitions toward the south and Turkey, Russia had not built its railroad network in that direction, and communications were bad. The bureaucracy was riddled with corruption and inefficiency; and it was unprepared for war. The Navy was weak and technologically backward; the Army, although very large, was inadequate in a modern war. By war’s end, the Russian leadership was determined to reform the Army and the society. In 1853, Russia looked to claim the island of Crimea in the Black Sea, so as to have access to an ice-free port, as well as better shipping and trade routes. Western Europeans perceived the Russians as exploitive of the weakening Ottoman Empire and a threat to their naval trade. Britain, France, the Kingdom of Sardinia, and the Ottoman Empire joined forces in the Crimean War against the Russians. In April 1854, Austria signed a defensive pact with Prussia. Thus, Russia found itself in a war with the majority of Europe. The European allies landed in Crimea and laid siege to the well-fortified Russian base at Sevastopol. The Russians lost battles at Alma in September 1854, followed by lost battles at Balaklava and Inkerman. After the prolonged Siege of Sevastopol (1854 – 55) the base fell, exposing Russia’s inability to defend a major fortification on its own soil. The defeats humiliated Russia and the tsar. In 1855, Nicholas I developed pneumonia. Rather than seeking medical treatment, he laid quietly at home, devastated by news of the Crimean War. He died in March 1855. The new tsar, Alexander II, would prove the strongest of the Romanov tsars. However, his early years were also marked with defeat. On January 15, 1856, he pulled Russia out of the war on very unfavorable terms, which included the loss of a naval fleet on the Black Sea. The Last Great Tsar: Alexander II Alexander II was born into a world of excessive privilege. As such, he received a liberal education that immersed him in concepts of the Enlightenment. He understood better than any tsar of the modern era, the importance of increasing rights for the people. Embarrassed by the Russian defeat in Crimea, he decided to focus on domestic improvements and modernization for Russia. To modernize the country, he needed to start, quite literally, from the ground up. The 1861 Emancipation of the Serfs Six years into his reign, Alexander II undertook the most radical and progressive reform in Russian history. He freed all serfs (over 23 million people) in a major agrarian reform, stimulated in part by his view that “it is better to liberate the peasants from above” than to wait until they won their freedom by uprisings “from below.” The Emancipation Reform of 1861 in Russia was the first and most important of liberal reforms effected during Alexander II’s reign (1855 – 1881). The reform effectively abolished serfdom throughout the Russian Empire. Serfs gained the full rights of free citizens, including rights to marry without having to gain consent, to own property, and to own a business. Moreover, the edict prescribed that peasants would be able to buy land from the landlords. In Georgia the emancipation took place later, in 1864, and on much better terms for the nobles than in Russia. Effects of Emancipation Although the emancipation reform led to Alexander II’s nickname, “Alexander the Liberator,” its results were far from ideal. Household serfs were the worst affected as they gained only their freedom and no land. In reality, the reforms created a new system in which the monarch had to coexist with an independent court, free press, and local governments that operated differently and more freely than in the past. This would further set the tsar and his people on a collision course in the succeeding years. The reforms also transformed the Russian economy. The individuals who led the reform were in favor of an economic system similar to that of other European countries, which promoted the ideas of capitalism and free trade. The idea of the reformers was to promote development and encourage private property ownership, free competition, entrepreneurship, and hired labor. They hoped this would bring about an a more laissez-faire economic system with minimal regulations and tariffs. Soon after the reforms, there was a substantial rise in the amount of grain production for sale. Alexander's Other Reforms Alexander is remembered best for his liberation of Russia’s serfs but his reforms stretched far further. He was a relatively progressive tsar who was bent on modernizing Russia. During his twenty-five years as tsar, he passed many reforms that collectively are dubbed, “The Great Reforms.” He afforded Russian Jews greater status and protection. This measure was significant because many of his successors would implement pogroms. Alexander also reformed the Orthodox church, state education, and modernized infrastructure throughout Russia. Media restrictions were relaxed. Russian armies and navies were modernized along the lines of those in Western Europe, although never to the same extent. Very successfully, Alexander also reformed the Russian judiciary system. He removed the old, cumbersome system of the Russian legal courts, and streamlined how courts across Russia should operate. This new, unified, court system resulted in many significant improvements, including the right to jury trial. The January Uprising While Alexander enjoyed success at home in Russia, people were less content on the fringes of the Russian empire. In particular, the Poles and their allies, Lithuanians, detested Russian rule. A new generation of military and political leaders heard stories of the semi-independence their parents had enjoyed in the Kingdom of Poland, and in the 1860s, Poles yearned to have that independence restored. In January 1863, the Poles launched a revolt against Russian rule. The uprising, despite lasting eighteen months, stood little chance of success. The Poles were motivated by their desire for restoration of even partial independence, but they were, again outgunned and outmanned by the Russian forces. Similarly, they were poorly organized. Rather than face the Russian armies head-on, the Poles resorted to guerilla warfare, which further enraged the Russians. This was, to them, a dishonorable way of fighting. Eventually, the Poles were captured. Hundreds were executed. Thousands more were deported to labor camps in Siberia. For decades, the tsar carried-out reprisals against the Poles. More than 15,000 were sent to labor camps in Siberia, and their homes or farms confiscated. The January Uprising ended in a Polish defeat, just at the Russo-Polish war had. But it was not without a smaller victory for the Poles. In order to shatter the economic backbone of many of the Polish upper class (who had supported the uprising), Alexander II freed the serfs in Poland. Death of Alexander II Alexander II was a reformer and likely the best tsar of the modern era. He was, however, still an autocrat in an increasingly discontent Russia. Despite many reforms, he stopped short of giving the people direct power in government. This frustrated and enraged many Russians, especially the growing class of young intellectuals and political men and women. On March 13, 1881, the tsar was returning from a review of the troops to the Winter Palace in St. Petersburg in his bullet-proof, closed carriage. All at once, a bomb was hurled beneath the carriage wheels. It killed one of Alexander’s Cossack guards, but the tsar exited the carriage, unhurt. According to some accounts, the tsar said, “Thank God I am unhurt.” From the crowd, a young man yelled, “Do not thank God, yet!” A second assassin pushed through the audience and threw a bomb at the tsar’s feet. It exploded, killing the assassin, and mortally wounding the tsar. His legs were shattered, and blood gushed forth from them. His chest and face were likewise mangled. Desperate to reach the Winter Palace, his guards hurried with the dying tsar. Members of the Romanov family, including the future tsars, Alexander III and Nicholas II, watched as the great “liberator tsar” breathed his last. At 3:30 that afternoon, Alexander II died in his office—almost twenty years to the day after he had signed the document that liberated the serfs. Legacy: Reactionaries and Reformers The years after Napoleon’s defeat were peculiar in Russia. In many ways, Russia attempted to modernize, but only to the extent to which their tsars could also remain autocrats. A trend developed. A progressive tsar such as Alexander I would reign and deliver a few freedoms to peoples within the Russian Empire. Immediately, the succeeding tsar would react to these measures with more conservative measures that tightened their grip on Russia. Then the next tsar would try, once again, to launch reforms. A cycle of reactionaries and reformists trickled through Russia's tsars. And although the Russian tsars were capable in many ways, none of them ever acted on the imminent danger of a discontented and growing intellectual class. Even Alexander II could not be so progressive as to share power with a parliamentary system. By trying to maintain a supreme, autocratic government in the world’s largest empire, the Romanov tsars sowed the seeds of their own, ultimate destruction. Attributions Images courtesy of Wikimedia Commons Boundless World History "Russia after Napoleon" https://courses.lumenlearning.com/suny-hccc-worldhistory2/chapter/russia-after-napoleon/ "Territorial Gains under Alexander I" "Decembrist Revolt" https://courses.lumenlearning.com/suny-hccc-worldhistory2/chapter/the-decembrist-revolt/ "The Wars of Nicholas I" https://courses.lumenlearning.com/suny-hccc-worldhistory2/chapter/the-wars-of-nicholas-i/ "Emancipation of the Serfs" https://creativecommons.org/licenses/by-sa/4.0/	oercommons	2025-03-18T00:37:03.308677	Neil Greenwood	{ "license": "Creative Commons - Attribution - https://creativecommons.org/licenses/by/4.0/", "url": "https://oercommons.org/courseware/lesson/87945/overview", "title": "Statewide Dual Credit World History, European Imperialism and Crises 1871-1919 CE, Chapter 11: Reactions, Imperial Russia in the First Half of the 19th Century", "author": "Anna McCollum" }
https://oercommons.org/courseware/lesson/87922/overview	Spanish South America Overview Simón Bolívar South American independence movements demonstrate the importance of Simon Bolivar and his linking with San Martin. Bolivar led militaries throughout South America to be successful in removing the Spanish from South America. Learning Objectives - Evaluate the differences between the Caribbean and Southern American Age of Revolutions. - Analyze the impact of Napoleonic Wars on the South American Age of Revolutions. Key Terms / Key Concepts - Gran Colombia: name used today for the state that encompassed much of northern South America and part of southern Central America from 1819 to 1831; a territory including present-day Colombia, Venezuela, Ecuador, Panama, northern Peru, western Guyana, and northwest Brazil - New Granada: the name given on May 27, 1717 to the jurisdiction of the Spanish Empire in northern South America, which corresponds to modern Colombia, Ecuador, Panama, and Venezuela - Battle of Carabobo: a battle fought between independence fighters led by Venezuelan General Simón Bolívar and the Royalist forces led by Spanish Field Marshal Miguel de la Torre (Bolívar’s decisive victory at Carabobo led to the independence of Venezuela and establishment of the Republic of Gran Colombia.) - Army of the Andes: a military force created by the United Provinces of the Río de la Plata (Argentina) and mustered by general José de San Martín in his campaign to free Chile from the Spanish Empire (In 1817, it crossed the Andes Mountains from the Argentine province of Cuyo at the current-day province of Mendoza, Argentina, and it succeeded in dislodging the Spanish from the country.) - Crossing of the Andes: one of the most important feats in the Argentine and Chilean wars of independence, in which a combined army of Argentine soldiers and Chilean exiles invaded Chile, leading to Chile’s liberation from Spanish rule (The crossing of the Andes was a major step in the strategy devised by José de San Martín to defeat the royalist forces at their stronghold of Lima, Viceroyalty of Perú, and secure the Spanish American independence movements.) Spanish South America El Libertador: Simón Bolívar Simón Bolívar (July 24, 1783 – December 17, 1830) was a Venezuelan military and political leader who played a key role in the establishment of Venezuela, Bolivia, Colombia, Ecuador, Peru, and Panama as sovereign states independent of Spanish rule. Bolívar was born into a wealthy, aristocratic Creole family and like others of his day was educated abroad at a young age, arriving in Spain when he was 16 and later moving to France. While in Europe, he was introduced to the ideas of Enlightenment philosophers, which gave him the ambition to replace the Spanish as rulers. Taking advantage of the disorder in Spain prompted by the Peninsular War, Bolívar began his campaign for Venezuelan independence in 1808, appealing to the wealthy Creole population through a conservative process. He established an organized national congress within three years. Despite several hindrances, including the arrival of an unprecedentedly large Spanish expeditionary force, the revolutionaries eventually prevailed, culminating in a patriot victory at the Battle of Carabobo in 1821 that effectively made Venezuela an independent country. Following this triumph over the Spanish monarchy, Bolívar participated in the foundation of the first union of independent nations in Latin America: Gran Colombia. He was president of Gran Colombia from 1819 to 1830. Through further military campaigns, he ousted Spanish rulers from Ecuador, Peru, and Bolivia (which was named after him). He was simultaneously president of Gran Colombia (current Venezuela, Colombia, Panamá, and Ecuador) and Peru, while his second in command Antonio José de Sucre was appointed president of Bolivia. He aimed at a strong and united Spanish America able to cope not only with the threats emanating from Spain and the European Holy Alliance but also with the emerging power of the United States. At the peak of his power, Bolívar ruled over a vast territory from the Argentine border to the Caribbean Sea. In his 21-year career, Bolívar faced two main challenges. First was gaining acceptance as undisputed leader of the republican cause. Despite claiming such a role since 1813, he began to achieve acceptance only in 1817, and consolidated his hold on power after his dramatic and unexpected victory in New Granada in 1819. His second challenge was implementing a vision to unify the region into one large state, which he believed (and most would agree, correctly) would be the only guarantee of maintaining independence from the Spanish in northern South America. His early experiences under the First Venezuelan Republic and in New Granada convinced him that divisions among republicans, augmented by federal forms of government, only allowed Spanish American royalists to eventually gain the upper hand. Once again, it was his victory in 1819 that gave him the leverage to bring about the creation of a unified state, Gran Colombia with which to oppose the Spanish Monarchy on the continent. Bolívar is, along with Argentine General José de San Martín, considered one of the great heroes of the Hispanic independence movements of the early 19th century. Failed Dream of a Unified Latin America At the end of the wars of independence (1808 – 1825), many new sovereign states emerged in the Americas from the former Spanish colonies. Throughout this revolutionary era, Bolívar envisioned various unions that would ensure the independence of Spanish America vis-à-vis the European powers—in particular Britain—and the expanding United States. In his 1815 Cartagena Manifesto, Bolívar had already advocated that the Spanish American provinces should present a united front to the Spanish in order to prevent being re-conquered piecemeal, but he had not yet proposed a political union of any kind. During the wars of independence, the fight against Spain was marked by an emerging sense of nationalism. It was unclear what the new states that replaced the Spanish Monarchy should be. Most of those who fought for independence identified with both their birth provinces and Spanish America as a whole, both of which they referred to as their patria—a term roughly translated as “fatherland” and “homeland.” For Bolivar, Hispanic America was the fatherland. He dreamed of a united Spanish America and in the pursuit of that purpose not only created Gran Colombia but also the Confederation of the Andes. The conference gathered in Peru and Bolivia. Moreover, he envisaged and promoted a network of treaties that would hold together the newly liberated Hispanic American countries. Nonetheless, he was unable to control the centrifugal process that pushed in all directions. On January 20, 1830, as his dream fell apart, Bolívar delivered his last address to the nation, announcing that he would be stepping down from the presidency of Gran Colombia. At the time, “Colombians” referred to the people of Gran Colombia (Venezuela, New Granada, and Ecuador), not modern-day Colombia. In his speech, a distraught Bolívar urged the people to maintain the union and to be wary of the intentions of those who advocated for separation: “Colombians! Today I cease to govern you. I have served you for twenty years as soldier and leader. During this long period we have taken back our country, liberated three republics, fomented many civil wars, and four times I have returned to the people their omnipotence, convening personally four constitutional congresses. These services were inspired by your virtues, your courage, and your patriotism; mine is the great privilege of having governed you… Colombians! Gather around the constitutional congress. It represents the wisdom of the nation, the legitimate hope of the people, and the final point of reunion of the patriots. Its sovereign decrees will determine our lives, the happiness of the Republic, and the glory of Colombia. If dire circumstances should cause you to abandon it, there will be no health for the country, and you will drown in the ocean of anarchy, leaving as your children’s legacy nothing but crime, blood, and death. Fellow Countrymen! Hear my final plea as I end my political career; in the name of Colombia I ask you, beg you, to remain united, lest you become the assassins of the country and your own executioners.” Bolívar ultimately failed in his attempt to prevent the collapse of the union.Gran Colombia was dissolved later that year and replaced by the republics of Venezuela, New Granada, and Ecuador. Ironically, these countries were established as centralist nations and would be governed for decades this way by leaders who, during Bolívar’s last years, accused him of betraying republican principles and wanting to establish a permanent dictatorship. These separatists, among them José Antonio Páez and Francisco de Paula Santander, justified their opposition to Bolívar for this reason and publicly denounced him as a monarch. Southern Cone Independence Southern South American Independence: San Martín José de San Martín was an Argentine general and the prime leader of the southern part of South America’s successful struggle for independence from the Spanish Empire. Born in Yapeyú, Corrientes, in modern-day Argentina, he left his mother country at the early age of seven to study in Málaga, Spain. In 1808, after taking part in the Peninsular War against Napoleon’s France, San Martín contacted South American supporters of independence from Spain. In 1812, he set sail for Buenos Aires and offered his services to the United Provinces of the Río de la Plata, present-day Argentina. After the Battle of San Lorenzo and time commanding the Army of the North during 1814, he organized a plan to defeat the Spanish forces that menaced the United Provinces from the north, using an alternative path to the Viceroyalty of Peru. This objective first involved the establishment of a new army, the Army of the Andes, in Cuyo Province, Argentina. From there, he led the Crossing of the Andes to Chile and triumphed at the Battle of Chacabuco and the Battle of Maipú (1818), thus liberating Chile from royalist rule. Then he sailed to attack the Spanish stronghold of Lima, Peru. On July 12, 1821, after seizing partial control of Lima, San Martín was appointed Protector of Peru, and Peruvian independence was officially declared on July 28. On July 22, after a closed-door meeting with fellow libertador Simón Bolívar at Guayaquil, Ecuador, Bolívar took over the task of fully liberating Peru. San Martín unexpectedly left the country and resigned the command of his army, excluding himself from politics and the military, and moved to France in 1824. The details of the July 22 meeting would be a subject of debate by later historians. San Martín is regarded as a national hero of Argentina and Peru, and together with Bolívar, one of the Liberators of Spanish South America. The Order of the Liberator General San Martín (Orden del Libertador General San Martín), created in his honor, is the highest decoration conferred by the Argentine government. Wars of Independence: Argentina, Chile, Peru San Martín entered the Argentine War of Independence about a year after it started. The reasons that he left Spain in 1811 to join the Spanish American wars of independence as a patriot remain contentious among historians. The action would seem contradictory and out of character, because if the patriots were waging an independentist and anti-Hispanic war, then he would be a traitor or deserter. There are a variety of explanations by different historians. Some argue that he returned because he missed South America and the war of independence justified changing sides to support it. Others contend that the wars in the Americas were not initially separatist but between supporters of absolutism and liberalism, which thus maintains a continuity between San Martín’s actions in Spain and in Latin America. The Argentine War of Independence started with the May Revolution and other military campaigns with mixed success. The undesired outcomes of the Paraguay and Upper Peru campaigns led the Junta (the provisional government after the May Revolution) to be replaced by an executive Triumvirate in September 1811. A few days after his arrival in Buenos Aires, San Martín was interviewed by the First Triumvirate. They appointed him a lieutenant colonel of cavalry and asked him to create a cavalry unit, as Buenos Aires did not have good cavalry. He began to organize the Regiment of Mounted Grenadiers with Alvear and Zapiola. As Buenos Aires lacked professional military leaders, San Martín was entrusted with the protection of the whole city, but kept focused on the task of building the military unit. A year later the Triumvirate was renewed, and San Martín was promoted to colonel. San Martín came up with a plan: organize an army in Mendoza, cross the Andes to Chile, and move to Peru by sea, all while another general defended the north frontier. This would place him in Peru without crossing the harsh terrain of Upper Peru, where two campaigns had already been defeated. To advance this plan, he requested the governorship of the Cuyo province, which was accepted. San Martín immediately began to organize the Army of the Andes. He drafted all citizens who could bear arms and all slaves from ages 16 to 30, requested reinforcements to Buenos Aires, and reorganized the economy for war production. San Martín proposed that the country declare independence immediately, before the crossing. That way, they would be acting as a sovereign nation and not as a mere rebellion, but the proposal never was accepted. Needing even more soldiers, San Martín extended the emancipation of slaves to ages 14 to 55, and even allowed them to be promoted to higher military ranks. He proposed a similar measure at the national level, but Pueyrredón encountered severe resistance. He included the Chileans who escaped Chile after the disaster of Rancagua, and organized them in four units: infantry, cavalry, artillery, and dragoons. At the end of 1816, the Army of the Andes had 5,000 men, 10,000 mules, and 1,500 horses. San Martin organized military intelligence, propaganda, and disinformation to confuse the royalist armies (such as the specific routes taken in the Andes), boost the national fervor of his army, and promote desertion among the royalists. In early 1817, San Martín led the Crossing of the Andes into Chile, obtaining a decisive victory at the battle of Chacabuco on February 17, which allowed the exiled Chilean leader Bernardo O’Higgins to enter Santiago de Chile unopposed and install a new independent government. In December 1817, a popular referendum was set up to decide on the Independence of Chile. On February 18, 1818, the first anniversary of the battle of Chacabuco, Chile declared its independence from the Spanish Crown. From there, San Martín took the Army of the Andes to fight in Peru. To begin the liberation of Peru and prepare for the invasion, Argentina and Chile signed a treaty on February 5, 1819. General José de San Martín believed that the liberation of Argentina wouldn’t be secure until the royalist stronghold in Peru was defeated. Peru had armed forces nearly four times the strength of those of San Martín. With this disparity, San Martín tried to avoid battles. He tried instead to divide the enemy forces in several locations, as during the Crossing of the Andes, and trap the royalists with a pincer movement with either reinforcements of the Army of the North from the South or the army of Simón Bolívar from the North. He also tried to promote rebellions and insurrection within the royalist ranks and promised the emancipation of any slaves that deserted their Peruvian masters to join his army. When he reached Lima, San Martín invited all of the populace of Lima to swear oath to the Independence cause. The signing of the Act of Independence of Peru was held on July 15, 1821. San Martín became the leader of the government, even though he did not want to lead. He was appointed Protector of Peru. After several years of fighting, San Martín abandoned Peru in September 1822 and left the whole command of the Independence movement to Simon Bolivar. The Peruvian War culminated in 1824 with the defeat of the Spanish Empire in the battles of Junin and Ayacucho. Guayaquil Conference The Guayaquil Conference was a meeting that took place on July 26, 1822, in Guayaquil, Ecuador, between José de San Martín and Simón Bolívar, to discuss the future of Perú (and South America in general). San Martín arrived in Guayaquil on July 25, where he was enthusiastically greeted by Bolívar. However, the two men could not come to an agreement, despite their common goals and mutual respect, even when San Martín offered to serve under Bolívar. Both men had very different ideas about how to organize the governments of the countries that they had liberated. Bolívar was in favor of forming a series of republics in the newly independent nations, whereas San Martín preferred the European system of rule and wanted to put monarchies in place. San Martín was also in favor of placing a European prince in power as King of Peru when it was liberated. The conference, consequently, was a failure, at least for San Martín. San Martín, after meeting with Bolívar for several hours on July 26, stayed for a banquet and ball given in his honor. Bolívar proposed a toast to “the two greatest men in South America: the general San Martín and myself,” whereas San Martín drank to “the prompt conclusion of the war, the organization of the different Republics of the continent and the health of the Liberator of Colombia.” After the conference, San Martín abdicated his powers in Peru and returned to Argentina. Soon afterward, he left South America entirely and retired in France. Primary Source: Simón de Bolívar: Message to the Congress of Angostura, 1819 We are not Europeans; we are not Indians; we are but a mixed species of aborigines and Spaniards. Americans by birth and Europeans by law, we find ourselves engaged in a dual conflict: we are disputing with the natives for titles of ownership, and at the same time we are struggling to maintain ourselves in the country that gave us birth against the opposition of the invaders. Thus our position is most extraordinary and complicated. But there is more. As our role has always been strictly passive and political existence nil, we find that our quest for liberty is now even more difficult of accomplishment; for we, having been placed in a state lower than slavery, had been robbed not only of our freedom but also of the right to exercise an active domestic tyranny. . .We have been ruled more by deceit than by force, and we have been degraded more by vice than by superstition. Slavery is the daughter of darkness: an ignorant people is a blind instrument of its own destruction. Ambition and intrigue abuses the credulity and experience of men lacking all political, economic, and civic knowledge; they adopt pure illusion as reality; they take license for liberty, treachery for patriotism, and vengeance for justice. If a people, perverted by their training, succeed in achieving their liberty, they will soon lose it, for it would be of no avail to endeavor to explain to them that happiness consists in the practice of virtue; that the rule of law is more powerful than the rule of tyrants, because, as the laws are more inflexible, every one should submit to their beneficent austerity; that proper morals, and not force, are the bases of law; and that to practice justice is to practice liberty. Although those people [North Americans], so lacking in many respects, are unique in the history of mankind, it is a marvel, I repeat, that so weak and complicated a government as the federal system has managed to govern them in the difficult and trying circumstances of their past. But, regardless of the effectiveness of this form of government with respect to North America, I must say that it has never for a moment entered my mind to compare the position and character of two states as dissimilar as the English-American and the Spanish-American. Would it not be most difficult to apply to Spain the English system of political, civil, and religious liberty: Hence, it would be even more difficult to adapt to Venezuela the laws of North America. Nothing in our fundamental laws would have to be altered were we to adopt a legislative power similar to that held by the British Parliament. Like the North Americans, we have divided national representation into two chambers: that of Representatives and the Senate. The first is very wisely constituted. It enjoys all its proper functions, and it requires no essential revision, because the Constitution, in creating it, gave it the form and powers which the people deemed necessary in order that they might be legally and properly represented. If the Senate were hereditary rather than elective, it would, in my opinion, be the basis, the tie, the very soul of our republic. In political storms this body would arrest the thunderbolts of the government and would repel any violent popular reaction. Devoted to the government because of a natural interest in its own preservation, a hereditary senate would always oppose any attempt on the part of the people to infringe upon the jurisdiction and authority of their magistrates. . .The creation of a hereditary senate would in no way be a violation of political equality. I do not solicit the establishment of a nobility, for as a celebrated republican has said, that would simultaneously destroy equality and liberty. What I propose is an office for which the candidates must prepare themselves, an office that demands great knowledge and the ability to acquire such knowledge. All should not be left to chance and the outcome of elections. The people are more easily deceived than is Nature perfected by art; and although these senators, it is true, would not be bred in an environment that is all virtue, it is equally true that they would be raised in an atmosphere of enlightened education. The hereditary senate will also serve as a counterweight to both government and people; and as a neutral power it will weaken the mutual attacks of these two eternally rival powers. The British executive power possesses all the authority properly appertaining to a sovereign, but he is surrounded by a triple line of dams, barriers, and stockades. He is the head of government, but his ministers and subordinates rely more upon law than upon his authority, as they are personally responsible; and not even decrees of royal authority can exempt them from this responsibility. The executive is commander in chief of the army and navy; he makes peace and declares war; but Parliament annually determines what sums are to be paid to these military forces. While the courts and judges are dependent on the executive power, the laws originate in and are made by Parliament. Give Venezuela such an executive power in the person of a president chosen by the people or their representatives, and you will have taken a great step toward national happiness. No matter what citizen occupies this office, he will be aided by the Constitution, and therein being authorized to do good, he can do no harm, because his ministers will cooperate with him only insofar as he abides by the law. If he attempts to infringe upon the law, his own ministers will desert him, thereby isolating him from the Republic, and they will even bring charges against him in the Senate. The ministers, being responsible for any transgressions committed, will actually govern, since they must account for their actions. A republican magistrate is an individual set apart from society, charged with checking the impulse of the people toward license and the propensity of judges and administrators toward abuse of the laws. He is directly subject to the legislative body, the senate, and the people: he is the one man who resists the combined pressure of the opinions, interests, and passions of the social state and who, as Carnot states, does little more than struggle constantly with the urge to dominate and the desire to escape domination. This weakness can only be corrected by a strongly rooted force. It should be strongly proportioned to meet the resistance which the executive must expect from the legislature, from the judiciary, and from the people of a republic. Unless the executive has easy access to all the administrative resources, fixed by a just distribution of powers, he inevitably becomes a nonentity or abuses his authority. By this I mean that the result will be the death of the government, whose heirs are anarchy, usurpation, and tyranny. . . Therefore, let the entire system of government be strengthened, and let the balance of power be drawn up in such a manner that it will be permanent and incapable of decay because of its own tenuity. Precisely because no form of government is so weak as the democratic, its framework must be firmer, and its institutions must be studied to determine their degree of stability...unless this is done, we will have to reckon with an ungovernable, tumultuous, and anarchic society, not with a social order where happiness, peace, and justice prevail. Source: From: Simón Bolívar, An Address of Bolivar at the Congress of Angostura (February 15, 1819), Reprint Ed., (Washington, D.C.: Press of B. S. Adams, 1919), passim. Scanned by: J. S. Arkenberg, Dept. of History, Cal. State Fullerton. Prof. Arkenberg has modernized the text. Attributions Attributions Images courtesy of Wikimedia Commons Boundless World History https://courses.lumenlearning.com/boundless-worldhistory/chapter/north-america/	oercommons	2025-03-18T00:37:03.340575	Neil Greenwood	{ "license": "Creative Commons - Attribution - https://creativecommons.org/licenses/by/4.0/", "url": "https://oercommons.org/courseware/lesson/87922/overview", "title": "Statewide Dual Credit World History, The Period of Revolution 1650-1871 CE, Chapter 9: Revolution, Spanish South America", "author": "Anna McCollum" }
https://oercommons.org/courseware/lesson/87889/overview	English Colonization Overview English Colonization The English were very different than the Spanish, Portuguese, French, or the Dutch in their colonization methods. This was very important point. The English focused mostly on trade, with limited engagements with indigenous populations overall. The English also promoted self reliance and governments. Learning Objectives - Compare and contrast the differences of the English and the other colonizers. - Analyze the differences between the English colonial systems of the East and West. - Evaluate the role of indigenous, African, and Europeans in the English colonial system. - Analyze the impact of the indentured servants on the English system. Key Terms / Key Concepts Jamestown: The first permanent English settlement in the Americas, established by the Virginia Company of London as "James Fort" on May 4, 1607, and considered permanent after brief abandonment in 1610. It followed several earlier failed attempts, including the Lost Colony of Roanoke. Roanoke: Also known as the Lost Colony; a late 16th-century attempt by Queen Elizabeth I to establish a permanent English settlement in the Americas. The colony was founded by Sir Walter Raleigh. The colonists disappeared during the Anglo-Spanish War, three years after the last shipment of supplies from England. English The English model of colonization brought key elements of the Spanish, French, and Dutch colonies together in one approach. The lateness of the English colonization meant that they were heavily influenced by the Spanish and provided a foil to the Spanish colonization. One of the critical components of the English colonization models is the lack of cohesion between the colonies. By not following a uniformed model of colonization, this would cause great difficulty and future rebellions between the English and their colonial worlds. The English seemed to be the most interested in both gaining territory and gaining money. The English approach to the North American colonies is one that is centered around hedonistic capitalism and religious freedoms. The English colonization in the Indian subcontinent is one that is also divided between the New World and the Indian Subcontinent, where the English divisions proved central to the ultimate division of the Mughal Empire and eventual British East Indies Company Raj. During the first wave of colonization, the English were the last European country to begin to colonize. Partly due to the lack of resources and technology that other Europeans had, the English had a very difficult time to establish a colonial presence. The Treaty of Tordaellsias was another problem that the English colonists had to overcome. The treaty divided the world between the Spanish and the Portuguese, but left out the other European colonizers, and by having the word of the Pope, this meant that the English were not about to disobey the Christian Church to gain colonies. Early English explorers were divided in their approaches to colonization. Some of the early English focused their attention on the northern reaches of the world, attempting to find the mythical Northwest Passage. Explorers such as John Cabot, who explored the lands of Nova Scotia, Newfoundland, and Labrador near Canada. Cabot sailed in the late 15th century for the English king Henry VIII. The English established a colony on these islands but they were never successful, partially due to the political and economic turmoil in England during the Tutor Dynasty. The lack of resources from the Canadian coastline also made it difficult to ensure deeper connections to the English colonization and community. Other English colonizers and settlers followed a different path, focusing instead on finding ways to integrate and take from the Spanish. Many of these colonizers were interested in attacking the Spanish and causing disruptions to the Spanish supply lines that were small but significant wounds for the Spanish to overcome. English sailors such as Sir Francis Drake, helped to wreak havoc on the Spanish supplies in Latin America. Sir Francis Drake was born in 1540 CE in England and grew up during the Elizabethan Era of England. Drake spent his early life around the sea and traveling for the English as a merchant and trader around the Northern Sea Ports in Europe. Recent historians note that some of Drake’s economic success rested upon slave trading in his early 20s. By venturing into African waters, Drake was provoking the Portuguese, who had a massive hold on the slave trade at the time. Drake’s antagonism of the Portuguese early on in his career would be the bedrock of his political and economic fortunes. From there, Drake began to attack the Spanish ships and their cargo. By raiding several of the Spanish ships, he began to amass a fortune of silver and gold leaving the New World. Drake became very well known in the Spanish and English worlds for different reasons. The Spanish became very upset by the constant raiding and destruction, while the English queen Elizabeth began to find favor in Drake and started having his seat at the English Court. This type of harassment of the Spanish was important for the English because it provided much needed funds that went to help the English to continue to grow and expand their colonial operations, and secondly, it provided key navigational and structural techniques on how to be better sailors. Sir Francis Drake’s circumnavigation of the world proved to be very profitable, not only did he gain massive amounts of Peruvian gold and silver, but it demonstrated that the English were on their way to becoming a global empire. Upon his return to England, in 1581 CE, Drake was knighted by Elizabeth and his fortunes continued to grow. Queen Elizabeth relied on Drake to not only provide silver and gold to the English empire, but also to help fuel the English colonization. The antagonistic relationship that Elizabeth had with the Spanish King Phillip II, meant that Elizabeth publicly disavowed Drake, but secretly pushed him to continue his harassment of the Spanish. Ultimately this harassment led the Spanish to build an armada to attack and stop these attacks. Drake knew that the Spanish were building massive warships and his expertise from years of harassing the Spanish proved effective. Drake helped to design the English strategy of smaller ships that were lighter and easier to move in the water against the larger and bulkier Spanish ships. Drake’s strategy proved successful, for when the Spanish arrived and attempted to invade England, the English ships were able to repel and keep the Spanish from landing. The English defeat of the Spanish Armada in 1588 CE was the turning point for the English naval policy. The English became the rulers of the sea with their superior ships and weapons. Drake was one of the key members of a group known as the Buccaneers, who were English pirates in the New World. Buccaneers created significant supply and critical shortages of Spanish silver and gold from the New World. This was a massive problem for the Spanish, that would eventually lead to their downfall as a colonial world power. Sir Francis Drake paved the way for other English explorers and settlers, as the English naval understandings grew, so too did the new desire for growing colonies in the New World. One of the critical differences between the English and the Portuguese and Spanish was the English use of the joint-stock companies. In today’s world, the voyage to the New World would be equivalent to going to Mars. It is extremely dangerous, expensive, and hard to get to this location. If you were interested in going to Mars, think about the funds that you have currently, it probably be much more than one individual could fund. But, if you were able to talk to your friends and their families and demonstrate how it would benefit them when you and your company makes it to Mars, that you might get funds. You would need to write a receipt that demonstrated the money they give you is proportional to the amount that you need, but also they get a part of that profit. The super high risk is worth a super high reward. This approach today would be called a stock and is how many of the companies in the United States are financed, through buying and selling of stocks. In the 15th to 17th centuries, it was incredibly expensive to go to the New World. By offering stock options, companies took the incredible individual risk of the adventure from very high, then to spread throughout the stock holders and made this lower. The use of the joint-stock company would not only benefit the risk/profit of the voyage, but also it created a group of investors that became increasingly wealthy due to the spreading of the rewards reaped from the successful adventures. Overtime, the English removed the word joint, and these companies became simply stock companies. The Dutch had a similar investment type of colonization with the Dutch East Indies and West Indies Companies. These provided travel funds and lobbied for colonization and opening of markets. The British companies, on the other hand, were central for establishing colonization in the North American world. The English exploration flourished following the defeat of the Spanish Armada in 1588 CE. New expeditions led by Sir Walter Raleigh to the New World would eventually pave the way for the first successful English colony. The changing North American political map was very important for the English to find a region that they could establish a colony. The Spanish dominated the South America and Florida, while the French had gained a colonial reign in the extreme northern region of North America. The English had to find the region between these two European powers to establish their own settlements. The English first attempt was in North Carolina’s Outer Banks region at the colony of Roanoke in 1585 CE. The colony failed for many reasons, including not enough English support and failures of political leadership to supply the colony with much needed resources and maintenance. The second attempt at colonization was at Jamestown, in 1607 CE. It is the Jamestown colony that demonstrates how fragmented the early English vision of colonization was. Many of the English future colonists read and discussed the tales and writings of the Spanish conquest. These future English colonists thought that there were many empires like the Aztec and Inca in the Americas, that if the English could establish a colony, they could put themselves at the top of an indigenous empire. The charter of the Jamestown colony puts forward that the goals of the colony were to, “give and take Order, to dig, mine, and search for all Manner of Mines of Gold, Silver, and Copper, as well within any Part of their said several Colonies…” One of the main reasons for establishing a colony of Jamestown was to gain as much mineral resources, such as gold and silver, as possible, meant that the majority of the population that were middle and upper class males that were interested in getting wealthy and powerful in the Americas. English Colonial America: Differences of Plymouth and Jamestown This mindset was one of the central problems that the future colonists of Jamestown had, because their interest in extracting wealth, meant that the Jamestown was not established for long term growth by having families or individuals who had practical farming skills. Hence, the year following the establishment of Jamestown, there was a prolonged period of starvation. The Jamestown colony was on the verge of failing until in 1611 CE. Learning Objectives - Analyze the impact of Jamestown on the English system. - Evaluate the government and economics of Jamestown. Key Terms / Key Concepts Plymouth: An English colonial venture in North America from 1620 to 1691, first surveyed and named by Captain John Smith. The settlement served as the capital of the colony and at its height, it occupied most of the southeastern portion of the modern state of Massachusetts. Navigation Acts: A series of English laws that restricted the use of foreign ships for trade between every country except England. They were first enacted in 1651, and were repealed nearly 200 years later in 1849. They reflected the policy of mercantilism, which sought to keep all the benefits of trade inside the empire, and minimize the loss of gold and silver to foreigners. Tobacco revitalized the Jamestown colony by introducing a large cash crop that could easily be produced in the region and provided great wealth to growers. Tobacco was one of the key crops of the Colombian Exchange, where Once the settlers arrived in the Virginia area, they found there were indigenous peoples, but many of the English remarked that the American landscape was very empty and devoid of life. This is probably because of the disease that were introduced during the Spanish colonial period and had decimated the indigenous population. The other component is that the English were expecting to find large groups like the Spanish and there were none of these that were still left in the North American continent at the time of English arrival. The groups that the English did find, were local bands of Powhatans that were a part of the Algonquin indigenous groups. The Powhatans were friendly to the English and showed these settlers how to farm and grow local foods. The English, who were more interested in gold and expansion, thought that the local Powhatans would be the basis of their new English empire, wanted the indigenous populations to do the work to grow the food. This meant that the Powhatans quickly left the English after demonstrations of how to grow their own food. It is important to note, that the majority of the first English settlers were males, similar to the Spanish colonization model. The biggest difference in the Spanish and English colonial societies relationship with indigenous populations is that the English were not interested in starting families with the indigenous populations. There was a very distinct separation between the English and the indigenous populations. The English, on the other hand, were interested in expansion and this meant that the Powhatans had to defend their homes and ways of life if they were to survive against the English settlement. The English found that their luck of finding large empires of gold and silver were extremely limited and thus, they were beginning to run out of resources and scarcity of the winter set in in 1609-1610 CE. This winter saw limited food and individuals went as far as cannibalism and digging up the bodies of recently deceased for food. Of the nearly 500 people in Jamestown, only 61 were alive in the Spring of 1610 CE. The Jamestown colony struggled in the first few years seems like an understatement. The introduction of tobacco was a major economic success and turned the fortunes of the English colony of Jamestown around. Tobacco was introduced in 1611 CE, by Sir Walter Raleigh. The English loved tobacco since it was introduced to Europe by the Spanish almost a century before. The English had many smokehouses throughout London and it was even seen as a nuance by King James I, who wrote about the harmful affects of the drug. By having tobacco grown in Virginia, meant that the English colonies could make massive profits and keep the money inside of the English economic system. This had such a dramatic effect when tobacco was successfully grown in Virginia, that much of the focus of the English were to find ways to build up the economics of the Virginia colonies. There is a great irony that the saving grace of the Jamestown colony was not food that could easily be consumed by the grower, after the Starving Time of Jamestown. The trade of goods for tobacco was the key way that the colonists could purchase their goods from the English company store. This relationship also had a dramatic effect on labor of the Jamestown colony as well. Tobacco is a heavy labor intensive crop, from planting to curing, there is much time and effort put into making tobacco. The land has to be set by the farmer to produce tobacco by cleaning away the land, then it has to be sewn into the ground. Afterwards, the crop has to be tended, which takes upwards of four months to go from seed to crop, usually meaning that there is constant watering and removal of insects. The harvest usually happens in the late summer, usually July to August, where the large leaves need to be “cured,” meaning that they are to be stored and dried out. From here, the crop is to be shipped and chopped into finer parts before it can be made into cigars, which was the popular way of consuming tobacco in the 16th century. The English want for the addictive plant meant that there was a large amount of money to be made in Virginia. The problem was the intensity of the labor was usually much more than a small farmer could manage. This meant that the English developed a unique labor system called indentured servitude. This was where an American farmer could go to England and offer a contract for a set time frame for work to be completed. Many of the indentured servant contracts were for seven years for men, and usually were for three years for women. English law was written that the indentured servant system appeared to benefit both the servant and the farmer in many ways. The farmer got a worker for a set time and could make any demands of the worker that the farmer wanted. Also, the farmer got land, usually near their original home area for bringing an English person to the Americas. The servant also was rewarded in English law. Many of the servants were lower class and could not afford to travel to seek fortunes in the Americas. This was a way to get to the Americas, as a positive trade off. For the men, once completing their contract, they were promised lands as well that they too could then become farmers in Virginia. While this appears to benefit both sides, there are significant problems with the indentured servant system. First, the average lifespan of the indentured servant was approximately 3 years in colonial Virginia, while many of the male contracts were for 7. This is due to harsh working environments, demands of the master, and diseases such as malaria that were rampant in the colonial Americas. Historians often note that this is very similar to a form of slavery. Female indentured servants were usually domestic workers and had laws that protected them from forced marriages to their masters during the indentured servant contract. The lack of women in Virginia meant that women had a premium experience and many times the contracts were shortened because of the valuable domestic services that women provided. The downside, is that women were not given the same opportunities after their contract expired, and many ended their contracts with marriage to the master without being granted their own lands. Also, the lands that were given to newly freed male indentured servants usually were at the western territories of the Virginia colony, that were often in disputes with indigenous populations because the English would without treaty simply give these lands without asking the indigenous populations. The harshness of the indentured servant life resulted in many running away from their owners. Primary sources linked here demonstrate how difficult it would have been to identify indentured servants that ran-away. The system of indentured servants was one that was very risky and fraught with problems, from harsh working conditions, to contract time that meant the workers often never benefitted from their contract, to those that earned their freedom not able to have lands that were not in dispute with indigenous populations. The breaking of the indentured servant system was the Nathaniel Bacon Rebellion in 1675-1676 CE. Nathaniel Bacon was an indentured servant that worked to gain his freedom and lands, but because of political problems that the Virginia governor faced, could not successfully get these. In the 1670s period, the Virginia governor William Berkley saw the increasing problems with the indigenous population. Berkley’s decision was to make peace treaties with the indigenous populations on the western borders of Virginia that said that the English would travel or own no more lands west of a line of demarcation. The indigenous populations were happy and this stopped many raids and fighting between the colonists and the English settlers. But Berkley had a secondary problem, that much of those lands were where indentured servants were promised and a growing population of newly freed indentured servants who felt that the promise of their contract was not being fulfilled. Nathaniel Bacon was a leader of this growing group of discontented newly emancipated indentured servants. He led a small force against the governor of Virginia, demanding their contract lands. Bacon was successful in torching the Jamestown settlement and chasing Berkeley from Virginia. In the resulting chaos, Bacon led his men in anger against the indigenous populations and raided and murdered several different groups in the Virginia region. Bacon was able to capture Berkeley and drew a gun pointed at Berkeley’s chest demanding changes, but Berkeley would not budge on his orders. This meant that Bacon knew that his demands would not be met and held Jamestown for months. It took almost a year before the rebellion broke apart, mostly due to Bacon dying of dysentery. The result of the Bacon Rebellion was clear to the colonial administration, that something had to be done to clearly distinguish the indentured servants, freedom, and who owned land. Bacon’s Rebellion was the key turning point because indentured servitude was no longer favored as a key method of labor in the English colonial system. Instead, the English started relying on the system of African slavery that started in 1619 CE. Slavery in the English system started early but changed as a direct result of the Nathaniel Bacon Rebellion. The first slaves arrived in the English North America in Virginia in 1619 CE. At first, the colonial society was not clear what this meant for the African populations. Africans originally were brought as indentured servants. It is important to note that this was essentially slavery, and that the treatment of the African population that was brought to the early Virginia colony was very difficult. By the 1630s CE, there were several emancipated African populations earned their freedom and lands. Following the Nathaniel Bacon’s rebellion, all African populations were transformed into enslaved. The form of slavery that the English developed their system known as chattel slavery, where those that were enslaved and all their descendants were enslaved for all future times. This system was very brutal because it meant that if an individual was born into slavery, that their family and descendants would remain enslaved forward. By enslaving African populations, this meant that it was very clear to the English colonists who was free and who was enslaved. This type of slavery continued from the middle of the 17th to the middle of the 19th century and would form many of the social and political problems of the American colonies unifying to the American Civil War. The role of African populations in English society was very unique as well, at the bottom tier meant that they were treated very terribly by all in the English system. African American women were subject to abuses by both the male and the female white owners. Labor went beyond simply producing crops, but also extended into the family support work, such as domestic labor as well. The English system of race was heavily influenced by their historic relationships in England and would have a significant influence on future colonization. The English had a very different historic relationship with race than other European colonizers. For example, the Spanish invasion in 711 CE of the Berbers from Northern Africa had a profound impact on the Spanish integration of diverse populations into their society. The English, on the other hand, were invaded by other Europeans throughout their history. This has a profound impact on the English understanding of race and ethnicity. Because of the lack of race meant that as the English were expanding throughout the world in the Early Modern period. The English had a very difficult time integrating and treating others, such as African and indigenous populations into the English society. For example, the English did not integrate the indigenous into their colonial society in Jamestown. The indigenous populations were push to the outside of the English system. Also the English would take lands and break treaties with the indigenous populations. The mistreatment of the indigenous population would only intensify moving forward as the English traveled throughout the world and would continue this lack of integration of populations. The treatment of the Afro-English populations was also demonstrated in the 17th century of exclusion. The relationship of power between the English and other populations becomes an either/or situation; where the individual is either English, or they do not have any political or economic power. The English would carry these ideas far beyond the North American shores, into the Indian subcontinent as well during subsequent colonization. In 1672, the Royal African Company was inaugurated, receiving from King Charles a monopoly of the trade to supply slaves to the British colonies of the Caribbean. From the outset, slavery was the basis of the British Empire in the West Indies and later in North America. Until the abolition of the slave trade in 1807, Britain was responsible for the transportation of 3.5 million African slaves to the Americas, a third of all slaves transported across the Atlantic. The introduction of the Navigation Acts led to war with the Dutch Republic. In the early stages of this First Anglo-Dutch War (1652-1654), the superiority of the large, heavily armed English ships was offset by superior Dutch tactical organization. English tactical improvements resulted in a series of crushing victories in 1653, bringing peace on favorable terms. This was the first war fought largely, on the English side, by purpose-built, state-owned warships. After the English monarchy was restored in 1660, Charles II re-established the navy, but from this point on, it ceased to be the personal possession of the reigning monarch, and instead became a national institution, with the title of “The Royal Navy.” As the English were developing their North American southern colony, they began a second colonial project in the American north. The English development of the colony of Plymouth took lessons of the first English colonization. To understand the issues of the Plymouth colony’s origin, it is important to start with the Protestant Reformation and the political and cultural transformations in the English system. When Henry VIII created the Anglican Church started the deep divisions in the English Christian community. These would intensify with subsequent English rulers and the English Civil War. The reign of Charles I intensified the want and desire for reformation of the Anglican Church for more purity. These reformers would be come known as the Puritans, wanting to purify Catholicism from the Anglican Church. Many of these individuals wanted full separation from the Anglican Church. Many of the Puritans were middle to upper class and had wealth. They were strict adherents to the Calvinist thought about reading and writing for the individual as well as putting importance of family ahead of social belonging. Because of the political turmoil in England, many of these individuals left England to go to the Netherlands because of similar Protestantism and freedoms of movements. The English that went to the Netherlands were there for approximately 10 years before they found the culture too unfamiliar and yearned for their children to be raised in more English customs and culture. The Puritans gained a company charter in 1619 CE, to establish the Plymouth colony. The congregation could apply for a company charter for the New World to establish an area that they could be in control of and practice their own faith. The English crown granted them a charter to land near Virginia and allowed the Puritans to leave in June 1620 CE. The planning and settlement of Plymouth helped to demonstrate the key differences between the Puritans and Jamestown. The first difference was the members of the voyage in the Mayflower were middle class and traveled with complete families. Having women and families was a key difference between the Jamestown and Plymouth colonies. The stability of family meant that Plymouth’s population did not suffer the way that Jamestown did having families. Families also provided structure to the Plymouth society as well. The second difference between the English colonizations was the Plymouth colony centered around the Puritan Church. In Jamestown colony, the Christian church was not the center of society, whereas in the Plymouth colony the Puritan church was the key to society. The relationship of the Puritan Church went well beyond the cultural, it also went to the political. Another key difference between the English colonization and the Spanish, French, Portuguese, and Dutch was the role of the government in the colonial society. In the Spanish and Portuguese, the colonial governments were established by the crown and many of the decrees were established by the monarchy. The French crown also held great control over the colonial world, but had a bit more leniency between the French individual and the crown. The Dutch also allowed for more control and the company charter had the majority of the political and economic stability of the colony. The English, on the other hand, allowed their North American colonies to establish their own governments. The Jamestown colony established the House of Burgess, where men, of good standing, white, property owning, and over 21 could elect their representative at the colonial level. This would prove to be a very important relationship because the Jamestown colony’s establishment meant that the colonies could raise their own taxes and establish their smaller rules for political understandings. The Puritans, also established their own rules of government that began with the Mayflower Compact. This was a charter that every male on the Mayflower agreed that they could participate by either direct elections or holding direct vote in the colony. The difference between the House of Burgess and the Mayflower Compact was that the Puritan society stipulated that participation in the colonial government was predicated on the participation in the Puritan church. This also highlights the differences between the House of Burgess and the Mayflower Compact by showing how important the role of the Christian church was between these two societies. Both, the House of Burgess and the Mayflower Compact, these societies could levy taxes for their perspective colonial governments. Yet, the British crown did not ask the colonies to pay into the larger British tax system. Meaning, that if you were in the colonial societies, that you did not pay the British taxes. It is unclear why the British would allow such a very important oversight of the colonial world, but it would prove to be very important when considering the divisions between the colonies and the English with the relationship of taxes. Self representing democracies were essential for the British system of colonization and provided a key difference between the different colonial models. The Plymouth colony eventually became known as the Plymouth plantation and was relatively successful early on in their social organizations. The Plymouth colony had a short period of starvation, that was much less dramatic than the Jamestown colony. The Plymouth colony could not plant or produce tobacco, thus the need for indentured servants and slaves was much less. Most of the farming in the Plymouth colony was subsistence or export of key materials such as timber. The less labor needs, meant that the Plymouth colony functioned on trade and trading much heavier than the Jamestown colonial world and would develop in a very different direction. Overtime, the Puritans split because of religious and cultural differences and thus individuals Brooke away from the Plymouth colony to establish their own colonial worlds. Anne Hutchinson and Thomas Hooker would eventually leave the Plymouth colony and founded their own colonies nearby in Rhode Island and Connecticut. The model of the role of the church and state remained throughout these newly formed and developed colonial worlds. The English developed different colonial models in the Jamestown and Plymouth colonies. The role of church and state, the economics, the culture, even as far as gender relationships were early on, defined and held to the core ideas of each of these respective regions. While both of these colonial models were important, it is easier to imagine these are the two poles of the North American colonial model, that on one side is Jamestown and the other is Plymouth, the subsequent colonies that emerged were blended these ideas in more of a grey between. For example, the American south developed in the Jamestown model, but different colonies in North Carolina to Maryland, were different on key issues. The same can be said for New England colonies as well. The region that was between these two poles was most notable the Middle colonies, of Pennsylvania, New York, New Jersey, and Delaware. These colonies took elements of both sets of colonial models as inspiration for their colonies. Pennsylvania is an excellent example of such a blend. William Penn established the colony for religious freedom for Quakers, a Protestant religion that believed that the chosen were touched by God and would shake or quake. This was a peaceful Protestant group that believed that there was a role for me, women, and indigenous in the community. Pennsylvania had great farming region and relied some on indentured servant labor, but not many slaves entered into the Pennsylvanian world. This blend of elements from Jamestown and Plymouth defined the Middle Colonies and would be shared throughout the North American world. The North American colonial experimentation demonstrates the English system was very difficult and had unique qualities to colonization. The English reliance on harassing the Spanish and establishing their own empire base was one of significant importance for the English. The establishment of a colonial society that had a self representation in government also provided a unique challenge and standard for the English as well. While the English system in the North American world had its unique similarities and differences, the British colonization of the Indian subcontinent held some of these similar idiosyncrasies. The English were also interested in exploring South Asia, specifically in the Indian subcontinent region. The British followed many of the Dutch and French settlements in the region to establish settlments, but were utlimately successful by incorporating a model of company control, similar to Jamestown. This would prove benefitial in the colonization and conquest of India, when the British East Indies Company came to control the region. This will be explored later, but note that many of the same cultural, political, economic, and social systems established by the English here in the early days of exploration, would continue forward with the English colonization of South Asia as well. Primary Source: Nathaniel Bacon's Rebellion: The Declaration Bacon’s Rebellion: The Declaration Nathaniel Bacon (1676) Economic and social power became concentrated in late seventeenth-century Virginia, leaving laborers and servants with restricted economic independence. Governor William Berkeley feared rebellion: “six parts of Seven at least are Poore, Indebted, Discontented and Armed.” Planter Nathaniel Bacon focused inland colonists’ anger at local Indians, who they felt were holding back settlement, and at a distant government unwilling to aid them. In the summer and fall of 1676, Bacon and his supporters rose up and plundered the elite’s estates and slaughtered nearby Indians. Bacon’s Declaration challenged the economic and political privileges of the governor’s circle of favorites, while announcing the principle of the consent of the people. Bacon’s death and the arrival of a British fleet quelled this rebellion, but Virginia’s planters long remembered the spectacle of white and black acting together to challenge authority. 1. For having, upon specious pretenses of public works, raised great unjust taxes upon the commonalty for the advancement of private favorites and other sinister ends, but no visible effects in any measure adequate; for not having, during this long time of his government, in any measure advanced this hopeful colony either by fortifications, towns, or trade. 2. For having abused and rendered contemptible the magistrates of justice by advancing to places of judicature scandalous and ignorant favorites. 3. For having wronged his Majesty’s prerogative and interest by assuming monopoly of the beaver trade and for having in it unjust gain betrayed and sold his Majesty’s country and the lives of his loyal subjects to the barbarous heathen. 4. For having protected, favored, and emboldened the Indians against his Majesty’s loyal subjects, never contriving, requiring, or appointing any due or proper means of satisfaction for their many invasions, robberies, and murders committed upon us. 5. For having, when the army of English was just upon the track of those Indians, who now in all places burn, spoil, murder and when we might with ease have destroyed them who then were in open hostility, for then having expressly countermanded and sent back our army by passing his word for the peaceable demeanor of the said Indians, who immediately prosecuted their evil intentions, committing horrid murders and robberies in all places, being protected by the said engagement and word past of him the said Sir William Berkeley, having ruined and laid desolate a great part of his Majesty’s country, and have now drawn themselves into such obscure and remote places and are by their success so emboldened and confirmed by their confederacy so strengthened that the cries of blood are in all places, and the terror and consternation of the people so great, are now become not only difficult but a very formidable enemy who might at first with ease have been destroyed. 6. And lately, when, upon the loud outcries of blood, the assembly had, with all care, raised and framed an army for the preventing of further mischief and safeguard of this his Majesty’s colony. 7. For having, with only the privacy of some few favorites without acquainting the people, only by the alteration of a figure, forged a commission, by we know not what hand, not only without but even against the consent of the people, for the raising and effecting civil war and destruction, which being happily and without bloodshed prevented; for having the second time attempted the same, thereby calling down our forces from the defense of the frontiers and most weakly exposed places. 8. For the prevention of civil mischief and ruin amongst ourselves while the barbarous enemy in all places did invade, murder, and spoil us, his Majesty’s most faithful subjects. Of this and the aforesaid articles we accuse Sir William Berkeley as guilty of each and every one of the same, and as one who has traitorously attempted, violated, and injured his Majesty’s interest here by a loss of a great part of this his colony and many of his faithful loyal subjects by him betrayed and in a barbarous and shameful manner exposed to the incursions and murder of the heathen. And we do further declare these the ensuing persons in this list to have been his wicked and pernicious councilors, confederates, aiders, and assisters against the commonalty in these our civil commotions. Sir Henry Chichley William Claiburne Junior Lieut. Coll. Christopher Wormeley Thomas Hawkins William Sherwood Phillip Ludwell John Page Clerke Robert Beverley John Cluffe Clerke Richard Lee John West Thomas Ballard Hubert Farrell William Cole Thomas Reade Richard Whitacre Matthew Kempe Nicholas Spencer Joseph Bridger John West, Hubert Farrell, Thomas Reade, Math. Kempe And we do further demand that the said Sir William Berkeley with all the persons in this list be forthwith delivered up or surrender themselves within four days after the notice hereof, or otherwise we declare as follows. That in whatsoever place, house, or ship, any of the said persons shall reside, be hid, or protected, we declare the owners, masters, or inhabitants of the said places to be confederates and traitors to the people and the estates of them is also of all the aforesaid persons to be confiscated. And this we, the commons of Virginia, do declare, desiring a firm union amongst ourselves that we may jointly and with one accord defend ourselves against the common enemy. And let not the faults of the guilty be the reproach of the innocent, or the faults or crimes of the oppressors divide and separate us who have suffered by their oppressions. These are, therefore, in his Majesty’s name, to command you forthwith to seize the persons above mentioned as traitors to the King and country and them to bring to Middle Plantation and there to secure them until further order, and, in case of opposition, if you want any further assistance you are forthwith to demand it in the name of the people in all the counties of Virginia. Nathaniel Bacon General by Consent of the people. William Sherwood Source: "Declaration of Nathaniel Bacon in the Name of the People of Virginia, July 30, 1676,"Massachusetts Historical Society Collections, 4th ser., 1871, vol. 9: 184–87. Attributions Attributions Images courtesy of Wikimedia Commons: https://upload.wikimedia.org/wikipedia/commons/4/4f/Clive.jpg Boundless World History https://www.coursehero.com/study-guides/boundless-worldhistory/england-and-parliamentary-monarchy/ Work based around the ideas of Patricia Seed: Ceremonies of Possession in Europe's Conquest of the New World, 1492–1640	oercommons	2025-03-18T00:37:03.377842	Neil Greenwood	{ "license": "Creative Commons - Attribution - https://creativecommons.org/licenses/by/4.0/", "url": "https://oercommons.org/courseware/lesson/87889/overview", "title": "Statewide Dual Credit World History, The Making of Early Modern World 1450-1700 CE, Chapter 6: Exploration, English Colonization", "author": "Anna McCollum" }
https://oercommons.org/courseware/lesson/87921/overview	Central America Overview Mexican War of Independence The Central American Independence Movement was very important because there were two very key problems that were established. There were two distinct waves of reform, one a social revolution and then a political independence movement. Learning Objectives - Evaluate the impact of the Napoleonic Wars on Central American independence movements. - Evaluate the impact of the Hidalgo Revolution on the Mexican Independence movement. Key Terms / Key Concepts Mestizos: a person of mixed race, especially the offspring of a Spaniard and an American Indian New Spain: a colonial territory of the Spanish Empire, in the New World north of the Isthmus of Panama (It was established following the Spanish conquest of the Aztec Empire in 1521, and following additional conquests, it was made a viceroyalty in 1535. The first of four viceroyalties Spain created in the Americas, it comprised Mexico, Central America, much of the Southwestern and Central United States, and Spanish Florida as well as the Philippines, Guam, Mariana, and Caroline Islands.) Miguel Hidalgo y Costilla: a Mexican Roman Catholic priest and a leader of the Mexican War of Independence hagiographic: a biography of a saint or an ecclesiastical leader in any of the world’s spiritual traditions. (The term, especially in contemporary times, is often used as a pejorative reference to biographies and histories whose authors are perceived to be uncritical of or reverential to their subject.) Ignacio Allende: a captain of the Spanish Army in Mexico who came to sympathize with the Mexican independence movement (He attended the secret meetings organized by Josefa Ortiz de Domínguez where the possibility of an independent New Spain was discussed. He fought along with Miguel Hidalgo y Costilla in the first stage of the struggle, eventually succeeding him in leadership of the rebellion.) Plan of Iguala: a revolutionary proclamation promulgated on February 24, 1821, in the final stage of the Mexican War of Independence from Spain; stated that Mexico was to become a constitutional monarchy whose sole official religion would be Roman Catholicism and that the Peninsulares and Creoles of Mexico would enjoy equal political and social rights Agustín de Iturbide: a Mexican army general and politician (During the Mexican War of Independence, he built a successful political and military coalition that took control in Mexico City on September 27, 1821, decisively gaining independence for Mexico. After the secession of Mexico was secured, he was proclaimed President of the Regency in 1821. A year later, he was announced as the Constitutional Emperor of Mexico, reigning briefly from May 19, 1822, to March 19, 1823. He is credited as the original designer of the first Mexican flag.) Start of the Mexican War of Independence September 16 is celebrated as Mexican Independence Day. The Mexican War of Independence was an armed conflict. It was the culmination of a political and social process which ended the rule of Spain in the territory of New Spain in 1821. The war had its antecedent in the French invasion of Spain in 1808. And it extended from the publication of Grito de Dolores by Father Miguel Hidalgo y Costilla on September 16, 1810 to the entrance of the Army of the Three Guarantees, led by Augustín de Iturbide, in to Mexico City on September 27, 1821. The movement for independence was inspired by the Age of Enlightenment and the liberal revolutions of the last part of the 18th century. By that time, the educated elite of New Spain began to reflect on the relations between Spain and its colonial kingdoms. Changes in the social and political structure occasioned by Bourbon reforms and a deep economic crisis in New Spain caused discomfort among the Creole (native-born) elite. Political events in Europe had a decisive effect on events in most of Spanish America. In 1808, King Charles IV and Ferdinand VII abdicated in favor of French leader Napoleon Bonaparte, who left the crown of Spain to his brother Joseph Bonaparte. The same year, the ayuntamiento (city council) of Mexico City, supported by viceroy José de Iturrigaray, claimed sovereignty in the absence of the legitimate king. That led to a coup against the viceroy, which when suppressed ended with the leaders of the movement being jailed. Despite the defeat in Mexico City, small groups of conspirators met in other cities of New Spain to raise movements against colonial rule. In 1810, after being discovered, Querétaro conspirators chose to take up arms on September 16 in the company of peasants and indigenous inhabitants of Dolores (Guanajuato), who were called to action by the secular Catholic priest Miguel Hidalgo, former rector of the Colegio de San Nicolás Obispo. The Hidalgo Revolt Miguel Hidalgo y Costilla, who later became known as a top theologian, was a priest and member of a group of educated Criollos in Querétaro. When his older brother died in 1803, Hidalgo took over as priest for the town of Dolores. In 1810, Hidalgo concluded that a revolt was needed because of injustices against the poor of Mexico. By this time, Hidalgo was known for his achievements at the prestigious San Nicolás Obispo school in Valladolid (now Morelia), where he later served as rector. Hidalgo hosted secret gatherings in his home to discuss whether it was better to obey or to revolt against a tyrannical government, as he defined the Spanish colonial government in Mexico. Famed military leader Ignacio Allende was among his attendees. Hidalgo was in Dolores on September 15, 1810, with other rebel leaders including commander Allende, when they learned their conspiracy had been discovered. Hidalgo ran to the church, calling for all the people to gather, where from the pulpit he called upon them to revolt. They all shouted in agreement. They were a comparatively small group and poorly armed with whatever was at hand, including sticks and rocks. On the morning of September 16, 1810, Hidalgo called upon the remaining locals who happened to be in the market, and again, from the pulpit, exhorted the people of Dolores to join him. Most did. Hidalgo had a mob of some 600 men within minutes. This became known as the Grito de Dolores or Cry of Dolores. Hidalgo’s Grito didn’t condemn the notion of monarchy or criticize the current social order in detail, but his opposition to the events in Spain and the current viceregal government was clearly expressed in his reference to bad government. The Grito also emphasized loyalty to the Catholic religion, a sentiment with which both Creoles and Peninsulares could sympathize. Hidalgo was met with an outpouring of support. Intellectuals, liberal priests, and many poor people followed Hidalgo with enthusiasm. Hidalgo also permitted Indians and mestizos to join his war. Hidalgo and Allende marched their army through towns including San Miguel and Celaya, where the angry rebels killed all the Spaniards they found. Along the way they adopted the standard of the Virgin of Guadalupe as their symbol and protector. When they reached the town of Guanajuato on September 28, they found Spanish forces barricaded inside the public granary. Among them were some “forced” Royalists—Creoles who had served and sided with the Spanish. By this time, the rebels numbered 30,000 and the battle was horrific. They killed more than 500 Spanish and creoles, then marched on toward Mexico City. The Viceroy quickly organized a defense, sending out the Spanish general Torcuato Trujillo with 1,000 men, 400 horsemen, and 2 cannons, all that could be found on such short notice. On October 30, Hidalgo’s army encountered Spanish military resistance at the Battle of Monte de las Cruces, which ended with Hidalgo achieving victory after the cannons were captured and the surviving Royalists retreated to the City. Despite having the advantage, Hidalgo retreated against the counsel of Allende. This retreat on the verge of apparent victory has puzzled historians and biographers ever since. They generally believe that Hidalgo wanted to spare the numerous Mexican citizens in Mexico City from the inevitable sacking and plunder that would have ensued. His retreat is considered Hidalgo’s greatest tactical error. Rebel survivors sought refuge in nearby provinces and villages. The insurgent forces planned a defensive strategy at a bridge on the Calderón River, pursued by the Spanish army. In January 1811, Spanish forces fought the Battle of the Bridge of Calderón and defeated the insurgent army, forcing the rebels to flee towards the United States-Mexican border, where they hoped to escape. Unfortunately, Hidalgo’s army was intercepted by the Spanish army. Hidalgo and his remaining soldiers were captured in the state of Coahuila at the Wells of Baján (Norias de Baján). All of the rebel leaders were found guilty of treason and sentenced to death, except for Mariano Abasolo. He was sent to Spain to serve a life sentence in prison. Allende, Jiménez, and Aldama were executed on June 26, 1811, shot in the back as a sign of dishonor. Hidalgo, as a priest, had to undergo a civil trial and review by the Inquisition. He was eventually stripped of his priesthood, found guilty, and executed on July 30. The heads of Hidalgo, Allende, Aldama, and Jiménez were preserved and hung from the four corners of the granary of Guanajuato as a warning to those who dared follow in their footsteps. Following the execution of Hidalgo, José María Morelos took over leadership of the insurgency. He achieved the occupation of the cities of Oaxaca and Acapulco. In 1813, he convened the Congress of Chilpancingo to bring representatives together and, on November 6 of that year, the Congress signed the first official document of independence, known as the “Solemn Act of the Declaration of Independence of Northern America.” A long period of war followed. In 1815, Morelos was captured by Spanish colonial authorities, tried, and executed for treason. Legacy and Analysis of the Hidalgo Revolt Father Hidalgo is today remembered as the Father of his Country, the great hero of Mexico’s War for Independence. There are numerous hagiographic biographies about him. The truth about Hidalgo is more complex. His was the first serious insurrection on Mexican soil against Spanish authority, and his achievements with a poorly armed mob were significant. He was a charismatic leader and worked well with Allende despite their differences. After decades of abuse of Creoles and poor Mestizos, Hidalgo found that there was a vast well of resentment and hatred of the Spanish government. He provided the catalyst for Mexico’s poor to vent their anger on the hated Spaniards, but his “army” was impossible to manage or control. His leadership decisions, most importantly his retreat from Mexico City, contributed to his defeat. Hidalgo’s shortcomings have made historians ask, “What if?” Historians can only speculate about the result if Hidalgo had pushed into Mexico City in November 1810. Hidalgo appeared to be too proud or stubborn to listen to the sound military advice offered by Allende and others and press his advantage. Finally, Hidalgo’s approval of the violent sacking and looting by his forces in Guanajuato and other towns alienated the group most vital to any independence movement: middle-class and wealthy Creoles like himself. They were needed to develop a new identity and government for Mexico, one that would allow Mexicans to break from Spain. Hidalgo achieved mythic status after his death. His martyrdom was an example to others who picked up the fallen banner of freedom and independence. He influenced later fighters such as José María Morelos, Guadalupe Victoria, and others. Today, Hidalgo’s remains are held in a Mexico City monument known as “the Angel of Independence,” along with other Revolutionary heroes. Vicente Guerrero and Colonel Agustín de Iturbide After the suppression of Hidalgo’s revolt, from 1815 to 1821 most fighting for independence from Spain was by small and isolated guerrilla bands. From these, two leaders arose: Guadalupe Victoria (born José Miguel Fernández y Félix) in Puebla and Vicente Guerrero in Oaxaca, both of whom gained allegiance and respect from their followers. After Hidalgo was stopped, the Spanish viceroy believed the situation under control and issued a general pardon to every rebel who would lay down his arms. By early 1820,after ten years of civil war and the death of two of its founders, the independence movement was stalemated and close to collapse. The rebels faced stiff Spanish military resistance and the apathy of many of the most influential criollos. In what was supposed to be the final government campaign against the insurgents, in December 1820 Viceroy Juan Ruiz de Apodaca sent a force led by a royalist criollo Colonel Agustín de Iturbide to defeat Guerrero’s army in Oaxaca. Iturbide, a native of Valladolid (now Morelia), gained renown for his zeal against Hidalgo’s and Morelos’s rebels during the early independence struggle. A favorite of the Mexican church hierarchy, Iturbide symbolized conservative criollo values; he was devoutly religious and committed to the defense of property rights and social privileges. He also resented his lack of promotion and failure to gain wealth. Iturbide’s assignment to the Oaxaca expedition coincided with a successful military coup in Spain against the monarchy of Ferdinand VII. The coup leaders, part of an expeditionary force assembled to suppress the independence movements in the Americas, had turned against the monarchy. They compelled the reluctant Ferdinand to reinstate the liberal Spanish Constitution of 1812 that created a constitutional monarchy. When news of the liberal charter reached Mexico, Iturbide perceived it both as a threat to the status quo and a catalyst to rouse the criollos to gain control of Mexico. The tides turned when conservative Royalist forces in the colonies chose to rise up against the liberal regime in Spain; it was a total turnaround compared to their previous opposition to the peasant insurgency. After an initial clash with Guerrero’s forces, Iturbide assumed command of the royal army. At Iguala, he allied his formerly royalist force with Guerrero’s radical insurgents to discuss the renewed struggle for independence. While stationed in the town of Iguala, Iturbide proclaimed three principles, or “guarantees,” for Mexican independence from Spain. Mexico would be an independent monarchy governed by King Ferdinand, another Bourbon prince, or some other conservative European prince; criollos would be given equal rights and privileges to peninsulares (those born in Spain); and the Roman Catholic Church in Mexico would retain its privileges and position as the established religion of the land. After convincing his troops to accept the principles, which were promulgated on February 24, 1821 as the Plan of Iguala, Iturbide persuaded Guerrero to join his forces in support of this conservative independence movement. A new army, the Army of the Three Guarantees, was placed under Iturbide’s command to enforce the Plan of Iguala. The plan was so broadly based that it pleased both patriots and loyalists. The goal of independence and the protection of Roman Catholicism brought together all factions. Iturbide’s army was joined by rebel forces from all over Mexico. When the rebel victory became certain, the Viceroy resigned. On August 24, 1821, representatives of the Spanish crown and Iturbide signed the Treaty of Córdoba, which recognized Mexican independence under the Plan of Iguala. On September 27, 1821, the Army of the Three Guarantees entered Mexico City, and the following day Iturbide proclaimed the independence of the Mexican Empire, as New Spain would henceforth be called. On the night of May 18, 1822, a mass demonstration led by the Regiment of Celaya, which Iturbide had commanded during the war, marched through the streets and demanded their commander-in-chief to accept the throne. The following day, the congress declared Iturbide emperor of Mexico. On October 31, 1822, Iturbide dissolved Congress and replaced it with a sympathetic junta. After Independence: The Mexican Empire The Spanish attempts to reconquer Mexico comprised episodes of war between Spain and the new nation. The designation mainly covers two periods: from 1821 to 1825 in Mexico’s waters, and a second period of two stages, including a Mexican plan to take the Spanish-held island of Cuba between 1826 and 1828, and the 1829 landing of Spanish General Isidro Barradas in Mexico to reconquer the territory. Although Spain never regained control of the country, it damaged the fledgling economy. After independence, Mexican politics were chaotic. The presidency changed hands 75 times over the next 55 years (1821 – 76). The newly independent nation was in dire straits after 11 years of the War of Independence. No plans or guidelines were established by the revolutionaries, so internal struggles for control of the government ensued. Mexico suffered a complete lack of funds to administer a country of over 4.5 million km². (In 1822, Mexico had annexed the Federal Republic of Central America, which includes present-day Costa Rica, El Salvador, Guatemala, Honduras, Nicaragua, and part of Chiapas.) And it faced the threats of emerging internal rebellions and of invasion by Spanish forces from their base in nearby Cuba. Mexico now had its own government, but Iturbide quickly became a dictator. He even had himself proclaimed emperor of Mexico, copying the ceremony used by Napoleon when he proclaimed himself emperor of France. No one was allowed to speak against Iturbide. He filled his government with corrupt officials who became rich by taking bribes and making dishonest business deals. Attributions Attributions Images courtesy of Wikimedia Commons Miguel Hidalgo con estandarte: https://upload.wikimedia.org/wikipedia/commons/7/7d/Miguel_Hidalgo_con_estandarte.jpg Boundless World History https://www.coursehero.com/study-guides/boundless-worldhistory/the-mexican-war-of-independence/ https://www.coursehero.com/study-guides/boundless-worldhistory/the-south-american-revolutions/	oercommons	2025-03-18T00:37:03.410402	Neil Greenwood	{ "license": "Creative Commons - Attribution - https://creativecommons.org/licenses/by/4.0/", "url": "https://oercommons.org/courseware/lesson/87921/overview", "title": "Statewide Dual Credit World History, The Period of Revolution 1650-1871 CE, Chapter 9: Revolution, Central America", "author": "Anna McCollum" }
https://oercommons.org/courseware/lesson/95301/overview	simple cuboidal epi_surface of ovary_400x, p000128 Overview \| simple cuboidal epi_surface of ovary_400x \| simple cuboidal epi_surface of ovary_400x simple cuboidal epi_surface of ovary_400x, \| one layer surface cells top layer is square looking with round nucleus \|	oercommons	2025-03-18T00:37:03.424722	Diagram/Illustration	{ "license": "Creative Commons - Attribution - https://creativecommons.org/licenses/by/4.0/", "url": "https://oercommons.org/courseware/lesson/95301/overview", "title": "simple cuboidal epi_surface of ovary_400x, p000128", "author": "Health, Medicine and Nursing" }
https://oercommons.org/courseware/lesson/91048/overview	Higher Education Syllabus Sharing. Schimizzi Overview Schimizzi 101 Why Schimizzi's Bio 101 Class has an Open Syllabus? Rationale for openly sharing this syllabus (Use this space to provide a short background on why there is value in openly sharing your syllabus.) Aspects of this syllabus that may want specific attention for remixing (Use this space to orient the professor to which sections of the syllabus might want need special attention for remixing based on student populations. Example - "This course features a high number of adults in a second career and they may not have expertise in __________________. This course features supports to help them slowly build their confidence with ____________.") Opportunities for collaboration (Use this space to identify specific parts of your course that you see as in the "continuous improvement" phase. This may be a section where you would appreciate seeing remixes so that you can grow from additional thought partnering. Example "This course is currently using peer feedback on the essay portion of assessment #2. The included peer rubric that is linked seems to have challenges with peers giving thorough feedback. Additional thoughts about including authentic peer feedback would be appreciated.) Syllabus Content (Copy and paste your syllabus into this space. You can also "Import from Google Docs" and attach Word Documents or PDFs.)	oercommons	2025-03-18T00:37:03.439012	03/18/2022	{ "license": "Creative Commons - Attribution - https://creativecommons.org/licenses/by/4.0/", "url": "https://oercommons.org/courseware/lesson/91048/overview", "title": "Higher Education Syllabus Sharing. Schimizzi", "author": "Joanna Schimizzi" }
https://oercommons.org/courseware/lesson/99505/overview	Life…will it prevail? Or will we end it all? Overview How can we show the ways our society prioritizes environmental issues? Life on Land, Life below water, Clean Water and Sanitation, and Climate Action .... Do surrounding communities prioritize the solving of environmental issues differently? How do communities unite individuals to be part of the solution to these environmental problems? SDG 6,13,14,15 https://docs.google.com/presentation/d/166oo8x0exEU0VZUmIjY1pfm_QUlw_9y-aK9mD0l6YAg/edit?usp=sharing	oercommons	2025-03-18T00:37:03.456767	12/17/2022	{ "license": "Creative Commons - Attribution - https://creativecommons.org/licenses/by/4.0/", "url": "https://oercommons.org/courseware/lesson/99505/overview", "title": "Life…will it prevail? Or will we end it all?", "author": "ying lin" }
https://oercommons.org/courseware/lesson/99841/overview	James Williams, Harold Mabern, Mulgrew Miller, Donald Brown, Geoff Keezer Memphis: Jazz Piano earlier years Overview A Look at Memphis Jazz Piano before James Williams, Donald Brown, and Mulgrew Miller made their significant contributions. In addition to the great Phineas Newborn jr., Charles Thomas and Harold Mabern also made a tremendous impact. Live music at local venues provided informal educational opportunities for students of all ages. Memphis Jazz Piano Pre-Triumvirate Charles Thomas Charles Thomas was a widely respected pianist who greatly influenced his Memphis peers including Harold Mabern, James Williams, and Donald Brown among many others. During his career, Thomas headlined numerous jazz festivals and accompanied vocalists such as Tony Bennett. After Ellington's death, the band leader's orchestra asked Thomas to take his place on the piano. But Thomas' tour with the Duke Ellington Orchestra didn't last long. Thomas "got tired of being Duke Ellington - he wanted to be Charlie Thomas," said his longtime manager, Jim Porter. So Thomas returned to Arkansas and played at such venues as the Black Orchid in Hot Springs during the 1960s. Thomas's longest running show was at the Atrium Bar at the Holiday Inn in west Little Rock, where he riffed out jazz patterns and improvised versions of pop songs every day from 5 to 9 p.m. and during Sunday brunches. Thomas didn’t record much until very late in his life. He was invited to appear with some noted piano buddies on the Japanese releases for the DIW label entitled “Memphis Convention” and “Memphis Piano Convention”. He also recorded several CDs for the French label Space Time. Jazz pianist Charles Thomas, who shunned the spotlight of touring with Duke Ellington's band to play in his home state of Arkansas, died Tuesday November 23, 1999 of prostate cancer. He was 64. Harold Mabern HAROLD MABERN a superb ensemble player and an inspiring accompanist, played with many of America's finest musicians and singers before becoming a bandleader in his own right. He was born on March 20 1936 in Memphis, Tennessee, the son of a timber-yard labourer. Impressed by his son's ability to pick out tunes from memory, his father saved up $60 to buy a piano. With no money for lessons, the teenaged Mabern began teaching himself, mainly by hanging around pianists. His immersion in Memphis blues influenced his later style of playing. At Manassas High School in the early 1950s, Mabern found himself surrounded by other would-be jazz musicians, including the saxophonists George Coleman, Frank Strozier and Charles Lloyd. In this encouraging atmosphere his technique developed rapidly and, on graduating, he and Strozier headed for Chicago to join a band with a rising reputation, MJT+3. Mabern recalled practicing up to 12 hours a day, and his playing attracted the notice of Chicago's ever-changing jazz scene. He was a big man, with hands to match, and played "two-handed piano", combining firmly marked rhythm, full chords and graceful melodic lines. In November 1959 Mabern decided to try his luck in New York. On his first night there he was standing outside Birdland, the city's most famous jazz venue, when he was greeted by the saxophonist Cannonball Adderley: "Hey, Big Hands! Looking for a gig? Come with me!" He soon found himself on the bandstand, accompanying the trumpeter Harry "Sweets" Edison. This was the beginning of the period in which Harold Mabern became known as the jazz world's Mr Reliable. A brief extract from the list of greats who relied on his large, safe hands would include Lionel Hampton, Sarah Vaughan, Miles Davis, Sonny Rollins, Betty Carter, JJ Johnson, Milt Jackson, Hank Mobley and Wes Montgomery. One date that Mabern wished he could forget was February 19 1972, when he was playing with the trumpeter Lee Morgan at Slugs nightclub. In the early hours of the morning, Morgan was shot dead on the bandstand by a jealous lover. Mabern recorded prolifically under the leadership of others, but albums of his own were sparse at first. A Few Miles From Memphis, his debut, was released in 1968. More followed, but he was in such demand that he did not have the time to promote them. It was not until 1989, when his album Straight Street, recorded for the Japanese label DIW, met with great success in Japan, that he began what amounted to his second career. Leading his own trio, and sometimes larger groups, he toured extensively, recording for DIW and later for Venus, another Japanese label. He took part in two remarkable piano ensembles, the Piano Choir - six pianists on conventional pianos or electric keyboards - and the Contemporary Piano Ensemble, with four players. From 1981 until his death Mabern taught in the music faculty at William Paterson University, Wayne, New Jersey. Being self-taught, he liked to refer to his students as fellow-learners, and several later became fellowperformers, too, such as the tenor saxophonist Eric Alexander and drummer Joe Farnsworth. Mabern's discography lists 26 albums under his own name and 91 as a sideman. These include many sessions led by close colleagues, such as Eric Alexander and his school friend George Coleman. Harold Mabern played in Britain on several occasions, recently in 2017 and 2018 with a quartet featuring Alexander, and with his trio at Ronnie Scott's in May. He is survived by a son and a daughter. Harold Mabern born March 20 1936, died September 18 2019	oercommons	2025-03-18T00:37:03.478471	Homework/Assignment	{ "license": "Creative Commons - Attribution - https://creativecommons.org/licenses/by/4.0/", "url": "https://oercommons.org/courseware/lesson/99841/overview", "title": "Memphis: Jazz Piano earlier years", "author": "Performing Arts" }
https://oercommons.org/courseware/lesson/84260/overview	Sample Assignment AOJ AOJ 144: Probation and Parole Overview In this course, you will analyze the essential elements of probation and parole by examining the history of sentencing and post-sentence release from its beginnings to the contemporary institution to which it has evolved. Integrated within this study, a variety of topics will be examined through an antiracist lens. The juvenile justice system, probation administration, sentencing, community-based corrections, the theory of rehabilitation, probation and parole officers, special programs, intermediate sanctions, and the future trends and issues related to probation and parole will all be considered with a key focus on social justice. Syllabus and Sample Assignment In this course, you will analyze the essential elements of probation and parole by examining the history of sentencing and post-sentence release from its beginnings to the contemporary institution to which it has evolved. Integrated within this study, a variety of topics will be examined through an antiracist lens. The juvenile justice system, probation administration, sentencing, community-based corrections, the theory of rehabilitation, probation and parole officers, special programs, intermediate sanctions, and the future trends and issues related to probation and parole will all be considered with a key focus on social justice.	oercommons	2025-03-18T00:37:03.498066	Syllabus	{ "license": "Creative Commons - Attribution - https://creativecommons.org/licenses/by/4.0/", "url": "https://oercommons.org/courseware/lesson/84260/overview", "title": "AOJ 144: Probation and Parole", "author": "Homework/Assignment" }
https://oercommons.org/courseware/lesson/97854/overview	Deconstructing Management Podcast Overview A podcast made by college students for college students. Access podcast at https://anchor.fm/deconstructingmanagement and on podcast listening apps. Overview: Are you bored by textbooks? Are you overwhelmed trying to keep up with the reading in all your college classes? Deconstructing Management is a podcast created by college students for college students. We make learning management not suck. Each episode is produced by different teams of students and aligns with the OpenStax Principles of Management textbook. We believe it's a better way to learn management, but we might be biased ;-) Licensed under CC BY 4.0 - creativecommons.org/licenses/by/4.0/ Access the textbook for free at openstax.org/details/books/principles-management . Author: Management Students of Nicole Colter Date Completed: 12/30/2021 A podcast made by college students for college students Access podcast at https://anchor.fm/deconstructingmanagement and on podcast listening apps Overview: Are you bored by textbooks? Are you overwhelmed trying to keep up with the reading in all your college classes? Deconstructing Management is a podcast created by college students for college students. We make learning management not suck. Each episode is produced by different teams of students and aligns with the OpenStax Principles of Management textbook. We believe it's a better way to learn management, but we might be biased ;-) Licensed under CC BY 4.0 - creativecommons.org/licenses/by/4.0/ Access the textbook for free at openstax.org/details/books/principles-management Author: Management Students of Nicole Colter Date Completed: 12/30/2021	oercommons	2025-03-18T00:37:03.511762	10/11/2022	{ "license": "Creative Commons - Attribution - https://creativecommons.org/licenses/by/4.0/", "url": "https://oercommons.org/courseware/lesson/97854/overview", "title": "Deconstructing Management Podcast", "author": "Nicole Colter" }
https://oercommons.org/courseware/lesson/79777/overview	Joshua Dover's Calculus 3 Project: Point in Cartesian, Polar, Cylindrical and Spherical coordinate systems Overview This Project has been completed as part of a standard Calculus 3 synchronous online course during Spring 2021 Semester at MassBay Community College, Wellesley Hills, MA. Introduction Point in Cartesian, Polar, Cylindrical and Spherical Coordinate Systems Joshua Dover Introduction If you were asked to describe an objects location, especially in space, it would be really hard without a system of references. Consider if you were telling a friend how to familiar location, like the grocery store, you would probably try and direct them from a known reference point. You might say something like "drive to the post office and take the first left after you pass it." This method helps you relay the information using a frame of reference. In mathematics, a point in is best described as a location or exact position, and it can exist on a plane, surface, or in space. It is considered to be one of the fundemental objects of Euclidean Geometry and has no size; therefore it lacks dimensions like width, height, and depth. In the 17th century, Descarte invented a coordinate system that united algebra and geometry, called Cartesian coordinates. Using this method geometric shapes, including lines and curves, could be drawn. This was fundemental for the development of calculus and was used to generalize vector spaces. Cartesian coordinates can even be used in graphs and three-dimensional images. From here several other methods were for desingating a points location were developed, they include: Polar, Cylindrical, and Spherical coordinate systems. Cartesian Coordinates Cartesian Coordinates, also known as rectangular coordinates, describe the location of a point in the plane, or in three-dimensional space. A plane is two dimensional flat surface and is usually divided by two axes, typically, x and y. Traditionally, the x-axis is the horizontal axis and the y-axis is the vertical one. Each axis operates with it's own number line that extends infinitely in either direction so that any real number can be expressed as a coordinate. Where the axes intersect is know as the origin and is desgingated by the coordinates (0, 0). On the x-axis, positions to the left of the origin have negative values while positions to the right are expressed wth positive values. The same applies to the vertical axis. As you move up from the origin the numbers are positive and as you move down from the origin the values are negative. A Cartesian coordinate in the two dimensional plane describes how far you move left or right in the horizontal direction and then how far up or down you move in the vertical direction to arrive at the designated point. They are expressed as a set of ordered pairs such as (-3, 2) where 3 refers to the distance along the x-axis from the origin in the negative direction and 2 refers to the distance vertically from the origin in the positive direction (see figure 1 below) [9]. Figure 1[9] User: n/a - Added: 12/14/09 In three-dimensional space the Cartesian coordinates are expressed as a triplet of ordered numbers and is based on three mutually perpendicular axes. The additional axis is usually referred to as the z-axis. Where the three axes meet is called the origin and it is desgniated by the points (0, 0, 0). Picturing three perpendicular axes can be difficult but a good way to picture it would a corner in a room. In this scenario the corner represents the origin and the xy plane would be the floor. One axis would extend horizontally out from the corner in each direction. This only allows you to picture one quardrant but if you imagine the lines continuing out past the wall you would have the entire plane. The seam of the corner would be the z axis and adds a vertical element to the xy plane. If that seam was extended past the floor you would have be able to plot negative values for z [9]. Three-dimensional Cartesian coordinates allow us to specify points in space and are usually expressed in the format (x, y, z). As in the two-dimensional version, values correspond to the distance from the origin along the respective axis. Polar Coordinates The polar coordinate system provides an alternative method of mapping points to ordered pairs. To find the coordinates of a point in the polar coordinate system, consider Figure 2. The point P has Cartesian coordinates (x, y). The line segment connecting the origin to the point P measures the distance from the origin to P and has length r. The angle between the positive x -axis and the line segment has measure θ. This observation suggests a natural correspondence between the coordinate pair (x, y) and the values r and θ. This correspondence is the basis of the polar coordinate system. Note that every point in the Cartesian plane has two values associated with it. In the polar coordinate system, each point also has two values associated with it: r and θ [1, section 1.3]. Figure 2 An arbitrary point in the Cartesian plane [1, section 1.3]. Using right-triangle trigonometry, the following equations are true for the point P: $\cos \theta=\dfrac{x}{r} ~~\text{so} ~~~x=r\cos\theta$ $\sin \theta = \dfrac{y}{r}~~\text{so}~~~y=r\sin \theta$ . Furthermore, $r^2=x^2+y^2 $ $\tan \theta =\dfrac{y}{x}$ Each point (x, y) in the Cartesian coordinate system can therefore be represented as an ordered pair (r, θ) in the polar coordinate system. The first coordinate is called the radial coordinate and the second coordinate is called the angular coordinate. In order to find a unique solution where the polar plot is in the same quadrant as the original point (x, y) it is necessary to restric the solutions of the equation tan θ = y/x. Normally, this equation has an infinite number of solutions, however, if we restrict the solutions to values between 0 and 2π then the solution will be in the quadrant relative to the original point. Also, the corresponding value of r is positive, so r2 = x2 + y2 [1, section 1.3]. In order to convert points between coordinate systems use the following equations: Given a point P in the plane with Cartesian coordinates (x, y) and polar coordinates (r, θ), the following conversion formulas hold true: x = r cos θ y = r sin θ $r^2=x^2+y^2 \\ \tan \theta =\dfrac{y}{x}$ These formulas can be used to convert from rectangular to polar or from polar to rectangular coordinates. Below are worked examples and tutorial videos. 1. How to convert the rectangular coordinates (3, 6) to polar coordinates: First, we will find r $r^2=x^2+y^2 \\ r^2=3^2+6^2\\ r^2=45\\ r=\sqrt {45} ~~or ~3\sqrt{5}$ Next, lets find θ $\tan{\theta}= \frac{y}{x}\\ \tan{\theta}= \frac{6}{3}\\ \theta = \tan^{-1}(2)\\ \theta \approx1.107$ Therefore, the polar coordinates are $(3\sqrt{5}, 1.107)$ . User: n/a - Added: 4/1/16 2. How to convert the polar coordinates $(8,\frac{2\pi}{3})$ to Cartesian coordinates First, lets find the x coordinate $x=8 \cos(\frac{2\pi}{3}) \\ x=8(-.05)\\ x=-4$ Next, lets find the y coordinate $y=8 \sin(\frac{2\pi}{3}) \\ x=8(\frac{2\pi}{3})\\ x=4\sqrt{3}$ Therfore, the Cartesian coordinate is $(-4, 4\sqrt{3}).$ User: n/a - Added: 6/7/11 Cylindrical Coordinates and Spherical Coordinates The Cartesian coordinate system provides a straightforward way to describe the location of points in space. Some surfaces can be difficult to model with equations based on the Cartesian system. Cylindrical and Spherical coordinates, based on extensions of polar coordinates, are used to describe a location on these difficult surfaces. Cylindrical coordinates are useful for dealing with problems involving cylinders, such as calculating the volume of a round water tank or the amount of oil flowing through a pipe. Similarly, spherical coordinates are useful for dealing with problems involving spheres, such as finding the volume of domed structures [1, section 2.7]. Cylindrical Coordinates By adding an axis (z) to the traditional Cartesian coordinate system (x,y), a three dimensional point can be plotted which is represented as a point with (x, y, z) components. The same technique can be applied to polar coordinates. By incorporating the z axis into the polar coordinate system, we have a new method to plot three dimensional points. This new system, known as the Cylindrical coordinate system, provides an extension of polar coordinates to three dimensions. In this new system a point in space is represented by the ordered triple (r, θ, z). The first two components (r, θ) are the polar coordinates of the point in the xy-plane, and z is the usual z-coordinate found in the Cartesian coordinate system (see Figure 3) [1, section 2.7]. In the xy-plane, the right triangle shown in Figure 3 [1, section 2.7] provides the key to converting cylindrical and Cartesian coordinates. In order to convert between Cylindrical (r, θ, z) and Cartesian (x, y, z) Coordinates use the following equations: From cylindrical coordinates to rectangular use: x = r cos θ y = r sin θ z = z coordinates From rectangular coordinates to cylindrical use: r2 = x2 + y2 $\tan \theta =\dfrac{y}{x}$ z = z coordinates Once again, the equation tan θ = y/x has an infinite number of solutions, but restricting θ to values between 0 and 2π will provide a unique solution based on the quadrant in which the original cartesian point is located [1, section 2.7]. Below are worked examples of conversions from Cartesian coordinates to cylindrical and cylindrical to Cartesian with tutorial videos. 1. How to convert the Cartesian coordinates (1, 5, 5) to cylindrical coordinates $r^2=x^2+y^2 \\ r^2=1^2+5^2\\ r^2=26\\ r=\sqrt{26}$ $\tan \theta =\dfrac{y}{x} \\ \tan \theta = \dfrac{5}{1} \\ \theta = \tan^{-1}(5)\\ \theta \approx 1.37$ Therefore, the cylindrical coordinates are $(\sqrt{26},1.37,5)$. User: n/a - Added: 7/22/14 2. How to convert the cylindrical coordinates $(4, \frac{11 \pi}{6},4)$ to Cartesian coordinates $x=r\cos \theta \\ x =4 \cos \Big(\dfrac{11 \pi}{6}\Big)\\ x=4 \Big(\dfrac{\sqrt{3}}{2}\Big) \\ x=2\sqrt{3}$ $y=r\sin \theta \\ x =4 \sin \Big(\dfrac{11 \pi}{6}\Big)\\ x=4 \Big(\dfrac{-1}{2}\Big) \\ x=-2$ Therefore, the rectangular coordinates are $ (2\sqrt{3},-2,4).$ User: n/a - Added: 7/22/14 Sperical Coordinates In the Cartesian coordinate system, the location of a point in space is described using an ordered triple in which each coordinate represents a distance. In the spherical coordinate system, the triple describes one distance and two angles. Cylidrical coordinates make it easier to describe a point on a cylinder and, in the same context, spherical coordinates make it simple to describe a point in a sphere. Grid lines for spherical coordinates are based on angle measurements, smiliar to the angle measurment used in polar coordinates [1, section 2.7]. In the spherical coordinate system, a point P in space (Figure 4) is represented by the ordered triple (ρ, θ, φ) where: • ρ (the Greek letter rho) is the distance between P and the origin (ρ ≠ 0); • θ is the same angle used to describe the location in cylindrical and polar coordinates; • φ (the Greek letter phi) is the angle formed by the positive z-axis and line segment ${OP}$ where O is the origin and 0 ≤ φ ≤ π. Figure 4 [1, section 2.7], Comparing spherical, rectangular, and cylindrical coordinates. The origin is represented as (0, 0, 0) in spherical coordinates. To convert spherical, cylindrical, and rectangular Coordinates use the following information: Rectangular coordinates and spherical coordinates of a point are related as follows: These equations are used to convert from spherical coordinates (ρ, θ, φ) to rectangular coordinates (x, y, z) x = ρ sin φ cos θ y = ρ sin φ sin θ z = ρ cos φ. These equations are used to convert from rectangular coordinates (x, y, z) to spherical coordinates (ρ, θ, φ) ρ2 = x2 + y2 + z2 $\tan \theta =\dfrac{y}{x} \\ \phi=\arccos \Big( \dfrac{z}{\sqrt{x^2+y^2+z^2}}\Big)$ These equations are used to convert from spherical coordinates (ρ, θ, φ) to cylindrical coordinates (r, θ, z) r = ρ sin φ θ = θ z = ρ cos φ The following equations are used to convert from cylindrical coordinates (r, θ, z) to spherical coordinates (ρ, θ, φ) ρ = r2 + z2 θ = θ $\phi=\arccos \Big( \dfrac{z}{\sqrt{r^2+z^2}}\Big)$ As before, we must be careful when using the formula tan θ = y/x to choose the correct value of θ. Below are worked examples on how to convert Cartesian coordinates to spherical coordinates and spherical coordinates to Cartesian coordinates. How to convert the Cartesian coordinates $(-5,-2,5)$ spherical coordinates $\rho^2=x^2+y^2+z^2\\ \rho^2=(-5)^2+(-2)^2+5^2\\ \rho^2=25+4+25\\ \rho^2=54\\ \rho^2=\sqrt{54} ~~~\text{or}~~~3\sqrt{6} $ $\tan \theta =\dfrac{y}{x} \\ \tan \theta = \dfrac{-2}{-5} \\ \theta = \tan^{-1}(\dfrac{2}{5}) \\ \theta \approx 0.3805~~~\text{ but this is in the first quadrant. To get this in the right quadrant we should had}~\pi~~\text{so}\\ \theta \approx 3.52$ $\cos \phi= \dfrac{z}{\sqrt{x^2+y^2+z^2}}\\ \cos \phi= \dfrac{5}{3\sqrt{6}}\\ \phi = \cos^{-1}\Big(\dfrac{5}{3\sqrt{6}}\Big)\\ \phi \approx 0,822$ User: n/a - Added: 7/24/14 How to convert the spherical coordinates $(3, \dfrac{\pi}{2},\dfrac{\pi}{4})$ to Cartesian coordinates. $x=\rho \sin \phi \cos \theta \\ x=3 \Big(\dfrac{\sqrt{2}}{2} \Big) (0)\\ x=0$ User: n/a - Added: 7/24/14 Conclusion The development of the Cartesian coordinate system united algebra and geometry by making it possible visualizing curves and functions. This made the concepts of both disciplines less abstract, and helped pave the way for the elements found in calculus. Additionally, there are many business, engineering, and mathematical applications for the graphs these points can be used to create. Through the addition of the polar, cylindrical, and spherical coordinate system, it became easier express the location of point in a circle, a cylinder, and a sphere repesctively. These additional coordinate systems are help engineers, scientist, and mathematicians increase our understanding and improve the world around us. References [1] Herman, E., & Strang, G. (77005), Calculus Volume 3, Houston, TX: OpenStax, 2018. [2] Mathispower4u, "Plotting Points on the Coordinate Plane," https://www.youtube.com/watch?v=s7NKLWXkEEE, 2009. [3] Mathispower4u, "Ex: Convert Cartesian Coordinates to Polar Coordinates," https://www.youtube.com/watch?v=byfFX7FMhzQ, 2016. [4] Mathispower4u, "Example: Convert a Point in Polar Coordinates to Rectangular Coordinates," https://www.youtube.com/watch?v=Txx9rvLnuTA, 2011 [5] Mathispower4u, "Ex 1: Convert Cartesian Coordinates to Cylindrical Coordinates," https://www.youtube.com/watch?v=3eA1UowemQs, 2014. [6] Mathispower4u, "Ex: Convert Cylindrical Coordinates to Cartesian Coordinates," https://www.youtube.com/watch?v=jNaPT_vcrNQ, 2014. [7] Mathispower4u, "Ex1: Convert Cartesian Coordinates to Spherical Coordinates," https://www.youtube.com/watch?v=ZI0f426X-rA, 2014. [8] Mathispower4u, "Ex1: Convert Spherical Coordinates to Cartesian Coordinates," https://www.youtube.com/watch?v=8J4B83Y-KHQ, 2014. [9] Nykamp DQ, “Cartesian coordinates,” From Math Insight, http://mathinsight.org/cartesian_coordinate [10] Udacity, "Cartesian Coordinates - Interactive 3D Graphic," https://www.youtube.com/watch?v=N4o3s5t0n9g, 2015.	oercommons	2025-03-18T00:37:03.549314	Igor Baryakhtar	{ "license": "Creative Commons - Attribution - https://creativecommons.org/licenses/by/4.0/", "url": "https://oercommons.org/courseware/lesson/79777/overview", "title": "Joshua Dover's Calculus 3 Project: Point in Cartesian, Polar, Cylindrical and Spherical coordinate systems", "author": "Homework/Assignment" }
https://oercommons.org/courseware/lesson/60981/overview	Thermochemistry: In-Class Assignment/Exercise with solutions Thermochemistry Power Point Lecture Thermochemistry: Atoms First Overview This lesson includes a powerpoint lecture and problem in-class exercise/assignment with corresponding solutions about thermochemistry. Thermochemistry: Atoms First Lesson This lesson includes a powerpoint lecture and problem in-class exercise/assignment with corresponding solutions about thermochemistry.	oercommons	2025-03-18T00:37:03.568419	Franco Pala	{ "license": "Creative Commons - Attribution - https://creativecommons.org/licenses/by/4.0/", "url": "https://oercommons.org/courseware/lesson/60981/overview", "title": "Thermochemistry: Atoms First", "author": "Lecture Notes" }
https://oercommons.org/courseware/lesson/97040/overview	Reading for Parents in Middle School Parent Involvement Overview This is an inquiry project done to research different strategies to increase parent involvement and their benefits, as well as a look into some stereotypes that can have a negative effect on a child's educational jouney at home. Introduction Introduction Parent involvement is something every school and educator should strive for. This does not always mean having an active PTA, but parents that are active in their child’s education. “There are several studies which show that parents can influence student achievement and social development.” (Becker, Epstein) In this module we explore different strategies that can and have been implemented in classrooms around the world, as well as different stereotypes that unfortunately fall onto parents and their ability to help their child achieve academic success. Main Points Parent Workshops Reading With Students at Home Contracts between Parents and Teachers Educational Levels of Parents Resources Becker, H. J., & Epstein, J. L. (1982). Parent involvement: A survey of teacher practices. The Elementary School Journal, 83(2), 85–102. https://doi.org/10.1086/461297 Parent Workshops Parents cannot be to blame for their child’s education, especially if they are not able to help with schoolwork at home. Whether this support looks like holding a meaningful conversation about the student’s needs, answering, or helping answer higher-level thinking questions, or helping with a set of math problems. More often you see “parent workshops” come into play in the school setting, to give parents more of the resources they need to help their student at home, so they are able to succeed in the classroom. Parent workshops sound great in theory, but in reality, it is hard to get a bunch of parents and their already busy schedules to coincide with a schedule created by an educator, or office staff. Not to mention of those parents many will most likely believe “that all teaching of academic skills should be left to the teacher in the classroom.” It is important to stress the benefits of education and how it should not stop when a child walks out of the class. There are many strategies educators can use to “help parents teach.” Some examples of these strategies are: - instruction for parents in techniques that can be used at home to further education outside of the classromm. - including parents in classroom activities during class time so they have an idea of how their child is receiving instruction. - requesting information from parents on how they have seen changes in their child. This video is an excellent example of giving parents resources that they can use to continue education at home. Other schools, like Peasley Middle School in Gloucester, Virginia, are implementing a parent workshop on a monthly basis, “as a way to help educate parents on practices to help their child at home, we decided that we could hold mini workshops once a month and feature specific strategies versus broad information.” Each month when the workshop takes place, a different subject is covered. The logistics of a strategy like this is very dependent on an open-minded classroom, open to discussion and disagreements. Building a team, including parents, students and teachers can be daunting but very rewarding if done correctly. In order to make this work you must be available to many sessions in order to cater to everyone’s busy schedule, while also balancing a healthy work-life routine. Resources Becker, H. J., & Epstein, J. L. (1982). Parent involvement: A survey of teacher practices. The Elementary School Journal, 83(2), 85–102. https://doi.org/10.1086/461297 StPaulPublicSchools. (2019, December 9). New parent-teacher conference model gaining popularity. YouTube. Retrieved September 13, 2022, from https://www.youtube.com/watch?v=13cWF7eYOVw&t=4s (video embedded) Reading with Students at Home One can never overestimate the importance of involving parents in their children’s education especially when it comes to reading. Reading is the basis of all subjects in education; math, science and history all involve some form of literacy. That is exactly why we all need to play our role in helping young minds develop their reading skills. It is never too early to begin reading to your child. When parents get involved in reading, it benefits students by increasing their interest and motivation. In fact, intrinsic motivation and parental involvement in literacy are two variables that are claimed to be key to children’s literary achievement as well as their self-efficacy. Children’s reading self-efficacy, how confident the student feels in their ability to read, is a great predictor of their future reading success. The article Parent Involvement: A Survey of Teacher Practices is a great resource to gain more information on the importance of involving parents in reading. Social and emotional development Social competence Resilience Self-control Increased academic performance throughout academic life Language comprehension Reading confidence Motivation to read Higher vocabulary For more detailed information on these benefits, you can visit this article. Because many parents are unaware of the benefits of reading at home, it is the job of teachers to provide support and information to parents. This means providing materials, strategies and activities to parents that they can use in their free-time to make reading an enjoyable experience for themselves and their children. Many teachers named two strategies that they use to get parents involved in their student’s literacy development: Encourage parents to take their children to the library Allow parents to borrow materials, such a books or activities, for short-term at home use While reading to your child in general is beneficial, parents should also allow their child to read to them. The video linked below explains different practices that parents can use when reading with their children to help build their literacy skills. The video explains that using strategies, such as word solving and discussing what the book was about, are great ways to begin building your child’s literacy skills at home. Resources Becker, H. J., & Epstein, J. L. (1982). Parent involvement: A survey of teacher practices. The Elementary School Journal, 83(2), 85–102. https://doi.org/10.1086/461297 Why it is important to involve parents in their children’s literacy development - ed. (n.d.). Retrieved September 11, 2022, from Contracts Between Parents and Teachers A Parent, Teacher and Student contract is designed to be able to have a written agreement made between the three parties involved. These outlines are based upon specific objectives or goals the student is to uphold for the school year. These contracts are meant to provide teachers with a way to communicate to the parents and students the teachers expectations with regards to learning goals and in-school behavior for students, it also gives the parents insight on what their student will need for that teacher's classroom. There are two types of contracts teachers available for teachers: Involved parent contracts Uninvolved parent contracts The involved parent contract requires them to supervise and assist during homework times or other projects that the teacher gives to their student. This does not always mean that the parents are required to provide instruction or clarification about their students' work but for parents to involve the structuring of the home environment to match the needs and responsibilities of the student. The uninvolved parent contract is just a formal agreement stating that the child will conduct good behavior and complete all assignments or set activities for said class. The parent does not engage in any direct instructional activities in this contract, but assists the teacher in shaping productive school behavior. There are important differences between the two contracts by teachers who teach different grade levels. The involved parent techniques are used mostly by teachers who teach the lower grade levels and the uninvolved parent techniques were used in the higher grade levels. This video is not directly talking about parent/student/teacher contracts but it talks about how important it is to have a strong partnership between teachers, parents and students. Having a strong partnership between parents and teachers helps students build better work habits and have a better attitude towards school. Students demonstrate better social skills, fewer behavioral problems and a greater ability to adapt to situations and get along; which parents and teachers benefit from too. Resources Becker, H. J., & Epstein, J. L. (1982). Parent involvement: A survey of teacher practices. The Elementary School Journal, 83(2), 85–102. https://doi.org/10.1086/461297 How to build a strong parent-teacher relationship. Andrea Loewen Nair. (2015, July 29). Retrieved September 13, 2022, from httpHow to build a strong parent-teacher relationship. Andrea Loewen Nair. (2015, July 29). Retrieved September 13, 2022, from http://www.andrealoewen.ca/how-to-build-a-strong-parent-teacher-relationship/ Williams, Aletha on November 7. (2019, September 26). Building parent-teacher relationships. Reading Rockets. Retrieved September 13, 2022, from https://www.readingrockets.org/article/building-parent-teacher-relationships Educational Levels of Parents Common stereotypes of students’ parents are described in three different ways: upper middle-class parents are described as “pushy.” Middle class parents are “helpful.” “incapable” is described to be the lower-class parents. With these comments, they appear to indicate that a parent's involvement in their student’s education is critical to what they can accomplish. Though, the main part of this section is the education levels of parents. For some families, it matters how much education the parents possess in order for their children to be more motivated in what they do in class. As I read some research about how students who tend to find motivation in school; they all go back to parents' involvement. Also, according to Responsive Classrooms article, “No matter (parents’) their income or background, students with involved parents are more likely to have higher grades and test scores, attend school regularly, have better social skills, show improved behavior, and adapt well to school.” Figure 1 is a graph that shows the difference in education levels of parents and how that impacts their children’s performance in a school classroom. As the graph indicates, there was a very strong relationship between more parent education and more parent involvement with school. Those with graduate or professional degrees attended general school meetings at an approximately twenty percent higher rate than parents who didn’t graduate from high school. In addition, of those two groups, the parents with the most education volunteered in school at forty three percent higher rate than the parents with the least education. This information comes from the article “What Part Does a Parent's Level of Education Play in Parental Involvement in Children’s Education?” The article also explains that parental involvement has been shown to be a strong indicator of student success at school. Understanding more about the characteristics of involved parents could help the teachers get more parents involved and help more students succeed. Once again below, a great example of this topic is shown as how it takes all three parts of a child’s education to be successful. Parents’ level of education becomes a leading factor in a child’s education. it can be the reason why a child is experiencing difficulties in school, even, in daily life. Usually there are two reasons that affect this theory. For one, a parent can be very highly educated or can possess some sort of education level. Two, parents can be zero to none on education levels. A lot of times this issue is noticed in schools with students that end up needing more time in subject lessons due to lack of help they get from home. while for others, they seem to be skyrocketing in the grade books due to a lot of assistance they receive from home. For instance, I myself come from a situation where both of my parents are very poorly educated. This meant that I had to be more serious about my education and make better choices in life. Due to my parents being migrants from Africa, adapting to the American school system was hard. One solution was me deciding to stay for after school programs where they helped with lessons I could not get in class. It was hard putting myself in the same shoes as my classmates. Home assignments that were given by teachers to do at home that involved parents were the most difficult.. Though I worked hard, I found a solution to help myself stay on the same level as my classmates; and I did that by going through early morning tutorials and after school. A great example of how parents' education levels impact a child's education can be seen in the video below. Another article that helps me with more information on this topic is “Emigration and Educational Attainment in Mexico.” There are, of course, other reasons why parental education may help predict schooling outcomes for children. For some parents, education may be a consumption good, as well as an investment good. “More educated parents may be individuals who place a high consumption value on education and who are willing to invest more heavily in educating their children.” From the article. Parents transmit values to their children regarding important life choices, including education. More educated parents may be positive role models in the educational choices of their children. As for the low educated, a student might still be having trouble being motivated because of home difficulties. Resources Becker, H. J., & Epstein, J. L. (n.d.). Parent Involvement: A Survey of Teacher Practices. The Elementary School Journal, Vol. 83, No. 2 (Nov., 1982), pp. 85-102. Retrieved February 11, 2015, from http://www.jstor.org/stable/1001098 CNN: Why parents matter in education - youtube. (n.d.). Retrieved September 12, 2022, from https://www.youtube.com/watch?v=wK-yIIOg5wo Emigration and educational attainment in Mexico. (n.d.). Retrieved September 12, 2022, from https://economics.ucr.edu/wp-content/uploads/2019/11/03-05-04Gordon-Hanson.pdf Title-I parental involvement news! – Federal & State Programs – Ben Bolt-Palito Blanco ISD. (n.d.). Retrieved September 11, 2022, from https://www.bbpbschools.net/apps/pages/index.jsp?uREC_ID=345909&type=d&pREC_ID=754303 What part does a parent's level of education play in parental involvement in children's education. The Wing Institute. (n.d.). Retrieved September 11, 2022, from https://www.winginstitute.org/what-part-does-parents Final Conclusion Parent involvement in their child’s education has been researched extensively, and the results are unanimous. Children who have parents who care and are involved in their educational journey in and out of the classroom tend to have more confidence in their abilities in the classroom. Asking parents to be involved can be hard to do, but if a parent is willing to put in the effort there are many strategies that can be implemented. In this module went into depth about how parents can help, and also why they may be reluctant to. Especially in section ‘Level of parents’ education. Teaching is a partnership between parents, students and educators. It is important to always be open to suggestions and to always be understanding of parents and their different beliefs, but to also hold your ground when it comes to your classroom management and teaching strategies, anytime you are implementing a strategy be sure you are able to back up the reasoning. That is how students can be more engaged in schools and how parents end up being satisfied by our roles as educators. With this, parents that also lack education can be more motivated to try to help their children in any way. “Communication and involvement from parents to teachers leads to success from teachers to students.” Resources Becker, H. J., & Epstein, J. L. (n.d.). Parent Involvement: A Survey of Teacher Practices. The Elementary School Journal, Vol. 83, No. 2 (Nov., 1982), pp. 85-102. Retrieved February 11, 2015, from http://www.jstor.org/stable/1001098	oercommons	2025-03-18T00:37:03.604558	Sarah Durden	{ "license": "Creative Commons - Attribution - https://creativecommons.org/licenses/by/4.0/", "url": "https://oercommons.org/courseware/lesson/97040/overview", "title": "Parent Involvement", "author": "Kendall Dodson" }
https://oercommons.org/courseware/lesson/122969/overview	Learning Object "Zero and first conditional" Overview Learning Object "Zero and first conditional" TESL, TEFL Learning Object "Zero and first conditional" Learning Object "Zero and first conditional" TESL, TEFL	oercommons	2025-03-18T00:37:03.622253	Lizeth Rojas	{ "license": "Creative Commons - Attribution - https://creativecommons.org/licenses/by/4.0/", "url": "https://oercommons.org/courseware/lesson/122969/overview", "title": "Learning Object \"Zero and first conditional\"", "author": "Lesson" }
https://oercommons.org/courseware/lesson/84536/overview	Proof of Differentiation Rules - The Derivative of the Sum of Two Functions: Calculus 1 Project by Nick Woodward Overview This Project has been completed as part of a standard 10 weeks Calculus 1 asynchronous online course with optional WebEx sessions during Summer 2021 Semester at MassBay Community College, Wellesley Hills, MA. Proof of Differentiation Rules - The Derivative of the Sum of Two Functions The Derivative of the Sum of Two Functions $[f(x)+g(x)]'=f'(x)+g'(x)$ To start, we first need to review the definition of a derivative: $$ f'(x)= \lim_{h \to 0} \dfrac{f(x+h)-f(x)}{h}$$ Next, we set up our equation that we will solve to prove the rule of the derivative of the sum of 2 functions $$ [f(x)+g(x)]'= \lim_{h \to 0} \dfrac{(f(x+h)+g(x+h))-(f(x)+g(x))}{h}$$ Once we have our variable substitued into our equation, we can distribute the negative value in the numerator $$~~~~~~~~~~~~~~~~=\lim_{h \to 0} \dfrac{f(x+h)+g(x+h)-f(x)-g(x)}{h}$$ Next, we can arrange our variables in the numerator to be a sum of 2 fractions which leaves us with the following $$~~~~~~~~~~~~~~~~~~~~~~=\lim_{h \to 0}\Big( \dfrac{f(x+h)-f(x)}{h}+\dfrac{g(x+h)-g(x)}{h}\Big)$$ After this, we can write this equation of the sum of 2 limits which yields the following equation $$~~~~~~~~~~~~~~~~~~~~~~=\lim_{h \to 0} \dfrac{f(x+h)-f(x)}{h}+\lim_{h \to 0}\dfrac{g(x+h)-g(x)}{h}$$ Next, we can recognize that the following limits are the definition of the derivative for f'(x) and g'(x) respectively $$~~~~~~~~~~~~~~~\lim_{h \to 0} \dfrac{f(x+h)-f(x)}{h}+\lim_{h \to 0}\dfrac{g(x+h)-g(x)}{h}=f'(x)+g'(x)$$ For further understanding of this topic, I highly recommend the following content: The first is a video explaining the definition of a derivative The next video explains the basic math behind this calculation and how we can separate the equation to be a sum of 2 fractions I would also recommend this in depth page that explains derivative notation which is a fundemental concept of this material	oercommons	2025-03-18T00:37:03.637067	Homework/Assignment	{ "license": "Creative Commons - Attribution - https://creativecommons.org/licenses/by/4.0/", "url": "https://oercommons.org/courseware/lesson/84536/overview", "title": "Proof of Differentiation Rules - The Derivative of the Sum of Two Functions: Calculus 1 Project by Nick Woodward", "author": "Activity/Lab" }
https://oercommons.org/courseware/lesson/122972/overview	Learning Object "Causative form" Overview Learning Object "Causative form" TESL; TEFL Learning Object "Causative form" TESL, TEFL	oercommons	2025-03-18T00:37:03.654105	Lizeth Rojas	{ "license": "Creative Commons - Attribution - https://creativecommons.org/licenses/by/4.0/", "url": "https://oercommons.org/courseware/lesson/122972/overview", "title": "Learning Object \"Causative form\"", "author": "Lesson" }
https://oercommons.org/courseware/lesson/60848/overview	Sternberg's Theory of Love Overview This covers the topic of Sternberg's Theory of Love. Love in the Modern World Author: Melissa Ness Editor: Heather Whittaker What is love? Other than a chemical reaction in our brains, love is made up of several components that have the potential to work together in harmony. According to Robert Sternberg’s Triangular Theory of Love, relationships are based on varying combinations of passion, love, and intimacy (Feurman, 2019). Each relationship consists of a dynamic combination of those three things. Love can be romantic or platonic based on the combination of these factors. Intimacy is linked to liking, commitment is linked to empty love, and passion is linked to infatuation. All these aspects need each other and Sternberg considered love to be incomplete if just one of them was missing. The first component of love is intimacy. It is defined as feelings of closeness, connectedness, and bonding (Feurman, 2019). Intimacy consists of two aspects of the triangle, passion, and commitment (Feurman, 2019). This often takes place at the beginning of relationships and is responsible for fantasies about the future or of that person. Infatuation may put two people under the impression they can make it work even if they have nothing they need to develop long-term commitment. Infatuation is often depicted in movies like its sister concept of "love at first sight." There may be no evidence that the other person will nurture a healthy, loving relationship, but that does not matter when infatuation is at the helm. In total, there are seven types of love that fall somewhere in between the three major subdivisions. The first being one I expanded on, infatuation. The others would be liking, empty love, fatuous love, romantic love, compassionate love, and the ideal consummate love. (Feurman, 2019). Each kind consists of one or two aspects from the triangle, and only one known as consummate love has the balance of all passion, intimacy, and commitment. The rest fall somewhere else along the spectrum, for example, romantic love consists of passion and intimacy but lacks commitment. Another being companionate love, filled with commitment and intimacy, yet no sign of passion. Last but not least is fatuous love which is very common in dating culture. Both passion and commitment are present but intimacy is lacking. All three types of love work together to create each relationship’s unique dynamic. Sternberg determined intimacy to be a very important aspect of love, the other type of love, decision and commitment along with empty love. This is what breaks many relationships, unfaithfulness and lust of someone outside of the relationship. Commitment requires a love that is mutual and both parties involved begin to move towards shared goals and remaining to each other. That may look different per relationship. For some couples, it will look like a monogamous relationship, while for others it could be an open relationship. Empty love is defined as commitment without passion or intimacy. Many relationships end up in this phase before separating. It is interesting how the interaction between all types of love work together yet have the power to separate people. Love is complicated; it is different for every person on the planet. Various potential partners fit our love stories to greater and lesser degrees, and we are more than likely to succeed in close relationships with people whose stories more rather than less match our own (Feurman, 2019). All aspects must work together in the right formula. Everyone has their own definitions for each term, and I believe that many of us are likely to foster relationships like those around us. One thing we can do is be proactive in educating ourselves on what a healthy relationship looks like, along with how to keep some sort of a balance with our partners for the best possible experience trying to balance intimacy, passion, and commitment. References: M. Feurman, Sternberg's triangular theory and the 7 types of love, July 2019. https://thoughtsfeeds.com/2019/10/17/sternbergs-triangular-theory-and-the-7-types-of-love/	oercommons	2025-03-18T00:37:03.668974	12/17/2019	{ "license": "Creative Commons - Attribution - https://creativecommons.org/licenses/by/4.0/", "url": "https://oercommons.org/courseware/lesson/60848/overview", "title": "Sternberg's Theory of Love", "author": "Heather Whittaker" }
https://oercommons.org/courseware/lesson/86935/overview	Evaluating Information on the Web Overview Use this guide as an example of lateral reading. Locating an Article Using Google, type your search term: climate change. Note the sources provided in the results. In this search, there are results from - EPA - BBC - Global Change - United Nations - NRDC Choose an article for evaluation. Searching Wikipedia Using the article from NRDC, "Climate Change: What You Need to Know," read laterally. Don't just rely on the .org domain! Step 1: Use Wikipedia to find out more about the source: NRDC, also known as the Natural Resources Defense Council. Use NRDC site: Wikipedia.org. Step 2: Note what Wikipedia says about the agency. The NRDC is - a 501(c)(3) non-profit international environmental advocacy group - an outgrowth of the Scenic Hudson Preservation Conference v. Federal Power Commission, which ruled environmental groups had the ability to sue the Federal Power Commission. - The NRDC has spearheaded several legal battles in favor of environmental protection, some that have lead to changes by the EPA. Note that Wikipedia says this article needs additional citations for verification. Continue to read other articles about the NRDC. Using Reliable, Well-Known Resources to Evaluate A Google search for the NRDC returns results from charity or non-profit tracking websites. However, two known, credible websites discuss the agency. From the information gathered, although the agency seems to have bias in that it leans left politically, the NRDC is a credible and authoritative source and usable for a paper. Ballotpedia Annenberg Classroom	oercommons	2025-03-18T00:37:03.684246	Crystal Newell	{ "license": "Creative Commons - Attribution - https://creativecommons.org/licenses/by/4.0/", "url": "https://oercommons.org/courseware/lesson/86935/overview", "title": "Evaluating Information on the Web", "author": "Student Guide" }
https://oercommons.org/courseware/lesson/74062/overview	https://www.opensocietyfoundations.org/explainers/value-inclusive-education https://www.youtube.com/watch?v=FQMCQ7Bx6d0 https://www.youtube.com/watch?v=lz40q5lydnQ Inclusive Classrooms Overview Inclusion Classrooms and why they are important and how to achieve them. What does Inclusive mean? Merriam Webster defines inclusion as "including everyone: especially allowing and accommodating people who have historically been excluded (as because of their race, gender, sexuality, or ability)" Open Society Foundation states that "Inclusive systems provide a better quality education for all children and are instrumental in changing discriminatory attitudes. Schools provide the context for a child's first relationship with the world outside their families, enabling the development of social relationships and interactions." Inclusivity is so important in the classroom as it leads to better education, more rounded social skills, and a higher self-esteem. Practicing it everyday and making sure your lessons, and language are inclusive is integral to the education system. Inclusive Language Inclusive langauge can make all the difference when dealing with anyone, especially students. People first language is the key to inclusive language. Some examples are instead of saying "disabled woman", you would say "woman with a disability", or "male nurse", you would just say "nurse". By using people first language you create a more inclusive and comfortable environment that is full of opportunities. The Diversity Movement has a great video on Youtube describing The Importance of Inclusive Language. Another YouTube video that invloves people first language is here.	oercommons	2025-03-18T00:37:03.704968	10/29/2020	{ "license": "Creative Commons - Attribution - https://creativecommons.org/licenses/by/4.0/", "url": "https://oercommons.org/courseware/lesson/74062/overview", "title": "Inclusive Classrooms", "author": "Kasse Parkinson" }
https://oercommons.org/courseware/lesson/96652/overview	Micrograph Lactococcus lactis gram stain 1000X p000176 Overview This micrograph was taken at 1000X total magnifcation on a brightfield microscope. The subject is Lactococcus lactis cells grown on agar at 37 degrees Celsius. The cells were heat-fixed to a slide and Gram stained prior to visualization. Image credit: Emily Fox Micrograph White background with small clusters of purple, round Lactococcus lactis cells.	oercommons	2025-03-18T00:37:03.722137	Diagram/Illustration	{ "license": "Creative Commons - Attribution - https://creativecommons.org/licenses/by/4.0/", "url": "https://oercommons.org/courseware/lesson/96652/overview", "title": "Micrograph Lactococcus lactis gram stain 1000X p000176", "author": "Health, Medicine and Nursing" }
https://oercommons.org/courseware/lesson/105110/overview	Using the Game: Minecraft to Teach Communication Competence Overview This activity helps students learn about communication competence and improve their computer-mediated communication competence skills. Students understand the importance of collaboration, team-building skills, and negotiation. The digital game, Minecraft, is used to help students craft better messages. Communication Studies Abstract This activity helps students learn about communication competence and improve their computer-mediated communication competence skills. Students understand the importance of collaboration, team-building skills, and negotiation. The digital game, Minecraft, is used to help students craft better messages. Courses: Any Lower or Upper Division Communication Courses; Small Group; Interpersonal, Leadership, and Introductory Communication Studies Courses; Public Speaking Keywords: Competence, Interpersonal, Minecraft, Team-Building Using the Game: Minecraft to Teach Communication Competence Introduction and Rationale Today’s students are defined as the new internet generation (Dzubian, Moskal, & Hartman, 2005). These young individuals have grown up with constant media exposure. Because of widespread media scandals and several misleading websites, they have been taught to be critical and wary of classical theoretical approaches. In addition, current college students have grown up with cell phones and personal computers as their standard technological tools. Often, these students will take their notes on their smartphones or tablets. Furthermore, they will often obtain their information from online sources rather than purchasing a traditional textbook. These media and technological influences also affect how they learn and retain information. Findings suggest that college students prefer texting over face-to-face conversations. Dzubian, Moskal, and Hartman (2005) found that current college students perform poorly in blended classrooms compared to other types of students. The reason is that they dislike and do not participate in the face-to-face component of the class. They would prefer only to communicate electronically. While college students possess superior computer skills, they frequently are still adolescents and are not hesitant about posting immature ideas and opinions. While online communication may pose drawbacks to college student communication, face-to-face interactions do not seem promising either. College students often need to consider how their remarks might be misinterpreted or misconstrued by others. They are less apt at reading nonverbal cues compared to other generations. In addition, they need to improve audience analysis and ethical communication. Research on current college students has shown that they have a hard time talking to others in an interpersonal context (Hartman & McCambridge, 2011). Employers have noted that they could be more effective at engaging in basic interpersonal skills because they have been surrounded by technology. For example, current college students are proficient at emailing and texting via electronic media. However, they need help to converse at a business lunch or express their ideas at a business meeting. Ultimately, when it comes to instructional communication, instructors are stuck choosing the lesser of two evils. Minecraft is a digital game that is also used in the classroom. Minecraft is a game about the placement of mining cubes. The cubes are made from various materials (e.g., tree trunks, water, ores, stone, and dirt). Players collect these cubes to create a formation. The game can be played individually or with others. The game's objective is to build a shelter for the evening before the monsters come out to prey on victims. After they complete the shelter, they repeat the process of adding to the shelter to make it more complex for monsters to attack and add valuable resources to survive. Minecraft allows students to be creative and sharpen their problem-solving skills. In addition, this is a social game that allows for practical communication skills. Students depend on other players to create their structures, and the chat feature teaches them better computer-mediated communication skills. Description of Activity Prior to the activity, ask students to complete the Self-Perceived Communication Competence Scale (McCroskey & McCroskey, 1988) and CMC Competence Scale (Spitzberg, 2005, v5) (Appendices 1 & 2). Next, ask the students to form dyads. All students will need a laptop, smartphone, or tablet with Internet access. Next, ask the students to go to https://education.minecraft.net/ and download a free trial of the game. Next, divide the class in half. Ask one-half of the students not to use the chat feature and the other half to use the chat feature. Next, students are instructed to build a shelter with their partners. Allow 20 minutes for them to build their structures. Another option would be to use one of the lesson plans on the website focused on communication and/or leadership. Students will work together to meet the objectives of that particular lesson. These additional lesson plans can be located under the resources tab. Allow students to talk about their experiences completing their Minecraft task with their partner. The instructor should also incorporate some concepts regarding communication competence and computer-mediated communication competence. Ask students to discuss these differences in detail and some of the challenges with these concepts related to this particular activity. If time allows, students can create a new computer mediated communication competence measure specific to Minecraft. Debriefing Paragraph After the activity, discuss their observations about their communication behaviors and perceptions of communication competence. In order to help students enhance their interpersonal communication skills with digital gaming, such as Minecraft, educators must create engaging and participative situations (Beckstrom, Manual, & Nightingale, 2008). Tucker (2006) found that students prefer team-based learning or cooperative strategies rather than direct learning from the instructor. Students want to be more involved in the learning process (Hanna, 2003). Thus, educators should place students in dyads or small groups so that students can interact with each other while in a digital gaming context. Hartman and McCambridge (2011) suggested that educators should stress how communication is an interactive process. Improving this process would include showing how each person has a unique communication style and how different individuals prefer to encode/decode messages. Instructors can help students recognize and identify their communication style and their level of communication competence. At the same time, instructors can help students realize that not everyone has different communication preferences. Students can use Minecraft to determine their communication styles and compare their results with others in the class. Appraisal/Evaluation of the Activity Students will appreciate the importance of communication in an online setting. Students will also learn how Minecraft can teach them about communication competence. Students love this activity because they are often interacting digitally. It is crucial for them to realize their communication behaviors and to understand if they are effective computer-mediated communicators. This activity creates an awareness of how messages are being understood and processed. This activity also helps students learn to work with others and develop small-group skills for dealing with conflict and misunderstandings. Using digital gaming, such as Minecraft, is an effective means of helping students communicate in a very technologically savvy society. References and Suggested Readings Barr, M. (2017). Video games can develop graduate skills in higher education students: A randomised trial. Computers & Education, 113, 86-97. Beckstrom, M., Manuel, J., & Nightingale, J. (2008). The wired utility meets the wired generation. Electric light and power. Retrieved from http://www.elp.com/index/display/articledisplay/342495/articles/electric-light-power/volume-86/issue-5/news-analysis/the-wiredutility-meets-the-wired-generation.html Dziuban, C., Moskal, P., & Hartman, J. (2005). Higher education, blended learning, and the generations: Knowledge is power: No more. Elements of quality online education: Engaging communities. Needham, MA: Sloan Center for Online Education. Hanna, D. E. (2003, July/August). Building a leadership vision: Eleven strategic challenges for higher education. Educause Review, 25-34. Hartman, J. L., & McCambridge, J. (2011). Optimizing Millennials’ Communication Styles. Business Communication Quarterly, 74(1), 22-44. doi:10.1177/1080569910395564 McCroskey, J. C., & McCroskey, L. L. (1988). Self-report as an approach to measuring communication competence. Communication Research Reports, 5(2), 108-113. Spitzberg, B. H. (2006). Preliminary development of a model and measure of computer-mediated communication (CMC) competence. Journal of Computer-Mediated Communication, 11(2), 629-666. Tucker, P. (2006). Teaching the millennial generation. Futurist, 40, Appendix 1 Self-Perceived Communication Competence Scale (SPCC) Directions: Below are twelve situations in which you might need to communicate. People's abilities to communicate effectively vary a lot, and sometimes the same person is more competent to communicate in one situation than in another. Please indicate how competent you believe you are to communicate in each of the situations described below. Indicate in the space provided at the left of each item your estimate of your competence. Presume 0 = completely incompetent and 100 = competent. _____1. Present a talk to a group of strangers. _____2. Talk with an acquaintance. _____3. Talk in a large meeting of friends. _____4. Talk in a small group of strangers. _____5. Talk with a friend. _____6. Talk in a large meeting of acquaintances. _____7. Talk with a stranger. _____8. Present a talk to a group of friends. _____9. Talk in a small group of acquaintances. _____10. Talk in a large meeting of strangers. _____11. Talk in a small group of friends. _____12. Present a talk to a group of acquaintances. Scoring: To compute the subscores, add the percentages for the items indicated and divide the total by the number indicated below. Public 1 + 8 + 12; divide by 3. Meeting 3 + 6 + 10; divide by 3. Group 4 + 9 + 11; divide by 3. Dyad 2 + 5 + 7; divide by 3. Stranger 1 + 4 + 7 + 10; divide by 4. Acquaintance 2 + 6 + 9 + 12; divide by 4. Friend 3 + 5 + 8 + 11; divide by 4. To compute the total SPCC score, add the subscores for Stranger, Acquaintance, and Friend. Then, divide that total by 3. Public \| > 86 High SPCC \| < 51 Low SPCC \| Meeting \| > 85 High SPCC \| < 51 Low SPCC \| Group \| > 90 High SPCC \| < 61 Low SPCC \| Dyad \| > 93 High SPCC \| < 68 Low SPCC \| Stranger \| > 79 High SPCC \| < 31 Low SPCC \| Acquaintance \| > 92 High SPCC \| < 62 Low SPCC \| Friend \| > 99 High SPCC \| < 76 Low SPCC \| Total \| > 87 High SPCC \| < 59 Low SPCC \| Higher SPCC scores indicate higher self-perceived communication competence with basic communication contexts (public, meeting, group, dyad) and receivers (strangers, acquaintance, friend). Appendix 2 CMC COMPETENCE SCALE (Spitzberg,2005, V.5) Instructions: We are interested in how people use various computer-mediated communication (CMC) technologies for conversing with others. For the purpose of this questionnaire, please consider CMC to include all forms of e-mail and computerbased networks (e.g., instant messaging, world-wide-web, chat rooms, personal data assistant, electronic bulletin boards, terminal-based video-telephony, etc.) for sending and receiving written messages with other people. For this survey, indicate the degree to which each statement regarding your use of various CMC media is true or untrue of you, using the following scale: 1 = NOT AT ALL TRUE OF ME 2 = MOSTLY NOT TRUE OF ME 3 = NEITHER TRUE NOR UNTRUE OF ME; UNDECIDED 4 = MOSTLY TRUE OF ME 5 = VERY TRUE OF ME MOTIVATION 01. I enjoy communicating using computer media. 02. I am nervous about using the computer to communicate with others. [R] 03. I am very motivated to use computers to communicate with others. 04. I look forward to sitting down at my computer to write to others. 05. Communicating through a computer makes me anxious. [R] KNOWLEDGE 06. I am very knowledgeable about how to communicate through computers. 07. I am never at a loss for something to say in CMC. 08. I am very familiar with how to communicate through email and the internet. 09. I always seem to know how to say things the way I mean them using CMC. 10. When communicating with someone through a computer, I know how to adapt my messages to the medium. EFFICACY 11. I don’t feel very competent in learning and using communication media technology. 12. I feel completely capable of using almost all currently available CMCs. 13. I am confident I will learn how to use any new CMCs that are due to come out. Journal of Computer-Mediated Communication 11 (2006) 629–666 ª 2006 International Communication Association 663 14. I’m nervous when I have to learn how to use a new communication technology. 15. I find changes in technologies very frustrating. 16. I quickly figure out how to use new CMC technologies. 17. I know I can learn to use new CMC technologies when they come out. 18. If a CMC isn’t user friendly, I’m likely not to use it. SKILLS COORDINATION 19. I know when and how to close down a topic of conversation in CMC dialogues. 20. I manage the give and take of CMC interactions skillfully. 21. I am skilled at timing when I send my responses to people who email me. 22. I am skilled at prioritizing (triaging) my email traffic. ATTENTIVENESS 23. I ask questions of the other person in my CMC. 24. I show concern for and interest in the person I’m conversing with in CMC. 25. I can show compassion and empathy through the way I write emails. 26. I take time to make sure my emails to others are uniquely adapted to the particular receiver I’m sending it to. EXPRESSIVENESS 27. I am very articulate and vivid in my CMC messages. 28. I use a lot of the expressive symbols [e.g., for ‘‘smile’’] in my CMC messages. 29. I try to use a lot of humor in my CMC messages. 30. I am expressive in my CMC conversations. COMPOSURE 31. I display a lot of certainty in the way I write my CMC messages. 32. I use an assertive style in my CMC writing. 33. I have no trouble expressing my opinions forcefully on CMC. 34. I make sure my objectives are emphasized in my CMC messages. 35. My CMC messages are written in a confident style. 36. I am skillful at revealing comp 39. how lively the interaction needs to be. 40. how much access the person I need to communicate with has to the medium. 41. how much information is involved in the message I need to communicate. 42. how much access I have to the channel or medium. 43. how long I need people to hang on to or remember the message. 44. how many different uses and forms are needed (e.g., hardcopy, image processing, voicemail, computer language, etc.) 45. how personal or intimate the information in the message is. 46. how quickly the receiver needs to react to the message. 47. the extent to which I need to get some ‘‘back and forth,’’ ‘‘give and take,’’ and interchange of ideas. 48. the extent to which I need some creative brainstorming. APPROPRIATENESS 49. I avoid saying things through that might offend someone. 50. I pay as much attention to the WAY I say things as WHAT I say. 51. I never say things that offend the other person. 52. I am careful to make my comments and behaviors appropriate to the situation. EFFECTIVENESS 53. I generally get what I want out of interactions. 54. I consistently achieve my goals in interactions. 55. My interactions are effective in accomplishing what I set out to accomplish. 56. I am effective in my conversations with others. CLARITY 57. I get my ideas across clearly in conversations with others. 58. My comments are consistently accurate and clear. 59. My messages are rarely misunderstood. 60. I feel understood when I interact with others. SATISFACTION 61. I am generally satisfied with my communication encounters. 62. I enjoy my interactions with others. 63. I feel good about my conversations. 64. I am generally pleased with my interactions. ATTRACTIVENESS 65. If I can engage someone in conversation, I can usually get them to like me. 66. I come across in conversation as someone people would like to get to know. 67. I make friends easily. 68. People generally enjoy my company when interacting with me. Journal of Computer-Mediated Communication 11 (2006) 629–666 ª 2006 International Communication Association 665 EFFICIENCY/PRODUCTIVITY 69. I get a tremendous amount accomplished through CMC. 70. My CMC interactions are more productive than my face-to-face interactions. 71. I am more efficient using CMC than other forms of communication. 72. CMC technologies are tremendous time-savers for my work. GENERAL USAGE/EXPERIENCE 73. I rely heavily upon my CMCs for getting me through each day. 74. I use computer-mediated means of communication almost constantly. 75. I can rarely go a week without any CMC interactions. 76. I am a heavy user of computer-mediated communication. 77. If I can use a computer for communicating, I tend to.	oercommons	2025-03-18T00:37:03.757697	Ryan Martinez	{ "license": "Creative Commons - Attribution - https://creativecommons.org/licenses/by/4.0/", "url": "https://oercommons.org/courseware/lesson/105110/overview", "title": "Using the Game: Minecraft to Teach Communication Competence", "author": "Narissra Punyanunt-Carter" }
https://oercommons.org/courseware/lesson/106094/overview	Introduction to Political Science Textbook Overview This is the OER textbook for POLS 1010 POLS 1010 OER Textbook This is an open educational textbook created for POLS 1010: Introduction to Political Science. It is the main text for the course and aligns with the test bank and lecture slides, also provided.	oercommons	2025-03-18T00:37:03.775764	06/30/2023	{ "license": "Creative Commons - Attribution - https://creativecommons.org/licenses/by/4.0/", "url": "https://oercommons.org/courseware/lesson/106094/overview", "title": "Introduction to Political Science Textbook", "author": "Jesse Cragwall" }
https://oercommons.org/courseware/lesson/61123/overview	Chapter 1 Chapter 2 Chapter 3 Chapter 4 College Algebra Textbook Overview College Algebra Textbook with chapters about Linears, Systems, Quadratics, and Functions CC x BY Ben Atchison College Algebra Textbook: Linears, Systems, Quadratics, and Functions College Algebra Textbook with chapters on Linears, Systems, Quadratics, and Functions	oercommons	2025-03-18T00:37:03.796041	Ben Atchison	{ "license": "Creative Commons - Attribution - https://creativecommons.org/licenses/by/4.0/", "url": "https://oercommons.org/courseware/lesson/61123/overview", "title": "College Algebra Textbook", "author": "Textbook" }
https://oercommons.org/courseware/lesson/61957/overview	T-Chart Example Without Pictures PDF T-Chart Example with Pictures Doc T-Chart Lecture T-Chart Lecture with Pictures PDF English Composition I: T-Chart Example Overview The lecture begins describing that a T-Chart can be especially effective when writing a compare and contrast essay to better organize the ideas and details which may have been discovered after using the other prewriting activities such as brainstorming or freewriting on a compare and contrast topic. My lecture then moves on to describe the general layout of a simple T-Chart (topic: the advantages and disadvantages of living on campus) and then goes into further detail with another T-Chart (topic: contrasting high school and college regarding course schedules, homework load, and housing). Lesson: T-Chart Example: Compare & Contrast High School and College The lecture begins describing that a T-Chart can be especially effective when writing a compare and contrast essay to better organize the ideas and details which may have been discovered after using the other prewriting activities such as brainstorming or freewriting on a compare and contrast topic. My lecture then moves on to describe the general layout of a simple T-Chart (topic: the advantages and disadvantages of living on campus) and then goes into further detail with another T-Chart (topic: contrasting high school and college regarding course schedules, homework load, and housing).	oercommons	2025-03-18T00:37:03.815823	Kristy Perry	{ "license": "Creative Commons - Attribution - https://creativecommons.org/licenses/by/4.0/", "url": "https://oercommons.org/courseware/lesson/61957/overview", "title": "English Composition I: T-Chart Example", "author": "Lesson" }
https://oercommons.org/courseware/lesson/61638/overview	Agriculture Math Packet Overview A packet of introductory calculations for use with agricultural students going into agronomy or production agriculture. Packet This is a packet for the units of Unit Proving, Fertilizer Calculations, Feeds and Feeding, Introduction to Statistics, and Pesticide Calculations.	oercommons	2025-03-18T00:37:03.831525	01/15/2020	{ "license": "Creative Commons - Attribution - https://creativecommons.org/licenses/by/4.0/", "url": "https://oercommons.org/courseware/lesson/61638/overview", "title": "Agriculture Math Packet", "author": "Kenan Layden" }
https://oercommons.org/courseware/lesson/119956/overview	English 1_Email Assignment English 1_July 23 Handout Summary Assessment You View + Letter Assignment Written Communication Overview overview area Assignments These course documents were designed for Second Chance Pell Grant student populations. They incorporate essential tools for students to learn effective communication in educational and professional settings. They cover topics such as crafting cover letters and professional emails, preparing well-organized documents and visuals, along with summarizing information within a variety of contexts. Development of these skills will support the student's success both academically and professionally.	oercommons	2025-03-18T00:37:03.850812	Holly Anderson	{ "license": "Creative Commons - Attribution - https://creativecommons.org/licenses/by/4.0/", "url": "https://oercommons.org/courseware/lesson/119956/overview", "title": "Written Communication", "author": "Rachel Becker" }
https://oercommons.org/courseware/lesson/65379/overview	Multilinguals are ...? Overview Multilinguals, those of us who use more than one language in everyday life, are... gifted semilinguals who are dominant in no mother tongue, for example? Apparently so, judging by the ways people keep talking about them. This is the first book that discusses, in light-hearted lay terms, the reasons behind the beliefs and myths about multilinguals that allow you to fill the blank in its title with almost any label and get away with it. Drawing on solid academic research, the book provides keys to the origin and endurance of the many intriguing names that multilinguals have been called, starting with the master-key to them all. The conclusion is that any oddities assigned to multilinguals are due to the language that is used to talk about them, not to multilingual behaviour itself. The book is abundantly illustrated and includes many cartoons. It is written for the general public, families, teachers, policy-makers, clinicians, and anyone who ever wondered about multilingualism, but is targeted exclusively at multilingual or monolingual readers (of English). Do we know what multilinguals are? Multilinguals use several languages in everyday life. Most people around the world are multilinguals, although they arouse attitudes ranging from awe at their giftedness or unusual intelligence to fear that they lack competence in any one language. This is the first book which discusses, in lay terms, the reasons behind the beliefs and myths traditionally associated with multilinguals. It is written for the general public and is relevant for families, teachers, speech-language clinicians, and anyone who ever wondered about multilingualism. The style is light, often witty, but founded on a thorough knowledge of solid academic research on this subject. The book is abundantly illustrated and includes many cartoons.	oercommons	2025-03-18T00:37:03.870269	Madalena Cruz-Ferreira	{ "license": "Creative Commons - Attribution - https://creativecommons.org/licenses/by/4.0/", "url": "https://oercommons.org/courseware/lesson/65379/overview", "title": "Multilinguals are ...?", "author": "Reading" }
https://oercommons.org/courseware/lesson/75238/overview	https://www.youtube.com/watch?v=yFN0nf6Hqk0 America's Failing Public School System Overview The issues within America's education system today. Issues with the Education System today America is failing to properly educate the young minds of today. There are many issues like having to do with the lack of skilled professionals and the lack of diversity within the education system. Many face the issue of being pushed through the system and have little or no resources on how to better educate themselves. Below is an atricle that discusses 18 issues with America's education system today. Please read it through and think to yourself if you have ever been impacted by these issues. "Waiting for Superman" Below is a clip from a documentary discussing the issues within the education system. The system has been facing these problems for many years now. However, none have been primarily resolved. This documentary shows the trials, errors, and successes many have gone thorugh to help better our education system. It is vital to not put the focus on the adults within the system, but rather the children. Politicians should be more focused on passing laws for the betterment of the children and not for the education professionals. For example, tenure and the Teacher's Union are major issues within the education system today. The public education system, although built to be run under the government and created to be equal, has ultimately failed our youth. Throughout the years, states and districts have shown the inequality many have had towards a better education.	oercommons	2025-03-18T00:37:03.888649	Natalie Rose	{ "license": "Creative Commons - Attribution - https://creativecommons.org/licenses/by/4.0/", "url": "https://oercommons.org/courseware/lesson/75238/overview", "title": "America's Failing Public School System", "author": "Primary Source" }
https://oercommons.org/courseware/lesson/88942/overview	"How to Ruin Your ASL Teacher's Day" (Tips on Making a Signed Video) Overview This will show students what is and is not acceptable when submitting videos in ASL. "How to Ruin Your ASL Teacher's Day" (Tips on Making a Signed Video) For this non-graded activity, you will be interacting with the H5P video below. Be sure to answer and submit all of the questions that appear while watching the video. - At the end of the video, click on the star at the bottom to review your answers. - Your answers will not be saved once you leave this page. - You do not earn credit for this activity, but it will increase your understanding.	oercommons	2025-03-18T00:37:03.902189	12/23/2021	{ "license": "Creative Commons - Attribution - https://creativecommons.org/licenses/by/4.0/", "url": "https://oercommons.org/courseware/lesson/88942/overview", "title": "\"How to Ruin Your ASL Teacher's Day\" (Tips on Making a Signed Video)", "author": "Colleen Sanders" }
https://oercommons.org/courseware/lesson/85929/overview	Play Overview Slide Deck about the importance of play- 2019 Importance of Play Slides of the Importance of Play	oercommons	2025-03-18T00:37:03.918473	09/18/2021	{ "license": "Creative Commons - Attribution - https://creativecommons.org/licenses/by/4.0/", "url": "https://oercommons.org/courseware/lesson/85929/overview", "title": "Play", "author": "Kathryn Quinn" }
https://oercommons.org/courseware/lesson/74006/overview	Education Standards What is the Americans with Disabilities Act Americans with Disabilities Act Overview This is a resource to teach high school through college level students about the Americans with Disabilities Act. The photo above is of George Bush Signing the Americans with Disabilities Act. "Photo of President George H. W. Bush signing the Americans with Disabilities Act inscribed to Justin Dart, Jr., 1990." by national museum of american history is licensed under CC BY-SA 2.0 Video Do you know what the Americans with Disabilities Act is? Watch this video to find out an overview of what the Americans with Disabilities Act is. Article Please read this article to learn all you need to know about the Americans with Disabilities Act. The Americans with Disabilities Act was first put into law in 1990. The Americans with Disabilities Act Ammendements Act in 2008, to change the defintion of disabiliity. The Americans with Disabilities Act prohibits discrimination against people with disabilities	oercommons	2025-03-18T00:37:03.941388	10/28/2020	{ "license": "Creative Commons - Attribution - https://creativecommons.org/licenses/by/4.0/", "url": "https://oercommons.org/courseware/lesson/74006/overview", "title": "Americans with Disabilities Act", "author": "Courtney Ogburn" }
https://oercommons.org/courseware/lesson/97222/overview	Reviews of Free ESOL Websites Overview This is a collection of links to free ESOL websites. These are the top ones, as reviewed and reported on by my students, from over a decade. Dozens of websites were reviewed and these made the final list. Reviews of Free ESOL Websites (PPT attached) These websites are the top ones found and reviewed by my students over a decade. Reviews of Free ESOL Websites	oercommons	2025-03-18T00:37:03.957765	09/14/2022	{ "license": "Creative Commons - Attribution - https://creativecommons.org/licenses/by/4.0/", "url": "https://oercommons.org/courseware/lesson/97222/overview", "title": "Reviews of Free ESOL Websites", "author": "Ransom Gladwin" }
https://oercommons.org/courseware/lesson/89746/overview	Letter From Abraham Lincoln to Albert G. Hodges, April 4, 1864 Overview President Lincoln addresses a group of border-state politicians about emancipation in a letter to Albert G. Hodges Description: President Lincoln addresses a group of border-state politicians about emancipation.	oercommons	2025-03-18T00:37:03.970122	Linda Coslett	{ "license": "Creative Commons - Attribution - https://creativecommons.org/licenses/by/4.0/", "url": "https://oercommons.org/courseware/lesson/89746/overview", "title": "Letter From Abraham Lincoln to Albert G. Hodges, April 4, 1864", "author": "Susan Jennings" }
https://oercommons.org/courseware/lesson/58269/overview	Brief Essay Outline “Definition” essay assignment: What is the “American Dream?” Essay outline Ethos, Pathos, Logos Formal Essay Rubric Formal Essay Rubric Formatting Dialogue Outline for "An Immigrant's Story" Practice Sheet #1: Integrating quotes into an essay Practice Sheet #2: Integrating quotes into an essay Summary Template Syllabus and agenda The Narrative Essay The Thesis Statement Write a news article (including the Who, What, When, Where, Why, How) on the incidents involving: Trayvon Martin, Eric Garner, Michael Brown, Tamir Rice Writing an Essay Powerpoint Composition I (ALP focus) Overview This is a Composition I course that can be modified for ALP use. All materials have been created by Dianne Traynor and uploaded by Joanna Gray. INTRODUCTION TO THE COURSE Open Educational Resources and “Found” Source Material English Composition 1 (May be adapted for Developmental Writing and Accelerated Learning Program (Alp) Author: Dianne Traynor Middlesex Community College (Bedford and Lowell campuses) Authorship date: July, 2019 Course Description: Overview: This course (Composition 1) has been structured to develop writing skills for collegiate and professional success. The thematic question used to provoke critical thinking in this course is, “WHO is America?” Through critical discussion of articles related to current problems facing America a, students will have the impetus to react to these issues through writing. The course focuses on essay organization and paragraph development, sentence formation, applied grammar and mechanics, and critical thinking. Author: Dianne Traynor Date added: September 24, 2019 License: Creative Common Attribution 4.0 Language: English Media Format: Downloadable docs Standards: Please align this resource to your standards Tags (5) Academic Writing, English, Grammar, Writing, Writing Mechanics Overview: This course uses current articles and videos which highlight problems America is facing today and gives the students the opportunity to speak out knowledgeably through writing on these issues. Development of language skills for written communication in collegiate, professional and personal success are the focus of this course through essay organization, paragraph development, sentence formation, applied grammar and mechanics, and critical thinking. The thematic question for the course is, “WHO is America?” Course Introduction: This writing in this course is heavily reliant on the student’s knowledge of current issues facing America today; therefore, reading comprehension is an integral skill for success. Information is disseminated through current articles and videos, which expose, explain, and often add suggestion for solution to the myriad of problems America is facing today. Discussion follows each reading, and “free writes” are employed prior to discussion so that student can gather their thoughts on the topic. Currently all articles used in this course can be viewed via internet links provided. As time passes, some articles may no longer be available; thus, more current and relevant articles may need to be substituted. Essay type and structure is presented through various texts that are openly-licensed and attributed to the authors. Attachments have been developed by the author of this course and fall under the CC Attribution license. 4.0 Product: 1. Students will write “brief” essays throughout the course, which are thesis-driven short essays of at least three paragraphs—intro, body, and conclusion. Only one piece of cited evidence is expected. These essays are intended to give students practice writing without fear of heavy criticism. The essays will be evaluated on correctly positioned thesis statement, use of introduction, body, and conclusion, and inclusion of cited evidence within the body. These “brief” essays are interspaced between the “formal” essays, which hold greater grade weight. 2. Students are expected to write 3 formal essays, which must include a well-developed thesis, an introduction, body, and conclusion, at least one cited piece of evidence obtained through the provided articles for each thesis “roadmap,” and a Works Cited page. These essays go through the writing process: free write, first draft, peer/instructor evaluation and polished draft. Course focus: Below are the focus areas to be explored along with suggested materials to be used to provide impetus for writing. All materials can be customized. Articles listed are currently available online (July, 2019) but may need to be updated as the discussed issues change or evolve. Current URLS are provided for all supplemental materials (videos and articles). All students are asked to provide a writing sample the first day of class to provide a measure of growth from the beginning of the course to the end. The subject of the writing sample is instructor generated. Thesis question: Why did you decide to attend college? Focus area 1: Syllabus and agenda Focus area 1: Syllabus/agenda presentation and how it references the thematic topic for the course: “WHO is America?” The Importance of a Thesis Statement Focus area 2: The importance of a thesis statement - Textbook: You, Writing! A Guide to College Composition (You, Writing! is licensed under a Creative Commons Attribution-NonCommercial- ShareAlike 4.0 International (CC BY-NC-SA 4.0). Authors: Alexandra Glynn (rights holder), Kelli Hallsten-Erickson, and Amy Jo Swing.) Link to this text: https://opendora.minnstate.edu/islandora/object/MINNSTATErepository%3A348 Read Chapter 5: The Thesis Statement - Instructor generated: How to Write a Thesis Statement ATTACHMENT 2 Focus Area #3: Developing the skills of a collegiate writer Focus area 3: Developing the skills of a collegiate writer: - PPT How to Write an Essay ATTACHMENT 3 - TEXT: WRITING SPACES: READINGS ON WRITING VOLUME 2, Edited by Charles Lowe and Pavel Zemliansky (licensed under the Creative Commons Attribution-Noncommercial-No Derivative Works 3.0) Link: http://parlorpress.com/pdf/writing-spaces-readings-on-writing-vol-2.pdf Read Article: “How to Read Like a Writer” By Mike Bunn page 71 - Instructor generated handout: “What is Annotation” ATTACHMENT 4 - TEXT: The Word on College Reading and Writing (PDF) (The Word on College Reading and Writing by Monique Babin, Carol Burnell, Susan Pesznecker, Nicole Rosevear, Jaime Wood is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License, except where otherwise noted. Link: https://open.umn.edu/opentextbooks/textbooks/the-word-on-college-reading-and-writing Page 11 Annotate and Take Notes - TEXT: The Word on College Reading and Writing (PDF) (The Word on College Reading and Writing by Monique Babin, Carol Burnell, Susan Pesznecker, Nicole Rosevear, Jaime Wood is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License, except where otherwise noted.) Link: https://open.umn.edu/opentextbooks/textbooks/the-word-on-college-reading-and-writing Page 74: Tone, Voice, and Point of View - Ethos, Pathos Logos - Video from Youtube (there are many that can be used on Ethos, Logos, Pathos) - Information and worksheet ATTACHMENT 5 - Notetaking: Use of Cornell notes will be throughout the course. Students are expected to annotate all readings and transfer notes on annotations to Cornell note pages (they may make their own or find a copy on the internet). - Instructor generated: “How to Write a Summary”. (students must include all of the information from this checklist into a well-written paragraph) ATTACHMENT 6 Students are asked to annotate, transfer annotations onto Cornell Notes, and write a well written summary on each of the following supplemental articles used in class: - How to cite evidence in an essay Integrating Quotes into an Essay Focus area 4: Integrating Quotes into an Essay - Read/annotate paraphrasing (integrating quotes) into an essay - Practice sheet #1: paraphrasing and quoting ATTACHEMENT 7 - Practice sheet #2: paraphrasing and quoting ATTACHMENT 8 - Text: You, Writing! A Guide to College Composition (You, Writing! is licensed under a Creative Commons Attribution-NonCommercial- ShareAlike 4.0 International (CC BY-NC-SA 4.0). Authors: Alexandra Glynn, Kelli Hallsten Erickson, and Amy Jo Swing.) Link: https://opendora.minnstate.edu/islandora/object/MINNSTATErepository%3A348 Read/annotate: How to cite evidence in an essay: Using sources pp. 151-155 Focus Area #5: Writing Formal Essays Focus area 5: Writing Formal essays Formal essay #1: Definition essay: What is the American Dream? - Text: Successful College Composition (2016 (PDF)): This text is a transformation of Writing for Success, a text adapted by The Saylor Foundation under a Creative Commons Attribution-NonCommercial-ShareAlike 3.0 License without attribution as requested by the work’s original creator or licensee. Kathryn Crowther, Lauren Curtright, Nancy Gilbert, Barbara Hall, Tracienne Ravita, and Kirk Swenson adapted this text under a grant from Affordable Learning Georgia to Georgia Perimeter College (GPC) in 2015. Section 1.3 was authored by Rebecca Weaver. This text is a revision of a prior adaptation of Writing for Success led by Rosemary Cox in GPC’s Department of English, titled Successful College Writing for GPC Students (2014, 2015) Link: https://www.affordablelearninggeorgia.org/documents/Successful_College_Composition_2016.pdf Read/annotate text chapter on “definition” essay, pages 105-106 - “Definition” essay assignment: What is the “American Dream?” ATTACHMENT 9 - Essay outline ATTACHMENT 10 - Instructor/peer review comment sheet ATTACHMENT 11 - Supplemental materials (URLs here may no longer be available. Instructor may find applicable sources) - What is the American Dream Today? https://www.thebalance.com/what-is-the-american-dream-today-3306027 - “The American Dream” by Anthony Brandt https://www.americanheritage.com/american-dream - “The American Dream is Alive and Well” by Samuel Abrams https://www.nytimes.com/2019/02/05/opinion/american-dream.html - Video Ted Talk “Living the American Dream” by Pooja Mahajan https://www.youtube.com/results?search_query=Living+the+American+Dream+by+Pooja+Mahajan - Video: (YouTube) “Unless You’re a Native American, You Came From Somewhere Else” https://www.youtube.com/watch?v=aiXuEk_CyWs&t=51s - Song: (YouTube) “God Bless the USA” by Lee Greenwood https://www.youtube.com/watch?v=Q65KZIqay4E Formal Essay #2 Narrative essay: “Through the Eyes of an Immigrant” - Text: Successful College Composition (2016) (PDF): This text is a transformation of Writing for Success, a text adapted by The Saylor Foundation under a Creative Commons Attribution-NonCommercial-ShareAlike 3.0 License without attribution as requested by the work’s original creator or licensee. Kathryn Crowther, Lauren Curtright, Nancy Gilbert, Barbara Hall, Tracienne Ravita, and Kirk Swenson adapted this text under a grant from Affordable Learning Georgia to Georgia Perimeter College (GPC) in 2015. Section 1.3 was authored by Rebecca Weaver. This text is a revision of a prior adaptation of Writing for Success led by Rosemary Cox in GPC’s Department of English, titled Successful College Writing for GPC Students (2014, 2015) Link: https://www.affordablelearninggeorgia.org/documents/Successful_College_Composition_2016.pdf Read/annotate text Chapter 3.1: Narration, pp. 89-91 - Handout: Formatting dialogue ATTACHMENT 12 Instructor generated: Narrative essay ATTACHMENT 13 Outline for “An Immigration Story” ATTACHMENT 14 - Instructor generated: instructor/peer evaluation sheet ATTACHMENT 15 Formal Essay #3: Persuasion Essay: What is the most significant reason for the racial tension that exists in America today? - Text: Successful College Composition (2016) (PDF): This text is a transformation of Writing for Success, a text adapted by The Saylor Foundation under a Creative Commons Attribution-NonCommercial-ShareAlike 3.0 License without attribution as requested by the work’s original creator or licensee. Kathryn Crowther, Lauren Curtright, Nancy Gilbert, Barbara Hall, Tracienne Ravita, and Kirk Swenson adapted this text under a grant from Affordable Learning Georgia to Georgia Perimeter College (GPC) in 2015. Section 1.3 was authored by Rebecca Weaver. This text is a revision of a prior adaptation of Writing for Success led by Rosemary Cox in GPC’s Department of English, titled Successful College Writing for GPC Students (2014, 2015) Link: https://www.affordablelearninggeorgia.org/documents/Successful_College_Composition_2016.pdf - Read and annotate Persuasion, Chapter 3.8, pp. 122-126 - Possible questions/ research ideas for the topic - Is racism dividing America through racial profiling? Supplemental materials - Implicit Bias test: https://secure.understandingprejudice.org/iat/racframe.htm - Ted Talk video (YouTube) “How Racial Profiling Hurts Everyone, Including the Police https://www.youtube.com/watch?v=LCX_Th-IjjE - Video: Racial/Ethnic Prejudice and Discrimination https://www.youtube.com/results?search_query=What+would+you+do+racial+profiling - Read/annotate/summarize: “Don’t Let the Loud Bigots Distract You. America’s Real Problem with Race Cuts Far Deeper https://time.com/5388356/our-racist-soul/ - Videos: “What Would You Do?” (How is implicit bias or stereotyping affecting the action of the people in each video?) - Pharmacy Calls Police on Black Woman - Black Customer Racially Profiled - White Waitress Wants Blacks to prepay for Meal - Videos: “What Would You Do?” (How is implicit bias or stereotyping affecting the action of the people in each video?) - Is American law enforcement out of control (racial profiling and police brutality; lack Lives Matter) - Instructor generated assignment: Write a news article (including the Who, What, When, Where, Why, How) on the incidents involving: Trayvon Martin, Eric Garner, Michael Brown, Tamir Rice ATTACHMENT 16 - Supplemental Materials - Read/annotate: “Why U.S. Police are Out of Control” https://consortiumnews.com/2015/08/20/why-us-police-are-out-of-control/ - Read/annotate: “Body Cameras were supposed to Help Improve Policing https://www.vox.com/2019/3/27/18282737/body-camera-police-effectiveness-study-george-mason - Video: (YouTube) “Understanding Black Lives Matters” https://www.youtube.com/watch?v=Sd-VUOgS3rE - Is the American prison system broken? Supplemental materials: - Video: Mass Incarceration Visualized https://www.youtube.com/watch?v=u51_pzax4M0 - Handout: Criminal Justice Fact Sheet https://www.naacp.org/criminal-justice-fact-sheet/ - Video: (YouTube) The Enduring Myth of Black Criminality https://www.youtube.com/watch?v=cQo-yYhExw0&t=126s - Handout: The Numbers Don’t Speak for Themselves: Racial Disparities and the Persistence of Inequality in the Criminal Justice System https://journals.sagepub.com/doi/full/10.1177/0963721418763931 - Video: Beyond Reform: (YouTube Ted Talk) Abolishing Prisons by Maya Schenwar https://www.youtube.com/watch?v=JFTRn_sIGiQ&t=206s - Should negative American history be erased? - Instructor generated assignment: Research the Charlottesville, Virginia riots. Write a one paragraph news article explaining: Who was involved, what happened, when did it happen, where did it happen, why did it happen, how did it happen? Write a paragraph reflection on what you think about this demonstration. - Supplemental materials: - Should negative American history be erased? - Video: (YouTube) “The Real History of the Confederate Flag https://www.youtube.com/watch?v=Tash7XtDCyM - Video: (YouTube) “Confederate Flag: A Symbol of Hate or History?” https://www.youtube.com/watch?v=qWfPQpB35xs - Article: “Steeped in Racism, Confederate Flag Evokes the Worst of Us” https://www.thelcn.com/lcn06/steeped-in-racism-confederate-flag-evokes-the-worst-of-us-20170817 - Video: (Youtube) “Why America is Wrestling with Confederate Monuments” https://www.youtube.com/watch?v=eNQ8F72Olh0 - Article: “Whose Memory? Whose Monuments? History, Commemoration, and the Struggle for an Ethical Past” Focus Area #6: The Brief Essay Focus area #6: The brief essay The purpose of the brief essay is to allow students to show understanding of current issues confronting Americans today through writing. Current articles on each subject area are provided (instructors may select their own). The brief essay is 1-2 pages in length, is thesis driven, has an introduction, body, and conclusion, and contains one cited piece of evidence obtained in assigned reading to support the thesis. The information used in the brief essays might be helpful when writing the formal essays. - Instructor generated “brief essay” outline ATTACHMENT 17 - Instructor- chosen issues that are being discussed in America today driven by a thesis question (each instructor could select areas that are of current concern and find applicable and current articles on each subject). - Immigration: What should America do about the immigration problem? Supplemental material: - Video: (YouTube) “America an Immigration Nation, 2017 https://www.youtube.com/watch?v=18pL2VmoMCQ - Article: “Let’s Have an Immigration Debate” realclearpolitics.com/articles/2019/01/14/lets_have_a_real_immigration_debate_139165.html - Immigration: Should birthright citizenship be upheld? Supplemental material: - Video (YouTube) “The Fight for Birthright Citizenship in America https://www.youtube.com/watch?v=788If50vyYU - Video (YouTube) “What is Birthright Citizenship?” https://www.youtube.com/watch?v=A5Ai9mFnZNo - Video (YouTube) “How the 14th Amendment Undermines Citizenship https://www.youtube.com/watch?v=qISar8CP9v0 - Article: “The Birthright Citizenship Debate https://www.mass.gov/orgs/highway-division - Article: “Immigration is About Us” https://townhall.com/columnists/joelgoodman/2017/02/10/immigration-is-about-us--not-them-n2283828 - Article: “4 Ways Trump can Fix America’s Immigration https://www.heritage.org/immigration/commentary/4-ways-trump-can-fix-americas-immigration-problem - Immigration: Should the term “illegal alien” be banned? Supplemental material: - Video: (YouTube) AP drops the term “illegal immigrant” https://www.youtube.com/watch?v=2h3oAMTfd1c - Video: (YouTube) “Should the term ‘Illegal Alien’ be banned?” https://www.youtube.com/watch?v=AezhO_QXAMM - Article: “Should the Term Illegal Alien be Used?” https://immigration.procon.org/view.answers.php?questionID=000757 - Politics: Are you a Republican or a democrat and WHY? Supplemental materials: - Article: Democrats vs Republicans https://www.diffen.com/difference/Democrat_vs_Republican - Video: (YouTube) “Political Crash Course” https://www.youtube.com/watch?v=VEmOUHxessE - Video: (YouTube) “The Political Systems https://www.youtube.com/watch?v=4FHqowXS4j4 - Video: (YouTube) “What are the Differences Between Republican and Democratic Parties https://www.youtube.com/watch?v=5SyLy-0Qgnw&t=15s - Politics: Should everyone living in America be allowed to vote? Supplemental materials: - Video: (YouTube) “The Fight for the Right to Vote in the United States https://www.youtube.com/watch?v=P9VdyPbbzlI - Article: “Should Convicted Felons Lose the Right to Vote?” https://psmag.com/social-justice/should-felons-lose-their-right-tov - Article: “Why Non-citizens Should be Allowed to Vote https://jacobinmag.com/2018/11/noncitizen-voting-undocumented-immigrants-midterm-elections - Article: “The Surprising Consequence of Lowering the Voting Age - Gun Control: How (or why) should the use of guns be controlled in America? Supplemental materials: - Article: “What is the 2nd Amendment? www.ducksters.com/history/us_government/second_amendment.php. Accessed 12 June 2019. - Video: (YouTube) “The Second Amendment: Firearms in the U.S.” https://www.youtube.com/watch?v=0TGcU0lmINk - Article: “The Right to Bear Arms: What Does it Really Mean? https://www.theguardian.com/us-news/2017/oct/05/second-amendment-right-to-bear-arms-meaning-history - Article: Pro/Con “Should More Gun Laws Be Enacted?” https://gun-control.procon.org/ - Family evolution: What is “family?” Supplemental materials: - Video: (YouTube) “The Changing American Family” https://www.youtube.com/watch?v=iFXbt5WSprI - Article: “The Evolution of the American Family https://online.csp.edu/blog/family-science/the-evolution-of-american-family-structure - Article: Benefits of Gay Marriage https://www.liveabout.com/the-benefits-of-gay-marriage-1411846?print - Video: “Effects of Growing Up With a Single Parent” https://www.youtube.com/watch?v=bnPF2K1Dz7E - Abortion: Should the right to abortion be upheld Supplemental materials: - Article: “Roe vs Wade: The Constitutional Right to Access Safe, Legal Abortion” https://www.plannedparenthoodaction.org/issues/abortion/roe-v-wade - Video: (YouTube) “What a New Supreme Court Means for Abortion https://www.youtube.com/watch?v=UI4g_amOTSg - Article: “Lawmakers Vote to Effectively Ban Abortion in Alabama” https://www.nytimes.com/2019/05/14/us/abortion-law-alabama.html - Video: (YouTube) “Pro and Anti-Abortion Rights Activists on Future of Alabama Abortion Bill”	oercommons	2025-03-18T00:37:04.086436	09/24/2019	{ "license": "Creative Commons - Attribution - https://creativecommons.org/licenses/by/4.0/", "url": "https://oercommons.org/courseware/lesson/58269/overview", "title": "Composition I (ALP focus)", "author": "Dianne Traynor" }
https://oercommons.org/courseware/lesson/94351/overview	What is a subject heading? Overview An animated presentation explaining the basic concept of a subject heading. Created in MS Powerpoint (version 2205), it can be edited to add your own content or branding. Can also be exported to video, see example here: https://www.youtube.com/watch?v=2HmkaMd_lgo ScrIpt for narration is found in the notes section of each slide. Description An animated presentation explaining the basic concept of a subject heading. Created in MS Powerpoint (version 2205), it can be edited to add your own content or branding. Can also be exported to video, see example here: https://www.youtube.com/watch?v=2HmkaMd_lgo ScrIpt for narration is found in the notes section of each slide.	oercommons	2025-03-18T00:37:04.104695	Information Science	{ "license": "Creative Commons - Attribution - https://creativecommons.org/licenses/by/4.0/", "url": "https://oercommons.org/courseware/lesson/94351/overview", "title": "What is a subject heading?", "author": "Higher Education" }
https://oercommons.org/courseware/lesson/88614/overview	Teaching First Gen College Students Recap Teaching First Generation College Students Overview This video is a short summary of what I've learned as an instructor taking the course: "Teaching First Generation College Students." First generation college students have unique needs and challenges when it comes to academics. The following are great resources for instructors teaching at the college level to assist first generation college students in their academic journey and ensure their ultimate success. Teaching First Generation College Students This video is a short summary of what I've learned as an instructor taking the course: "Teaching First Generation College Students." First generation college students have unique needs and challenges when it comes to academics. The following are great resources for instructors teaching at the college level to assist first generation college students in their academic journey and ensure their ultimate success. https://csulb.zoom.us/rec/share/5LC8A0c2W9DZHre_OnbChNW0qlTm8SEbMmlBsu1zKANsHBEFMVhOiJD_01IaYpk6.dQRDRIjyo4qJbieg?startTime=1639442019000	oercommons	2025-03-18T00:37:04.122557	12/10/2021	{ "license": "Creative Commons - Attribution - https://creativecommons.org/licenses/by/4.0/", "url": "https://oercommons.org/courseware/lesson/88614/overview", "title": "Teaching First Generation College Students", "author": "Banafshe Sharifian" }
https://oercommons.org/courseware/lesson/87246/overview	Digital Literacy Quiz Digital Wellbeing https://www.youtube.com/watch?v=h-VP58ncwJU Presentation of Empathy Skills What is Digital Literacy and Why It Matters Digital Citizenship Overview This course is about digital citizenship and its importance in using the internet. This quick and easy-to-follow module includes the four key aspects of digital citizenship and videos that contain further information on those key aspects. This resource can be utilized as a learning tool for both teachers and middle school-aged/high school-aged learners who are directly interacting with or new to how the internet works. This resource can also be utilized as a source to learn and practice digital citizenship together in the classroom. What Does Digital Citizenship Mean? In the 21st century, there are many types of citizenship, nationalities, and origins for the people around us. When we introduce ourselves to others, we may say: "Hello, my name is ____ and I am from ____." This introduction in the physical sense has informed the way that we interact with the world and how those interactions shape us. As we go into becoming a more digital age, it is even more important to think about how we are interacting with each other on the internet. If you are taking this module, you may be wondering to yourself, what in the world is digital citizenship and why is it so important? Before you continue with this module, I'd like for you to watch the video below to learn about Digital Citizenship. After watching the video above, you probably have a lot of questions about the aspects of Digital Citizenship. In this module, we will cover the 4 key concepts of digital citizenship, which are: - Empathy - Digital Literacy - Digital Divide - Digital Wellness Check out an additional video below with even more information. Empathy When we think about "Empathy" in the in-person sense, our mind immediately flickers to thoughts of interpreting and understanding how someone is feeling and why they are feeling that way. Online, empathy works in a similar manner, and having empathy online is crucial to being a good digital citizen. Empathy online means trying to understand another person's perspective and understanding them beyond the digital screen, because everyone online is a person with feelings that we must respect. Having empathy online means that we: - Remain responsive to others in a positive and open manner - Be understanding of a person's living situation, especially on video conferences - Refrain from making rude comments - Recognize that certain verbal expressions may be missed online, as everything is text-based - Always use respectful language - Be compassionate Below is a video resource showing empathy in action. Digital Literacy In simple terms, digital literacy is being able to understand the purpose of technology, and how to use that technology effectively. Picture this: you're a teacher during the pandemic and you have students who have never taken an online lesson. Digital literacy is the ability to understand how to navigate that environment, such as being able to open a web browser, view your emails, send text messages, write blogs, and communicate with your students or create resources for them using Powerpoint or Google Docs. Beyond that, digital literacy is understanding how to reach your students and the effectiveness of those online resources. While digital literacy is important in terms of understanding the basics of the internet, digital literacy is also extremely important in terms of understanding the dangers of the internet. Some of the dangers of the internet include: - Phishing - Viruses - Imitators (people who lie about their identity online) Below is a video resource which further breaks down digital literacy. Digital Divide The Digital Divide refers to the equity gap that exists after the digital and technological age. This divide exists between students who are able to access technology freely and students who are cut off from accessing that technology due to socioeconomic or other factors. These factors make come into fruition when students do not have computers at home or access to the internet in the same manner as other students. As an educator, it is important to learn about the digital divide because it shows one of the problems of the digital age and increases our ability to be valuable digital citizens. During the Coronavirus pandemic, we have seen this problem of a digital divide manifest itself in many ways. There are students who did not have access to computers or technology who were completely cut off from receiving an education. For those students, the school environment in person was their main interaction with learning. Understanding the digital divide helps teachers understand how to better serve students who do not have the same access and helps students gain similar access to their peers. The digital divide is based upon two key factors, which are: - Race: The number of African American students and Hispanic students who are impacted by the digital divide. African American students are impacted at home and at school, as schools that serve the majority of African American students are underfunded and therefore, have fewer computers. At home, fewer African American and Hispanic students have access to computers for school. - Income: Income is a huge factor of the digital divide, as many parents do not have the money to buy students computers and tablets to complete their schoolwork. Beyond that, a parent may be provided a laptop from school, but not have enough money for internet service. Below is a video resource that discusses the digital divide. Digital Wellness Digital wellness is essentially the practice of checking on your wellbeing in the digital environment and how that digital environment is impacting you in your personal and professional life. Digital wellness is the most important aspect of digital citizenship because it directly impacts a person outside of the classroom. For students, digital wellness includes how they interact with social media comments from friends or internalize new social media trends. There are certain trends, diets, and body types on the internet that may impact digital wellness. Digital wellness may also be impacted by mean or derogatory internet comments meant to make a person feel bad about themselves. In order to practice digital wellness, a person must: - Limit the amount of time they spend on social media, logging off when they feel overwhelmed. - Be alert of digital habits, including how much time is spent online. - Make rules for yourself, including times when you will or won't be on social media. - Practice and model kindness in an online setting. - Do not say anything that you would not say in person. - Create a social media routine. - Turn off social media or online activities when engaged with people in real life. Digital wellness is incredibly important to overall wellness and being a good digital citizen. Below is a video resource that discusses digital wellness. Conclusion In our module today, we covered how to be a digital citizen. Being a digital citizen is a long process and requires a lot of time and effort. However, if we all do our parts to become good digital citizens, the internet as a whole will improve for everyone. I hope that you learned some new information about digital literacy. Below is an optional quiz that you can take to test your knowledge.	oercommons	2025-03-18T00:37:04.154452	Valeria Astor	{ "license": "Creative Commons - Attribution - https://creativecommons.org/licenses/by/4.0/", "url": "https://oercommons.org/courseware/lesson/87246/overview", "title": "Digital Citizenship", "author": "Primary Source" }
https://oercommons.org/courseware/lesson/23393/overview	Nasi Lemak Overview Nasi lemak is a Malay fragrant rice dish cooked in coconut milk and pandan leaf. It is commonly found in Malaysia, where it is considered the national dish; it is also popular in neighbouring areas such as Singapore; Brunei, and Southern Thailand. Task : Go and Buy the Ingredients In order to try out the recipe given, first of all, you need to get all the ingredients required for preparing the dish. The ingredients too seek after will be for the Rice, Sambal, Condiments abd Vegetables. You are free to get all the ingredients from any where you like. Make sure the ingredients is fresh and newly produced. Check and observed before you purchase!	oercommons	2025-03-18T00:37:04.217508	05/17/2018	{ "license": "Creative Commons - Attribution - https://creativecommons.org/licenses/by/4.0/", "url": "https://oercommons.org/courseware/lesson/23393/overview", "title": "Nasi Lemak", "author": "Halim Jamal" }
https://oercommons.org/courseware/lesson/89529/overview	Copyright is a Spectrum Overview This resource offers a different perspective on copyright and its relationship with Creative Commons Licenses. Copyright is a Spectrum Note: This graphic does not intend to offer legal advice, it is offering a new perspective about copyright and its relation to Creative Commons. For true legal advice, consult a copyright lawyer.	oercommons	2025-03-18T00:37:04.235502	01/25/2022	{ "license": "Creative Commons - Attribution - https://creativecommons.org/licenses/by/4.0/", "url": "https://oercommons.org/courseware/lesson/89529/overview", "title": "Copyright is a Spectrum", "author": "Andrea Bearman" }
https://oercommons.org/courseware/lesson/98140/overview	Extended Hand to Big Toe Pose Overview A benefit of hand to big toe pose.	oercommons	2025-03-18T00:37:04.251385	10/21/2022	{ "license": "Creative Commons - Attribution - https://creativecommons.org/licenses/by/4.0/", "url": "https://oercommons.org/courseware/lesson/98140/overview", "title": "Extended Hand to Big Toe Pose", "author": "Annmarie Bedard" }
https://oercommons.org/courseware/lesson/72024/overview	script_to_create_imsmanifest_file script_to_fix_html zip file for importing OpenStax Chemistry 2e to Brightspace/D2L Overview Full text of Chemistry 2e from OpenStax in a form suitable for importing to Brightspace/D2L zip file for importing OpenStax Chemistry 2e to Brightspace/D2L I created this from the zip file provided by OpenStax by - converting the collection.xml file into an imsmanifest.xml file - cleaning up the html files a bit using <details></details> for objectives, summaries and solutions - creating a .css file which takes advantage of the various environments defined in the .html file The conversion and the cleanup are both done with perl scripts; I have attached those as well.	oercommons	2025-03-18T00:37:04.270643	09/03/2020	{ "license": "Creative Commons - Attribution - https://creativecommons.org/licenses/by/4.0/", "url": "https://oercommons.org/courseware/lesson/72024/overview", "title": "zip file for importing OpenStax Chemistry 2e to Brightspace/D2L", "author": "Erika Merschrod" }
https://oercommons.org/courseware/lesson/86967/overview	Improving Reading Skills Overview This is a resource for improving reading skills or habits. It is suitable for students or individuals that intends to find out steps for improving reading skills. Introduction Reading skill is essential for our day to day life. Reading helps build other skills like writing, researching, communication, etc. Above all, it is important to find out your purpose of reading before engaging in intensive or extensive reading techniques that will help you understand the content better. Read a thousand books and your words will flow like a river -Virginia Woolf. Ways to Improve Reading Skills Image: The Martin (CCO) Ways to Improve Reading Skill Reading skill is a habit that needs to be nurtured and upheld. You can improve reading skill through these steps below. - Find out the kind of resources you are interested in It is generally believed that people like involving themselves in what they are interested in. In the same way readers can find resources they like and would want to read. It could be of different genre such as comic, romance, non-fiction, etc. Join reading communities or clubs Register with book clubs that is closest to you. Meeting with people of same interest and goal will help you stay on track. Keep practicing and read often Practice leads to perfection. The more you read, you become better. Take note of new words Read alongside your writing materials or notepads. Take note of new words, look up their meanings, use them regularly to build your vocabulary Find out a conducive space/s that suits your reading needs Selecting a conducive reading environment is important. Some people read in a quite environment whereas others might prefer reading with music on. It is necessary to choose spaces you are comfortable with. This short video from the British Council further explains how to improve Reading Skills Video:British Council (CC BY) Summary Irrespective of the kind of resources you are interested in, you can make reading a hobby by reading consistently. You can start by reading resources that have few pages, as you progress in reading, you can decide to increase the volume of what you read. Having a small private library in your house or work place will help uphold reading skill. If you are not interested in hard copies, you can read online, download resources, download online reading and book/library software applications. Image: e-book (CCO) Attribute and Reference Attribution - Junior Libby. Books. Available online at https://www.publicdomainpictures.net/pictures/30000/velka/books-1345826320IHi.jpg Copyright CCO - The Martin. (2017). African Woman Reading. Available online at https://openclipart.org/detail/288006/african-woman-reading-more-colour Copyright CCO - British Council. (2017). How to Improve Your Reading skill. Video available at https://youtu.be/KLKZdMo7cLE Copyright CC BY - E-book. (2017). Available online at https://i0.hippopx.com/photos/353/519/709/e-book-e-reader-alcor-myth-e-paper-preview.jpg Copyright CCO Reference - Soren, R. (2021). How to Improve Your Reading skill. Available online at https://www.wikihow.com/Improve-Your-Reading-Skills	oercommons	2025-03-18T00:37:04.289645	Elementary Education	{ "license": "Creative Commons - Attribution - https://creativecommons.org/licenses/by/4.0/", "url": "https://oercommons.org/courseware/lesson/86967/overview", "title": "Improving Reading Skills", "author": "Education" }
https://oercommons.org/courseware/lesson/54361/overview	Introduction to Matter: Mixtures, Elements, and compounds Overview This module is a brief introduction to the definitions of mixture, compound, and element and includes a Ted Ed video on What's in a Mixture: the science of macaroni salad. Mixtures, Elements, and Compounds I like to ask students after they watch the Macaroni Salad (What's in a Mixture?) video how they would classify milk. They will often go further, asking "whole milk or skim?" We typically have a lively discussion. A mixture is a combination of materials that can be separated using physical methods like filtering, washing, using magnets, etc. A compound is two or more atoms "chemically" connected and we need to use chemical methods to separate or purify. An element is pure matter, or only one type of atom. Watch Ted Ed's What's In a Mixture for a primer on mixtures and how we separate them.	oercommons	2025-03-18T00:37:04.306833	05/15/2019	{ "license": "Creative Commons - Attribution - https://creativecommons.org/licenses/by/4.0/", "url": "https://oercommons.org/courseware/lesson/54361/overview", "title": "Introduction to Matter: Mixtures, Elements, and compounds", "author": "Amy Petros" }
https://oercommons.org/courseware/lesson/82809/overview	Critical Thinking and Evaluating Information Overview Original Source by Mary Johnson - Some sections have been deleted. LEARNING OBJECTIVES By the end of this section, you will be able to: Define critical thinking - Describe the role that logic plays in critical thinking - Describe how both critical and creative thinking skills can be used to problem-solve - Describe how critical thinking skills can be used to evaluate information - Identify strategies for developing yourself as a critical thinker Critical Thinking and Evaluating Information Critical Thinking and Evaluating Information The original resource has been adapted from Mary Johnson's Critical Thinking and Evaluating Information. Some sections have been deleted from the original source. https://creativecommons.org/licenses/by/4.0 Critical Thinking As a college student, you are tasked with engaging and expanding your thinking skills. One of the most important of these skills is critical thinking because it relates to nearly all tasks, situations, topics, careers, environments, challenges, and opportunities. It is a “domain-general” thinking skill, not one that is specific to a particular subject area. What Is Critical Thinking? Critical thinking is clear, reasonable, reflective thinking focused on deciding what to believe or do. It means asking probing questions like “How do we know?” or “Is this true in every case or just in this instance?” It involves being skeptical and challenging assumptions rather than simply memorizing facts or blindly accepting what you hear or read. Imagine, for example, that you’re reading a history textbook. You wonder who wrote it and why, because you detect certain biases in the writing. You find that the author has a limited scope of research focused only on a particular group within a population. In this case, your critical thinking reveals that there are “other sides to the story.” Who are critical thinkers, and what characteristics do they have in common? Critical thinkers are usually curious and reflective people. They like to explore and probe new areas and seek knowledge, clarification, and new solutions. They ask pertinent questions, evaluate statements and arguments, and they distinguish between facts and opinion. They are also willing to examine their own beliefs, possessing a manner of humility that allows them to admit lack of knowledge or understanding when needed. They are open to changing their mind. Perhaps most of all, they actively enjoy learning, and seeking new knowledge is a lifelong pursuit. This may well be you! No matter where you are on the road to being a critical thinker, you can always more fully develop and finely tune your skills. Doing so will help you develop more balanced arguments, express yourself clearly, read critically, and glean important information efficiently. Critical thinking skills will help you in any profession or any circumstance of life, from science to art to business to teaching. With critical thinking, you become a clearer thinker and problem solver. \| Critical Thinking IS \| Critical Thinking is NOT \| \|---\|---\| \| Skepticism \| Memorizing \| \| Examining assumptions \| Group thinking \| \| Challenging reasoning \| Blind acceptance of authority \| \| Uncovering biases \| Critical Thinking and Logic Critical thinking is fundamentally a process of questioning information and data. You may question the information you read in a textbook, or you may question what a politician or a professor or a classmate says. You can also question a commonly-held belief or a new idea. With critical thinking, anything and everything is subject to question and examination for the purpose of logically constructing reasoned perspectives. What Is Logic? The word logic comes from the Ancient Greek logike, referring to the science or art of reasoning. Using logic, a person evaluates arguments and reasoning and strives to distinguish between good and bad reasoning, or between truth and falsehood. Using logic, you can evaluate the ideas and claims of others, make good decisions, and form sound beliefs about the world.[1] Questions of Logic in Critical Thinking Let’s use a simple example of applying logic to a critical-thinking situation. In this hypothetical scenario, a man has a Ph.D. in political science, and he works as a professor at a local college. His wife works at the college, too. They have three young children in the local school system, and their family is well known in the community. The man is now running for political office. Are his credentials and experience sufficient for entering public office? Will he be effective in the political office? Some voters might believe that his personal life and current job, on the surface, suggest he will do well in the position, and they will vote for him. In truth, the characteristics described don’t guarantee that the man will do a good job. The information is somewhat irrelevant. What else might you want to know? How about whether the man had already held a political office and done a good job? In this case, we want to think critically about how much information is adequate in order to make a decision based on logic instead of assumptions. The following questions, presented in Figure 1, below, are ones you may apply to formulating a logical, reasoned perspective in the above scenario or any other situation: - What’s happening? Gather the basic information and begin to think of questions. - Why is it important? Ask yourself why it’s significant and whether or not you agree. - What don’t I see? Is there anything important missing? - How do I know? Ask yourself where the information came from and how it was constructed. - Who is saying it? What’s the position of the speaker and what is influencing them? - What else? What if? What other ideas exist and are there other possibilities? Figure 1 Problem-Solving with Critical Thinking For most people, a typical day is filled with critical thinking and problem-solving challenges. In fact, critical thinking and problem-solving go hand-in-hand. They both refer to using knowledge, facts, and data to solve problems effectively. But with problem-solving, you are specifically identifying, selecting, and defending your solution. Below are some examples of using critical thinking to problem-solve: - Your roommate was upset and said some unkind words to you, which put a crimp in the relationship. You try to see through the angry behaviors to determine how you might best support the roommate and help bring the relationship back to a comfortable spot. - Your campus club has been languishing due to lack of participation and funds. The new club president, though, is a marketing major and has identified some strategies to interest students in joining and supporting the club. Implementation is forthcoming. - Your final art class project challenges you to conceptualize form in new ways. On the last day of class when students present their projects, you describe the techniques you used to fulfill the assignment. You explain why and how you selected that approach. - Your math teacher sees that the class is not quite grasping a concept. She uses clever questioning to dispel anxiety and guide you to a new understanding of the concept. - You have a job interview for a position that you feel you are only partially qualified for, although you really want the job and you are excited about the prospects. You analyze how you will explain your skills and experiences in a way to show that you are a good match for the prospective employer. - You are doing well in college, and most of your college and living expenses are covered. But there are some gaps between what you want and what you feel you can afford. You analyze your income, savings, and budget to better calculate what you will need to stay in college and maintain your desired level of spending. Problem-Solving Action Checklist Problem-solving can be an efficient and rewarding process, especially if you are organized and mindful of critical steps and strategies. Remember to assume the attributes of a good critical thinker: if you are curious, reflective, knowledge-seeking, open to change, probing, organized, and ethical, your challenge or problem will be less of a hurdle, and you’ll be in a good position to find intelligent solutions. The steps outlined in this checklist will help you adhere to these qualities in your approach to any problem: \| STRATEGIES \| ACTION CHECKLIST[2] \| \| \|---\|---\|---\| \| 1 \| Define the problem \| \| \| 2 \| Identify available solutions \| \| \| 3 \| Select your solution \| \| Critical and Creative Thinking Critical and creative thinking (described in more detail in Chapter 6: Theories of Learning) complement each other when it comes to problem-solving. The following words, by Dr. Andrew Robert Baker, are excerpted from his “Thinking Critically and Creatively” essay. Dr. Baker illuminates some of the many ways that college students will be exposed to critical and creative thinking and how it can enrich their learning experiences. THINKING CRITICALLY AND CREATIVELY Critical thinking skills are perhaps the most fundamental skills involved in making judgments and solving problems. You use them every day, and you can continue improving them. The ability to think critically about a matter—to analyze a question, situation, or problem down to its most basic parts—is what helps us evaluate the accuracy and truthfulness of statements, claims, and information we read and hear. It is the sharp knife that, when honed, separates fact from fiction, honesty from lies, and the accurate from the misleading. We all use this skill to one degree or another almost every day. For example, we use critical thinking every day as we consider the latest consumer products and why one particular product is the best among its peers. Is it a quality product because a celebrity endorses it? Because a lot of other people may have used it? Because it is made by one company versus another? Or perhaps because it is made in one country or another? These are questions representative of critical thinking. The academic setting demands more of us in terms of critical thinking than everyday life. It demands that we evaluate information and analyze myriad issues. It is the environment where our critical thinking skills can be the difference between success and failure. In this environment we must consider information in an analytical, critical manner. We must ask questions—What is the source of this information? Is this source an expert one and what makes it so? Are there multiple perspectives to consider on an issue? Do multiple sources agree or disagree on an issue? Does quality research substantiate information or opinion? Do I have any personal biases that may affect my consideration of this information? It is only through purposeful, frequent, intentional questioning such as this that we can sharpen our critical thinking skills and improve as students, learners and researchers. While critical thinking analyzes information and roots out the true nature and facets of problems, it is creative thinking that drives progress forward when it comes to solving these problems. Exceptional creative thinkers are people that invent new solutions to existing problems that do not rely on past or current solutions. They are the ones who invent solution C when everyone else is still arguing between A and B. Creative thinking skills involve using strategies to clear the mind so that our thoughts and ideas can transcend the current limitations of a problem and allow us to see beyond barriers that prevent new solutions from being found. Brainstorming is the simplest example of intentional creative thinking that most people have tried at least once. With the quick generation of many ideas at once, we can block-out our brain’s natural tendency to limit our solution-generating abilities so we can access and combine many possible solutions/thoughts and invent new ones. It is sort of like sprinting through a race’s finish line only to find there is new track on the other side and we can keep going, if we choose. As with critical thinking, higher education both demands creative thinking from us and is the perfect place to practice and develop the skill. Everything from word problems in a math class, to opinion or persuasive speeches and papers, call upon our creative thinking skills to generate new solutions and perspectives in response to our professor’s demands. Creative thinking skills ask questions such as—What if? Why not? What else is out there? Can I combine perspectives/solutions? What is something no one else has brought-up? What is being forgotten/ignored? What about ______? It is the opening of doors and options that follows problem-identification. Consider an assignment that required you to compare two different authors on the topic of education and select and defend one as better. Now add to this scenario that your professor clearly prefers one author over the other. While critical thinking can get you as far as identifying the similarities and differences between these authors and evaluating their merits, it is creative thinking that you must use if you wish to challenge your professor’s opinion and invent new perspectives on the authors that have not previously been considered. So, what can we do to develop our critical and creative thinking skills? Although many students may dislike it, group work is an excellent way to develop our thinking skills. Many times I have heard from students their disdain for working in groups based on scheduling, varied levels of commitment to the group or project, and personality conflicts too, of course. True—it’s not always easy, but that is why it is so effective. When we work collaboratively on a project or problem we bring many brains to bear on a subject. These different brains will naturally develop varied ways of solving or explaining problems and examining information. To the observant individual we see that this places us in a constant state of back and forth critical/creative thinking modes. For example, in group work we are simultaneously analyzing information and generating solutions on our own, while challenging other’s analyses/ideas and responding to challenges to our own analyses/ideas. This is part of why students tend to avoid group work—it challenges us as thinkers and forces us to analyze others while defending ourselves, which is not something we are used to or comfortable with as most of our educational experiences involve solo work. Your professors know this—that’s why we assign it—to help you grow as students, learners, and thinkers! —Dr. Andrew Robert Baker, Foundations of Academic Success: Words of Wisdom Evaluating Information with Critical Thinking Evaluating information can be one of the most complex tasks you will be faced with in college. But if you utilize the following four strategies, you will be well on your way to success: - Read for understanding - Examine arguments - Clarify thinking - Cultivate “habits of mind” Read for Understanding When you read, take notes or mark the text to track your thinking about what you are reading. As you make connections and ask questions in response to what you read, you monitor your comprehension and enhance your long-term understanding of the material. You will want to mark important arguments and key facts. Indicate where you agree and disagree or have further questions. You don’t necessarily need to read every word, but make sure you understand the concepts or the intentions behind what is written. See the chapter on Active Reading Strategies for additional tips. Examine Arguments When you examine arguments or claims that an author, speaker, or other source is making, your goal is to identify and examine the hard facts. You can use the spectrum of authority strategy for this purpose. The spectrum of authority strategy assists you in identifying the “hot” end of an argument—feelings, beliefs, cultural influences, and societal influences—and the “cold” end of an argument—scientific influences. The most compelling arguments balance elements from both ends of the spectrum. The following video explains this strategy in further detail: Clarify Thinking When you use critical thinking to evaluate information, you need to clarify your thinking to yourself and likely to others. Doing this well is mainly a process of asking and answering probing questions, such as the logic questions discussed earlier. Design your questions to fit your needs, but be sure to cover adequate ground. What is the purpose? What question are we trying to answer? What point of view is being expressed? What assumptions are we or others making? What are the facts and data we know, and how do we know them? What are the concepts we’re working with? What are the conclusions, and do they make sense? What are the implications? Cultivate “Habits of Mind” “Habits of mind” are the personal commitments, values, and standards you have about the principle of good thinking. Consider your intellectual commitments, values, and standards. Do you approach problems with an open mind, a respect for truth, and an inquiring attitude? Some good habits to have when thinking critically are being receptive to having your opinions changed, having respect for others, being independent and not accepting something is true until you’ve had the time to examine the available evidence, being fair-minded, having respect for a reason, having an inquiring mind, not making assumptions, and always, especially, questioning your own conclusions—in other words, developing an intellectual work ethic. Try to work these qualities into your daily life. Developing Yourself As a Critical Thinker Critical thinking is a fundamental skill for college students, but it should also be a lifelong pursuit. Below are additional strategies to develop yourself as a critical thinker in college and in everyday life: - Reflect and practice: Always reflect on what you’ve learned. Is it true all the time? How did you arrive at your conclusions? - Use wasted time: It’s certainly important to make time for relaxing, but if you find you are indulging in too much of a good thing, think about using your time more constructively. Determine when you do your best thinking and try to learn something new during that part of the day. - Redefine the way you see things: It can be very uninteresting to always think the same way. Challenge yourself to see familiar things in new ways. Put yourself in someone else’s shoes and consider things from a different angle or perspective. If you’re trying to solve a problem, list all your concerns: what you need in order to solve it, who can help, what some possible barriers might be, etc. It’s often possible to reframe a problem as an opportunity. Try to find a solution where there seems to be none. - Analyze the influences on your thinking and in your life: Why do you think or feel the way you do? Analyze your influences. Think about who in your life influences you. Do you feel or react a certain way because of social convention, or because you believe it is what is expected of you? Try to break out of any molds that may be constricting you. - Express yourself: Critical thinking also involves being able to express yourself clearly. Most important in expressing yourself clearly is stating one point at a time. You might be inclined to argue every thought, but you might have greater impact if you focus just on your main arguments. This will help others to follow your thinking clearly. For more abstract ideas, assume that your audience may not understand. Provide examples, analogies, or metaphors where you can. - Enhance your wellness: It’s easier to think critically when you take care of your mental and physical health. Try taking activity breaks throughout the day to reach 30 to 60 minutes of physical activity each day. Scheduling physical activity into your day can help lower stress and increase mental alertness. Also, do your most difficult work when you have the most energy. Think about the time of day you are most effective and have the most energy. Plan to do your most difficult work during these times. And be sure to reach out for help if you feel you need assistance with your mental or physical health (see Maintaining Your Mental and Physical Health for more information). KEY TAKEAWAYS - Critical thinking is logical and reflective thinking focused on deciding what to believe or do. - Critical thinking involves questioning and evaluating information. - Critical and creative thinking both contribute to our ability to solve problems in a variety of contexts. - You can take specific actions to develop and strengthen your critical thinking skills.	oercommons	2025-03-18T00:37:04.336202	erin faherty	{ "license": "Creative Commons - Attribution - https://creativecommons.org/licenses/by/4.0/", "url": "https://oercommons.org/courseware/lesson/82809/overview", "title": "Critical Thinking and Evaluating Information", "author": "Reading" }
https://oercommons.org/courseware/lesson/66554/overview	Education Standards Uses Tools and Processes for OER Uses Tools and Processes of Precision Agriculture for OER Uses Tools and Processes Worksheet Variability in Precision Agriculture OER Variability in Precision Agriculture OER pdf Precision Agriculture Basics Overview Precision Agriculture Basics is three lesson plans to give students a basic understanding of Precision Agriculture. It includes: 1. Definition of Precision Agriculture 2. Uses, Tools and Processes of Precision Agriculture 3. Variability in Precision Agriculture Precision Agriculture Lesson 1 "Precision Agriculture Definition" - Typical Keywords: Site specific or subfield, GPS (geospatial), efficiency, management, data, technology, variable rate, environment, economic, variability - This Precision Agriculture (PA) definition has recently been recognized by the Board of directors as the official definition of the International Society for Precision Agriculture (ISPA) - “Precision Agriculture is a management strategy that gathers, processes and analyzes temporal, spatial and individual data and combines it with other information to support management decisions according to estimated variability for improved resource use efficiency, productivity, quality, profitability and sustainability of agricultural production.” - Breakdown of different parts of definition: - “management strategy the gathers, processes and analyzes data” - Data is gathered in the field. Examples: Yield data is gathered during harvest via a yield monitor in a combine. Planting data is gathered from a planter during seeding. Remote sensing data is gathered from satellites into a software platform. - Data is processed from the field into a cloud-based software package or brought from the combine/tractor via an usb device or data card and read into a software package. - Data is analyzed by the farmer or a precision agriculture consultant and used in making management decisions. - “temporal, spatial and individual data” - Temporal data: Data that specifically refers to times or dates. - Spatial data: Any data that can be mapped with a location (latitude/longitude) - Individual data: Data gathered or recorded by farmer. - “Variability” - Precision Agriculture assumes that fields are not uniform, but rather variable. Variability can occur in soils physical properties and topography of the land. Variability can also occur because of previous farming practices (no till versus conventional tillage), vegetation (alfalfa, pasture, cropland), management (renovated tree rows, old farmyards/fence lines) and etc. - “improved resource use efficiency, productivity, quality, profitability and sustainability of agricultural production” - Resources use efficiency includes land, labor, fuel, fertilizer, herbicide, fungicide, insecticide, seed, and ect. - Productivity refers to increasing yield - Quality would include fruit/vegetable size and firmness; protein content, oil content, test weight, plumpness and more. - Profitability is ability to generate more revenue than expenses. - According to the National Institute of Food and Agriculture, Sustainable agricultural practices are intended to protect the environment, expand the Earth’s natural resource base, and maintain and improve soil fertility. Based on a multi-pronged goal, sustainable agriculture seeks to: - Increase profitable farm income - Promote environmental stewardship - Enhance quality of life for farm families and communities - Increase production for human food and fiber needs - “management strategy the gathers, processes and analyzes data” Precision Agriculture Lesson One: Definition of Precision Agriculture Overview: Students will use the internet to develop a concise definition of Precision Agriculture. Objectives: The student will be able to explain basic concepts in precision agriculture. Materials Needed: Access to the internet Activity: - Individual activity: Each student will have search the internet and learn as much as they can about precision agriculture in 5 minutes. Students will each write 3 concepts that they learned. (5-10 minutes) - Place the students into groups of 2 or 3. Students will report the 3 concepts that they learned to their group. (2-5 minutes) - Using the concepts learned, have each group formulate a concise (less than 25 word) definition of Precision Agriculture (5-10 minutes) - Each group will read their definition of Precision Agriculture, while the teacher writes key words on the whiteboard. (5-10 minutes) - Teacher shares the official definition of Precision Agriculture (below). (5 minutes) - Teacher discusses the definition, including any terms students are familiar with. (below) (10-20 minutes) Precision Agriculture Lesson 2 "Uses, Tools and Processes" Teacher Resources: - Powerpoint has notes - PDF of Powerpoint, with notes - Student Worksheet - Example of typical Guidance System - http://www.rlhtechs.com/Trimble%20Ag/EZ%20500.htm - “Climate/Fieldview Drive” - Software Company Websites - Intelligent Devices - https://agriculture.trimble.com/product/greenseeker-system/ - https://agriculture.trimble.com/product/weedseeker-spot-spray-system/ - https://www.precisionplanting.com/products/product/smartfirmer - https://www.digitalmatter.com/Solutions/IoT-Agriculture-Sensors - https://www.scrdairy.com/herd-intelligence/hc24-solution.html - https://all3dp.com/beaniot-internet-of-things-agriculture/ Precision Agriculture Lesson Two: Uses, Tools and Processes of Precision Agriculture Overview: Students will be introduced to spatial data that is used in making management decisions in agriculture. Objectives: The student will be able to: -Explain the Uses of Precision Agriculture -Describe the Tools used in Precision Agriculture -List the Processes used in Precision Agriculture Materials Needed: Access to the internet Activity: - Teacher will go through the powerpoint presentation - While reviewing the powerpoint, students will complete the worksheet. Optional Activities: - Worksheet includes optional activities. Precision Agriculture Lesson 3 "Variability in Precision Agriculture" Teacher Resources: - Powerpoint Slides - Activities - Students will research one of the era’s of farming (Agriculture Revolution, Ridge and Furrow Farming, Industrial Revolution and Technological Revolution) - Discussion Questions: - What type of equipment/technology is utilized? - What new inventions happened during this time period? - How did new equipment/technology/inventions change farming practices? - Discussion Questions: - After seeing several examples of variability in a field, the students will come up with other examples of how field can be variable. - Discussion Point: “What are other examples of temporal variability in a field?” - Discussion Point: “What are some farming methods to manage variability in a field?” - Students will research one of the era’s of farming (Agriculture Revolution, Ridge and Furrow Farming, Industrial Revolution and Technological Revolution) Resource Websites: Precision Agriculture Lesson One: Variability in Precision Agriculture Overview: Students will discover why “variability” is the driving factor behind precision agriculture. Objectives: The student will explore different types of variation in a field and how precision agriculture technology can help manage the variability. Materials Needed: internet Activity: A powerpoint presentation, with notes, will explain field variability. Several discussion slides are a part of the powerpoint. - Students will research one of the era’s of farming - Discussion Questions: - What type of equipment/technology is utilized? - What new inventions happened during this time period? - How did new equipment/technology/inventions change farming practices? - Discussion Questions: - After seeing several examples of variability in a field, the students will come up with other examples of how field can be variable. - Discussion Point: “What are other examples of temporal variability in a field?” - Discussion Point: “What are some farming methods to manage variability in a field?”	oercommons	2025-03-18T00:37:04.395026	Carmel Miller	{ "license": "Creative Commons - Attribution - https://creativecommons.org/licenses/by/4.0/", "url": "https://oercommons.org/courseware/lesson/66554/overview", "title": "Precision Agriculture Basics", "author": "Homework/Assignment" }
https://oercommons.org/courseware/lesson/115931/overview	How did the Trans-Atlantic Slave Trade Impact African Civilizations? Overview This resource is a document based activity that consists of eight primary sources related to the trans-Atlantic slave trade. The assignment asks students to consider how the trans-Atlantic slave trade impacted African civilizations using primary sources. Attachments The attachment for this resource is contains instructions for a document based activity about the transatlantic slave trade and a packet of primary source documents, art, and artifacts for students to use in the activity. About This Resource The sample assignment included here was submitted by a participant in a one-day virtual workshop entitled, "Teaching the Global African Diaspora" for world history teachers hosted by the Alliance for Learning in World History. This is a draft document that may subsequently have been revised in light of feedback and discussion during the event. This resource was contributed by Elizabeth Mulcahy, a social studies educator in Virginia.	oercommons	2025-03-18T00:37:04.413481	Alliance for Learning in World History	{ "license": "Creative Commons - Attribution - https://creativecommons.org/licenses/by/4.0/", "url": "https://oercommons.org/courseware/lesson/115931/overview", "title": "How did the Trans-Atlantic Slave Trade Impact African Civilizations?", "author": "Homework/Assignment" }
https://oercommons.org/courseware/lesson/120572/overview	Logarithms and Their Friends Logarithms and Their Friends Overview Logaritms explained as being an exponent. Compares power functions and exponential functions: - A power function is different than an exponential function - The inverse of apower function is a root function - The inverse of an exponential function is a logarithmic function Shows when to use a power function and shows when to use an expoentail function. Includes many examples.	oercommons	2025-03-18T00:37:04.431803	10/09/2024	{ "license": "Creative Commons - Attribution - https://creativecommons.org/licenses/by/4.0/", "url": "https://oercommons.org/courseware/lesson/120572/overview", "title": "Logarithms and Their Friends", "author": "ROBERT BROWN" }
https://oercommons.org/courseware/lesson/82845/overview	Wikipedia Renewable Assignment on 1984 by George Orwell Overview This is an OER, Open Pedagogy project based on a reading of 1984 by George Orwell. Students will reseach a topic directly related to the novel and find a Wikipedia page that is lacking in information or analysis and edit the page to add substance to it. Proper citations are necessary. Deliverables include a project proposal, an annotated bibliography, an edited Wikipedia page, and a synopsis describing the plan, process, and outcome of their work. This synopsis will be presented and discussed in class at the end. Open Pedagogy Wikipedia Assignment Suggested for Composition I where 1984 by George Orwell is assigned	oercommons	2025-03-18T00:37:04.447984	06/26/2021	{ "license": "Creative Commons - Attribution - https://creativecommons.org/licenses/by/4.0/", "url": "https://oercommons.org/courseware/lesson/82845/overview", "title": "Wikipedia Renewable Assignment on 1984 by George Orwell", "author": "Katie Durant" }
https://oercommons.org/courseware/lesson/114905/overview	Wrap Around Support for Faculty Implementing OER Overview Archived session from the 2024 Arizona Regional OER Conference. Session Title: Wrap Around Support for Faculty Implementing OER. This resource includes the session abstract, presenter(s), resources, and recording. Session Abstract, Presenters, Resources, and Recording Session Abstract Faculty are key to implementing Open Educational Resources (OER). Yavapai College has effectively developed and currently offers strategic wrap around support for faculty adopting, adapting, and building OER. Through this approach, YC saved students $802,340 during fall 2020 through spring 2022. During this webinar, presenters will share the key components to this approach and offer resources that could be implemented on your campus. Presenter(s) - Thatcher Bohrman, Yavapai College - Megan Crossfield, Yavapai College - Andrea Schaben, Yavapai College Resources - OER LibGuide - Teaching & eLearning Website (OER Faculty Facing Website) - OER Training for Course Builders - OER Training for Teachers - OER Handbook for YC Program Recording	oercommons	2025-03-18T00:37:04.462940	04/03/2024	{ "license": "Creative Commons - Attribution - https://creativecommons.org/licenses/by/4.0/", "url": "https://oercommons.org/courseware/lesson/114905/overview", "title": "Wrap Around Support for Faculty Implementing OER", "author": "OERizona Conference" }
https://oercommons.org/courseware/lesson/80763/overview	Writing the Literacy Narrative Overview This Google hyperdoc walks students through the writing process for a literacy narrative in a series of steps. This can be used in a high school or college ELA course that requires personal narrative. Writing the Literacy Narrative Literacy Narrative - In this tutorial, you will walk through instruction and writing steps that will lead you to a literacy narrative. Please make a copy of this document (File>Make Copy) and complete all of the steps below: \| Literacy Narrative Requirements4 pages, double spaced (1000 words)MLA FormatSee your course and fill in your due dates \| \| \| Prewriting Check (Week 3) \| Due Date: \| \| Draft Due to Peer Editing Form (Week 4) \| Due Dates (there are 2 due dates): \| \| Final Draft (Week 5) \| Due Date: \| Grading Sometimes it’s nice to know how your paper will be graded before you start writing. Here are the key features of a well-written paper From Norton Field Guide chapter 10 \| A well-told story. As with most narratives, those about literacy often set up some sort of situation that needs to be resolved. That need for resolution makes readers want to keep on reading. Some literacy narratives simply explore the role that developing literacy of some kind played at some time in someone’s life, as when Felsenfeld “was knocked sideways” by classical music. And some, like Vallowe’s, speculate on the origins of the writer’s literacy. \| \| Vivid detail. Details can bring a narrative to life for readers by giving them vivid mental sensations of the sights, sounds, smells, tastes, and textures of the world in which your story takes place. The details you use when describing something can help readers picture places, people, and events;dialogue can help them hear what is being said. \| \| Some indication of the narrative’s significance. By definition, a literacy narrative tells something the writer remembers about learning to read, write, or gain competence in a specific area. In addition, the writing needs to make clear why the incident matters to them. You may reveal its significance in various ways. \| Step 1: Choosing a Topic In general, it’s a good idea to focus on a single event that took place during a relatively brief period of time--though sometimes learning to do or understand something ,au tale [;ace over an extended period. In that case, several snapshots or important moments may be needed. Here are some suggestions for topics: \| \| In the box below, make a list of possible topics, then choose one that you think will be interesting to you and to others. Choose at least one and spend 30 minutes freewriting, listing, clustering, or looping in the box below. This will be graded. You are welcome to do this by hand and upload an image in the box below if that suits you better. \| Step 2: Generating Ideas and Text \| In the columns below you will generate text. Much of it may be used later as you draft your paper, but don’t worry about that now. Use these exercises to help you get your ideas down. \| \| \| Purpose: Why do you want to tell this tory? To share a memory? Fulfill an assignment? Teach a lesson? Explore your past? \| \| \| Audience: Remember you will be posting your paper in a forum for peers to read. Are your readers likely to have had similar experiences? Would they tell similar stories? How much explaining will you have to do to help them understand your narrative? Can you assume that they will share your attitudes, or will you have to work at making them see your perspective? How much of your life are you willing to share with your audience? \| \| \| Stance: What attitude do you want to project? Affectionate? Neutral? Critical, Sincere? Serious? Humorous? Nostalgic? \| \| \| Describe the setting: Where does your story take place? List the places, and then describe the settings: What do you see? What do you hear? What do you smell? How and what do you feel? What do you taste? \| \| \| Think about the key people: Narratives include people whose actions play an important role in the story. Describe teacher person in a paragraph or so \| \| \| Recall or imagine some characteristic dialogue: A good way to bring people to life and move a story along is with dialogue, to let readers hear them rather than just hearing about them. Write 6-10 lines of dialogue between two people in your narrative. If you don’t recall an actual conversation, create one that could have happened. \| \| \| Write about what happened: This is the heart of any good narrative. Summarize what happened in a paragraph or so--you will of course expand when you write your draft \| \| \| Consider the Significance of the narrative: You need to make it clear why this event was significant to you and to your reader. How did it change you? Why was it meaningful? Why does it matter? \| Step 3: Organization of the Literacy Narrative \| Below are three different options for organizing your essay. Choose one of them (don’t be afraid to choose something other than chronological!). Click on the image and use the down arrow to open the drawing, make a copy, and fill in the boxes with elements from your story to help you outline your organization \| \| Paste in your link: \| \| Once you have completed Steps 1-3, submit a link to your copy of this document to your teacher as your Prewriting Check \| Step 4- Draft Use this MLA formatted writing template linked HERE to draft out your 4 page (1000 word) essay by making a copy and adding your own information. Add a link to your paper in the box below. Make sure it is set so that “Anyone with a link CAN EDIT” Do this by clicking SHARE in the top right corner. Then click “change” under the “get link” box, and use the down arrow to change so that anyone at MHA can edit. \| link to paper: \| Step 5: Get Feedback \| Submit your draft to paperrater.com. Use feedback to polish your essay. Here is a TUTORIAL for paperrater.com \| \| What feedback did you get from paperrater.com? Paste it in this box: \| Step 6- Peer Editing Go back to the course and submit your draft for peer editing. You will post your own draft, then edit two of your peers’ drafts. Read the directions carefully in the Peer Editing Forum. Step 7: Final Paper Once you have revised your draft, you will submit your final draft to your teacher in the course. You may also paste the draft below. Make sure it is shared so that anyone from MHA with a link can edit: \| Paste in Link: \| Link to the Literacy Narrative Google Doc Make a copy of this using File>Make a Copy	oercommons	2025-03-18T00:37:04.514344	Unit of Study	{ "license": "Creative Commons - Attribution - https://creativecommons.org/licenses/by/4.0/", "url": "https://oercommons.org/courseware/lesson/80763/overview", "title": "Writing the Literacy Narrative", "author": "Module" }
https://oercommons.org/courseware/lesson/120789/overview	Functions in C Language Overview Functions are an essential part of C programming, providing a way to break large programs into smaller and manageble chunks. This image describes the types of functions used in C language Functions in C Language Functions are an essential part of C programming, providing a way to break large programs into smaller and manageble chunks. This image describes the types of functions used in C language. Built in functions like printf(),scanf() are predefined functions in C library. User defined functions are written by programmer according to his requirement.	oercommons	2025-03-18T00:37:04.526830	10/17/2024	{ "license": "Creative Commons - Attribution - https://creativecommons.org/licenses/by/4.0/", "url": "https://oercommons.org/courseware/lesson/120789/overview", "title": "Functions in C Language", "author": "Navdeep Kaur" }
https://oercommons.org/courseware/lesson/115625/overview	Team Discussion: Cognitive Styles when Using Technology (SESMag) Overview What cognitive styles do you use to interact with technology? PRE-REQ: https://oercommons.org/courseware/lesson/115624 Pre-Requisites Team Discussion: Cognitive Styles Begin getting to know your team by contributing to the team discussion: 1. Describe your thoughts about the cognitive styles reading (1+ paragraph) 2. Respond to two different people. Include how your facet values are similar or different from your teammate's	oercommons	2025-03-18T00:37:04.540655	Psychology	{ "license": "Creative Commons - Attribution - https://creativecommons.org/licenses/by/4.0/", "url": "https://oercommons.org/courseware/lesson/115625/overview", "title": "Team Discussion: Cognitive Styles when Using Technology (SESMag)", "author": "Information Science" }
https://oercommons.org/courseware/lesson/80433/overview	Music Appreciation Overview This course is an interactive discussion of music through the ages and how we as a people from various walks of life can appreciate it. Appreciating Call and Response This section discusses the origins of step dancing in the African-American culture. The link below written by Nicola F. Mason of Eastern Kentucky University discusses the roots of this dance and its music from South Africa. Native Dance and Music: African American Steppin' Writing Prompt: 1. What is the traditional African name for gumboot dancing? What does it mean? How does this name represent the historical origins of gumboot dancing? 2. What other names are often used in reference to Steppin’? How do these names represent the historical origins of Steppin’? 3. “Gumboot dancing and Steppin’ are no longer restricted by place, purpose, or person.” What are the places, purposes, and persons referred to in this statement? 4. Discuss ways that learning about gumboot dancing and Steppin’ in the classroom can assist in developing cultural sensitivity in students. Gumboot Dancing and Steppin’ - Origins, Parallels, and Uses in the Classroom. (2021, February 5). Retrieved May 15, 2021, from https://human.libretexts.org/@go/page/87706	oercommons	2025-03-18T00:37:04.559895	05/15/2021	{ "license": "Creative Commons - Attribution - https://creativecommons.org/licenses/by/4.0/", "url": "https://oercommons.org/courseware/lesson/80433/overview", "title": "Music Appreciation", "author": "Duana Demus-Leslie" }
https://oercommons.org/courseware/lesson/75050/overview	CAREER READINESS FRAMEWORK Overview a basic framework for desingin program on career readiness CAREER READINESS FRAMEWORK (PIC) There are three stages and six steps in career readiness program: Stage1: Know Step 1- Who I am? Step 2- What I want to be? Stage 2: Prepare Step 3- Setting my resume Step 4- Networking Stage 3: Perform Step 5- Facing interview Step 6- Managing job offer, rejections, and career	oercommons	2025-03-18T00:37:04.577110	11/24/2020	{ "license": "Creative Commons - Attribution - https://creativecommons.org/licenses/by/4.0/", "url": "https://oercommons.org/courseware/lesson/75050/overview", "title": "CAREER READINESS FRAMEWORK", "author": "RONALD YESUDHAS" }
https://oercommons.org/courseware/lesson/83395/overview	APA 7th Edition: Set up an APA Format Paper in 6 Minutes Video APA 7th Style Guide PowerPoint APA Reference General APA Format How to Format a Paper in APA 7th Overview In scholarly writing, it is important to structure a paper in a manner that is concise and follows the general format set by writing professionals. The American Phycological Association (APA) format of writing is widely accepted and a good rule of thumb to follow when writing formal papers. This resource was constructed to give the basics of the newest APA 7th edition. Additional research will be needed for more specific situations and citations Objectives The objective of this lesson is to instruct students how to properly structure their paper using the APA 7th format in professional writing. There is additional information available on citations and references as it is important to uphold the ethics of writing and to always avoid plagiarism. To get the most information out of this lesson, students should review the included material below in the following order. 1. Review the information related to the general format of APA 7th. 2. Watch the video covering basics of APA 7th 3. Review and take notes over the PowerPoint. This PowerPoint is detailed and making your own notes will allow for quicker reference when you are doing your writing 4. Look at the additional images pertaining to APA 7th citations and reference list	oercommons	2025-03-18T00:37:04.599103	07/10/2021	{ "license": "Creative Commons - Attribution - https://creativecommons.org/licenses/by/4.0/", "url": "https://oercommons.org/courseware/lesson/83395/overview", "title": "How to Format a Paper in APA 7th", "author": "Daniel Childers" }
https://oercommons.org/courseware/lesson/67215/overview	BIOL 122 Concepts of Biology Overview https://openstax.org/details/books/concepts-biology BIOL 122 BIOL 122 Chapters used for course: Chapter1 & 2 Chapters 3 & 4 Chapters 5 & 6 Chapters 7 & 8 Chapters 9 & 10 Chapters 11 & 12 Chapters 16 & 17 Chapters 18 & 19 Chapters 20 & 21	oercommons	2025-03-18T00:37:04.615600	05/23/2020	{ "license": "Creative Commons - Attribution - https://creativecommons.org/licenses/by/4.0/", "url": "https://oercommons.org/courseware/lesson/67215/overview", "title": "BIOL 122 Concepts of Biology", "author": "Clement Gomes" }
https://oercommons.org/courseware/lesson/100325/overview	Course Syllabus Overview The attached file is our syllabus for the Introductory Statistics course that we are teaching as an OER course. The summary of the syllabus is as follows. - This course uses MyOpenMath for testing students' knkowledge via homework and quiz assessments. MyOpenMath is an open platform for students to use without any additional access fees like the one for our other statistics courses which charge an extra fee to use a different online platform. - This course uses MS Excel as the statistical tool. We have created templates for students to use to evaluate statistics for a given data. Students have access to all Microsoft products via their college account without any extra charge. Using Excel also eliminates the need for buying a calculator. - A big part of the course is the project, which is based on real world data. Students are provided with data in a spreadsheet by the instructor. Data is mined from public domains. Students are to submit their input using MS Word and MS Excel. - We are also using MS Teams to record additional video resources on using Excel for statistics. Syllabus The attached file is our syllabus for the Introductory Statistics course that we are teaching as an OER course. The summary of the syllabus is as follows. - This course uses MyOpenMath for testing students' knkowledge via homework and quiz assessments. MyOpenMath is an open platform for students to use without any additional access fees like the one for our other statistics courses which charge an extra fee to use a different online platform. - This course uses MS Excel as the statistical tool. We have created templates for students to use to evaluate statistics for a given data. Students have access to all Microsoft products via their college account without any extra charge. Using Excel also eliminates the need for buying a calculator. - A big part of the course is the project, which is based on real world data. Students are provided with data in a spreadsheet by the instructor. Data is mined from public domains. Students are to submit their input using MS Word and MS Excel. - We are also using MS Teams to record additional video resources on using Excel for statistics.	oercommons	2025-03-18T00:37:04.633040	01/30/2023	{ "license": "Creative Commons - Attribution - https://creativecommons.org/licenses/by/4.0/", "url": "https://oercommons.org/courseware/lesson/100325/overview", "title": "Course Syllabus", "author": "Hersh Patel" }

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