Have you ever taken a device apart to find out how it works? Many of us have done so, whether to attempt a repair or simply to satisfy our curiosity. A device’s internal workings are often distinct from its user interface on the outside. For example, we don’t think about microchips and circuits when we turn up the volume on a mobile phone; instead, we think about getting the volume just right. Similarly, the inner workings of the human body are often distinct from the external expression of those workings. It is the job of psychologists to find the connection between these—for example, to figure out how the firings of millions of neurons become a thought.
This chapter strives to explain the biological mechanisms that underlie behavior. These physiological and anatomical foundations are the basis for many areas of psychology. In this chapter, you will learn how genetics influence both physiological and psychological traits. You will become familiar with the structure and function of the nervous system. And, finally, you will learn how the nervous system interacts with the endocrine system.
By the end of this section, you will be able to:
- Explain the basic principles of the theory of evolution by natural selection
- Describe the differences between genotype and phenotype
- Discuss how gene-environment interactions are critical for expression of physical and psychological characteristics
Psychological researchers study genetics in order to better understand the biological factors that contribute to certain behaviors. While all humans share certain biological mechanisms, we are each unique. And while our bodies have many of the same parts—brains and hormones and cells with genetic codes—these are expressed in a wide variety of behaviors, thoughts, and reactions.
Why do two people infected by the same disease have different outcomes: one surviving and one succumbing to the ailment? How are genetic diseases passed through family lines? Are there genetic components to psychological disorders, such as depression or schizophrenia? To what extent might there be a psychological basis to health conditions such as childhood obesity?
To explore these questions, let’s start by focusing on a specific genetic disorder, sickle cell anemia, and how it might manifest in two affected sisters. Sickle-cell anemia is a genetic condition in which red blood cells, which are normally round, take on a crescent-like shape (Figure 3.2). The changed shape of these cells affects how they function: sickle-shaped cells can clog blood vessels and block blood flow, leading to high fever, severe pain, swelling, and tissue damage.
Many people with sickle-cell anemia—and the particular genetic mutation that causes it—die at an early age. While the notion of “survival of the fittest” may suggest that people suffering from this disorder have a low survival rate and therefore the disorder will become less common, this is not the case. Despite the negative evolutionary effects associated with this genetic mutation, the sickle-cell gene remains relatively common among people of African descent. Why is this? The explanation is illustrated with the following scenario.
Imagine two young women—Luwi and Sena—sisters in rural Zambia, Africa. Luwi carries the gene for sickle-cell anemia; Sena does not carry the gene. Sickle-cell carriers have one copy of the sickle-cell gene but do not have full-blown sickle-cell anemia. They experience symptoms only if they are severely dehydrated or are deprived of oxygen (as in mountain climbing). Carriers are thought to be immune from malaria (an often deadly disease that is widespread in tropical climates) because changes in their blood chemistry and immune functioning prevent the malaria parasite from having its effects (Gong, Parikh, Rosenthal, & Greenhouse, 2013). However, full-blown sickle-cell anemia, with two copies of the sickle-cell gene, does not provide immunity to malaria.
While walking home from school, both sisters are bitten by mosquitos carrying the malaria parasite. Luwi is protected against malaria because she carries the sickle-cell mutation. Sena, on the other hand, develops malaria and dies just two weeks later. Luwi survives and eventually has children, to whom she may pass on the sickle-cell mutation.
Malaria is rare in the United States, so the sickle-cell gene benefits nobody: the gene manifests primarily in minor health problems for carriers with one copy, or a severe full-blown disease with no health benefits for carriers with two copies. However, the situation is quite different in other parts of the world. In parts of Africa where malaria is prevalent, having the sickle-cell mutation does provide health benefits for carriers (protection from malaria).
The story of malaria fits with Charles Darwin’s theory of evolution by natural selection (Figure 3.3). In simple terms, the theory states that organisms that are better suited for their environment will survive and reproduce, while those that are poorly suited for their environment will die off. In our example, we can see that, as a carrier, Luwi’s mutation is highly adaptive in her African homeland; however, if she resided in the United States (where malaria is rare), her mutation could prove costly—with a high probability of the disease in her descendants and minor health problems of her own.
Genetic variation, the genetic difference between individuals, is what contributes to a species’ adaptation to its environment. In humans, genetic variation begins with an egg, about 100 million sperm, and fertilization. Fertile women ovulate roughly once per month, releasing an egg from follicles in the ovary. During the egg’s journey from the ovary through the fallopian tubes, to the uterus, a sperm may fertilize the egg.
The egg and the sperm each contain 23 chromosomes. Chromosomes are long strings of genetic material known as deoxyribonucleic acid (DNA). DNA is a helix-shaped molecule made up of nucleotide base pairs. In each chromosome, sequences of DNA make up genes that control or partially control a number of visible characteristics, known as traits, such as eye color, hair color, and so on. A single gene may have multiple possible variations, or alleles. An allele is a specific version of a gene. So, a given gene may code for the trait of hair color, and the different alleles of that gene affect which hair color an individual has.
When a sperm and egg fuse, their 23 chromosomes combine to create a zygote with 46 chromosomes (23 pairs). Therefore, each parent contributes half the genetic information carried by the offspring; the resulting physical characteristics of the offspring (called the phenotype) are determined by the interaction of genetic material supplied by the parents (called the genotype). A person’s genotype is the genetic makeup of that individual. Phenotype, on the other hand, refers to the individual’s inherited physical characteristics, which are a combination of genetic and environmental influences (Figure 3.4).
Most traits are controlled by multiple genes, but some traits are controlled by one gene. A characteristic like cleft chin, for example, is influenced by a single gene from each parent. In this example, we will call the gene for cleft chin “B,” and the gene for smooth chin “b.” Cleft chin is a dominant trait, which means that having the dominant allele either from one parent (Bb) or both parents (BB) will always result in the phenotype associated with the dominant allele. When someone has two copies of the same allele, they are said to be homozygous for that allele. When someone has a combination of alleles for a given gene, they are said to be heterozygous. For example, smooth chin is a recessive trait, which means that an individual will only display the smooth chin phenotype if they are homozygous for that recessive allele (bb).
Imagine that a woman with a cleft chin mates with a man with a smooth chin. What type of chin will their child have? The answer to that depends on which alleles each parent carries. If the woman is homozygous for cleft chin (BB), her offspring will always have cleft chin. It gets a little more complicated, however, if the mother is heterozygous for this gene (Bb). Since the father has a smooth chin—therefore homozygous for the recessive allele (bb)—we can expect the offspring to have a 50% chance of having a cleft chin and a 50% chance of having a smooth chin (Figure 3.5).
In sickle cell anemia, heterozygous carriers (like Luwi from the example) can develop blood resistance to malaria infection while those who are homozygous (like Sena) have a potentially lethal blood disorder. Sickle-cell anemia is just one of many genetic disorders caused by the pairing of two recessive genes. For example, phenylketonuria (PKU) is a condition in which individuals lack an enzyme that normally converts harmful amino acids into harmless byproducts. If someone with this condition goes untreated, he or she will experience significant deficits in cognitive function, seizures, and an increased risk of various psychiatric disorders. Because PKU is a recessive trait, each parent must have at least one copy of the recessive allele in order to produce a child with the condition (Figure 3.6).
So far, we have discussed traits that involve just one gene, but few human characteristics are controlled by a single gene. Most traits are polygenic: controlled by more than one gene. Height is one example of a polygenic trait, as are skin color and weight.
Where do harmful genes that contribute to diseases like PKU come from? Gene mutations provide one source of harmful genes. A mutation is a sudden, permanent change in a gene. While many mutations can be harmful or lethal, once in a while, a mutation benefits an individual by giving that person an advantage over those who do not have the mutation. Recall that the theory of evolution asserts that individuals best adapted to their particular environments are more likely to reproduce and pass on their genes to future generations. In order for this process to occur, there must be competition—more technically, there must be variability in genes (and resultant traits) that allow for variation in adaptability to the environment. If a population consisted of identical individuals, then any dramatic changes in the environment would affect everyone in the same way, and there would be no variation in selection. In contrast, diversity in genes and associated traits allows some individuals to perform slightly better than others when faced with environmental change. This creates a distinct advantage for individuals best suited for their environments in terms of successful reproduction and genetic transmission.
Genes do not exist in a vacuum. Although we are all biological organisms, we also exist in an environment that is incredibly important in determining not only when and how our genes express themselves, but also in what combination. Each of us represents a unique interaction between our genetic makeup and our environment; range of reaction is one way to describe this interaction. Range of reaction asserts that our genes set the boundaries within which we can operate, and our environment interacts with the genes to determine where in that range we will fall. For example, if an individual’s genetic makeup predisposes her to high levels of intellectual potential and she is reared in a rich, stimulating environment, then she will be more likely to achieve her full potential than if she were raised under conditions of significant deprivation. According to the concept of range of reaction, genes set definite limits on potential, and environment determines how much of that potential is achieved. Some disagree with this theory and argue that genes do not set a limit on a person’s potential with reaction norms being determined by the environment. For example, when individuals experience neglect or abuse early in life, they are more likely to exhibit adverse psychological and/or physical conditions that can last throughout their lives. These conditions may develop as a function of the negative environmental experiences in individuals from dissimilar genetic backgrounds (Miguel, Pereira, Silveira, & Meaney, 2019; Short & Baram, 2019).
Another perspective on the interaction between genes and the environment is the concept of genetic environmental correlation. Stated simply, our genes influence our environment, and our environment influences the expression of our genes (Figure 3.7). Not only do our genes and environment interact, as in range of reaction, but they also influence one another bidirectionally. For example, the child of an NBA player would probably be exposed to basketball from an early age. Such exposure might allow the child to realize his or her full genetic, athletic potential. Thus, the parents’ genes, which the child shares, influence the child’s environment, and that environment, in turn, is well suited to support the child’s genetic potential.
In another approach to gene-environment interactions, the field of epigenetics looks beyond the genotype itself and studies how the same genotype can be expressed in different ways. In other words, researchers study how the same genotype can lead to very different phenotypes. As mentioned earlier, gene expression is often influenced by environmental context in ways that are not entirely obvious. For instance, identical twins share the same genetic information (identical twins develop from a single fertilized egg that split, so the genetic material is exactly the same in each; in contrast, fraternal twins usually result from two different eggs fertilized by different sperm, so the genetic material varies as with non-twin siblings). But even with identical genes, there remains an incredible amount of variability in how gene expression can unfold over the course of each twin’s life. Sometimes, one twin will develop a disease and the other will not. In one example, Aliya, an identical twin, died from cancer at age 7, but her twin, now 19 years old, has never had cancer. Although these individuals share an identical genotype, their phenotypes differ as a result of how that genetic information is expressed over time and through their unique environmental interactions. The epigenetic perspective is very different from range of reaction, because here the genotype is not fixed and limited.
Genes affect more than our physical characteristics. Indeed, scientists have found genetic linkages to a number of behavioral characteristics, ranging from basic personality traits to sexual orientation to spirituality (for examples, see Mustanski et al., 2005; Comings, Gonzales, Saucier, Johnson, & MacMurray, 2000). Genes are also associated with temperament and a number of psychological disorders, such as depression and schizophrenia. So while it is true that genes provide the biological blueprints for our cells, tissues, organs, and body, they also have a significant impact on our experiences and our behaviors.
Let’s look at the following findings regarding schizophrenia in light of our three views of gene-environment interactions. Which view do you think best explains this evidence?
In a 2004 study by Tienari and colleagues, of people who were given up for adoption, adoptees whose biological mothers had schizophrenia and who had been raised in a disturbed family environment were much more likely to develop schizophrenia or another psychotic disorder than were any of the other groups in the study:
- Of adoptees whose biological mothers had schizophrenia (high genetic risk) and who were raised in disturbed family environments, 36.8% were likely to develop schizophrenia.
- Of adoptees whose biological mothers had schizophrenia (high genetic risk) and who were raised in healthy family environments, 5.8% were likely to develop schizophrenia.
- Of adoptees with a low genetic risk (whose mothers did not have schizophrenia) and who were raised in disturbed family environments, 5.3% were likely to develop schizophrenia.
- Of adoptees with a low genetic risk (whose mothers did not have schizophrenia) and who were raised in healthy family environments, 4.8% were likely to develop schizophrenia.
The study shows that adoptees with high genetic risk were most likely to develop schizophrenia if they were raised in disturbed home environments. This research lends credibility to the notion that both genetic vulnerability and environmental stress are necessary for schizophrenia to develop, and that genes alone do not tell the full tale.
By the end of this section, you will be able to:
- Identify the basic parts of a neuron
- Describe how neurons communicate with each other
- Explain how drugs act as agonists or antagonists for a given neurotransmitter system
Neurons are the central building blocks of the nervous system, 100 billion strong at birth. Like all cells, neurons consist of several different parts, each serving a specialized function (Figure 3.8). A neuron’s outer surface is made up of a semipermeable membrane. This membrane allows smaller molecules and molecules without an electrical charge to pass through it, while stopping larger or highly charged molecules.
The nucleus of the neuron is located in the soma, or cell body. The soma has branching extensions known as dendrites. The neuron is a small information processor, and dendrites serve as input sites where signals are received from other neurons. These signals are transmitted electrically across the soma and down a major extension from the soma known as the axon, which ends at multiple terminal buttons. The terminal buttons contain synaptic vesicles that house neurotransmitters, the chemical messengers of the nervous system.
Axons range in length from a fraction of an inch to several feet. In some axons, glial cells form a fatty substance known as the myelin sheath, which coats the axon and acts as an insulator, increasing the speed at which the signal travels. The myelin sheath is not continuous and there are small gaps that occur down the length of the axon. These gaps in the myelin sheath are known as the Nodes of Ranvier. The myelin sheath is crucial for the normal operation of the neurons within the nervous system: the loss of the insulation it provides can be detrimental to normal function. To understand how this works, let’s consider an example. PKU, a genetic disorder discussed earlier, causes a reduction in myelin and abnormalities in white matter cortical and subcortical structures. The disorder is associated with a variety of issues including severe cognitive deficits, exaggerated reflexes, and seizures (Anderson & Leuzzi, 2010; Huttenlocher, 2000). Another disorder, multiple sclerosis (MS), an autoimmune disorder, involves a large-scale loss of the myelin sheath on axons throughout the nervous system. The resulting interference in the electrical signal prevents the quick transmittal of information by neurons and can lead to a number of symptoms, such as dizziness, fatigue, loss of motor control, and sexual dysfunction. While some treatments may help to modify the course of the disease and manage certain symptoms, there is currently no known cure for multiple sclerosis.
In healthy individuals, the neuronal signal moves rapidly down the axon to the terminal buttons, where synaptic vesicles release neurotransmitters into the synaptic cleft (Figure 3.9). The synaptic cleft is a very small space between two neurons and is an important site where communication between neurons occurs. Once neurotransmitters are released into the synaptic cleft, they travel across it and bind with corresponding receptors on the dendrite of an adjacent neuron. Receptors, proteins on the cell surface where neurotransmitters attach, vary in shape, with different shapes “matching” different neurotransmitters.
How does a neurotransmitter “know” which receptor to bind to? The neurotransmitter and the receptor have what is referred to as a lock-and-key relationship—specific neurotransmitters fit specific receptors similar to how a key fits a lock. The neurotransmitter binds to any receptor that it fits.
Now that we have learned about the basic structures of the neuron and the role that these structures play in neuronal communication, let’s take a closer look at the signal itself—how it moves through the neuron and then jumps to the next neuron, where the process is repeated.
We begin at the neuronal membrane. The neuron exists in a fluid environment—it is surrounded by extracellular fluid and contains intracellular fluid (i.e., cytoplasm). The neuronal membrane keeps these two fluids separate—a critical role because the electrical signal that passes through the neuron depends on the intra- and extracellular fluids being electrically different. This difference in charge across the membrane, called the membrane potential, provides energy for the signal.
The electrical charge of the fluids is caused by charged molecules (ions) dissolved in the fluid. The semipermeable nature of the neuronal membrane somewhat restricts the movement of these charged molecules, and, as a result, some of the charged particles tend to become more concentrated either inside or outside the cell.
Between signals, the neuron membrane’s potential is held in a state of readiness, called the resting potential. Like a rubber band stretched out and waiting to spring into action, ions line up on either side of the cell membrane, ready to rush across the membrane when the neuron goes active and the membrane opens its gates (i.e., a sodium-potassium pump that allows movement of ions across the membrane). Ions in high-concentration areas are ready to move to low-concentration areas, and positive ions are ready to move to areas with a negative charge.
In the resting state, sodium (Na+) is at higher concentrations outside the cell, so it will tend to move into the cell. Potassium (K+), on the other hand, is more concentrated inside the cell, and will tend to move out of the cell (Figure 3.10). In addition, the inside of the cell is slightly negatively charged compared to the outside. This provides an additional force on sodium, causing it to move into the cell.
From this resting potential state, the neuron receives a signal and its state changes abruptly (Figure 3.11). When a neuron receives signals at the dendrites—due to neurotransmitters from an adjacent neuron binding to its receptors—small pores, or gates, open on the neuronal membrane, allowing Na+ ions, propelled by both charge and concentration differences, to move into the cell. With this influx of positive ions, the internal charge of the cell becomes more positive. If that charge reaches a certain level, called the threshold of excitation, the neuron becomes active and the action potential begins.
Many additional pores open, causing a massive influx of Na+ ions and a huge positive spike in the membrane potential, the peak action potential. At the peak of the spike, the sodium gates close and the potassium gates open. As positively charged potassium ions leave, the cell quickly begins repolarization. At first, it hyperpolarizes, becoming slightly more negative than the resting potential, and then it levels off, returning to the resting potential.
This positive spike constitutes the action potential: the electrical signal that typically moves from the cell body down the axon to the axon terminals. The electrical signal moves down the axon with the impulses jumping in a leapfrog fashion between the Nodes of Ranvier. The Nodes of Ranvier are natural gaps in the myelin sheath. At each point, some of the sodium ions that enter the cell diffuse to the next section of the axon, raising the charge past the threshold of excitation and triggering a new influx of sodium ions. The action potential moves all the way down the axon in this fashion until reaching the terminal buttons.
The action potential is an all-or-none phenomenon. In simple terms, this means that an incoming signal from another neuron is either sufficient or insufficient to reach the threshold of excitation. There is no in-between, and there is no turning off an action potential once it starts. Think of it like sending an email or a text message. You can think about sending it all you want, but the message is not sent until you hit the send button. Furthermore, once you send the message, there is no stopping it.
Because it is all or none, the action potential is recreated, or propagated, at its full strength at every point along the axon. Much like the lit fuse of a firecracker, it does not fade away as it travels down the axon. It is this all-or-none property that explains the fact that your brain perceives an injury to a distant body part like your toe as equally painful as one to your nose.
As noted earlier, when the action potential arrives at the terminal button, the synaptic vesicles release their neurotransmitters into the synaptic cleft. The neurotransmitters travel across the synapse and bind to receptors on the dendrites of the adjacent neuron, and the process repeats itself in the new neuron (assuming the signal is sufficiently strong to trigger an action potential). Once the signal is delivered, excess neurotransmitters in the synaptic cleft drift away, are broken down into inactive fragments, or are reabsorbed in a process known as reuptake. Reuptake involves the neurotransmitter being pumped back into the neuron that released it, in order to clear the synapse (Figure 3.12). Clearing the synapse serves both to provide a clear “on” and “off” state between signals and to regulate the production of neurotransmitter (full synaptic vesicles provide signals that no additional neurotransmitters need to be produced).
Neuronal communication is often referred to as an electrochemical event. The movement of the action potential down the length of the axon is an electrical event, and movement of the neurotransmitter across the synaptic space represents the chemical portion of the process. However, there are some specialized connections between neurons that are entirely electrical. In such cases, the neurons are said to communicate via an electrical synapse. In these cases, two neurons physically connect to one another via gap junctions, which allows the current from one cell to pass into the next. There are far fewer electrical synapses in the brain, but those that do exist are much faster than the chemical synapses that have been described above (Connors & Long, 2004).
There are several different types of neurotransmitters released by different neurons, and we can speak in broad terms about the kinds of functions associated with different neurotransmitters (Table 3.1). Much of what psychologists know about the functions of neurotransmitters comes from research on the effects of drugs in psychological disorders. Psychologists who take a biological perspective and focus on the physiological causes of behavior assert that psychological disorders like depression and schizophrenia are associated with imbalances in one or more neurotransmitter systems. In this perspective, psychotropic medications can help improve the symptoms associated with these disorders. Psychotropic medications are drugs that treat psychiatric symptoms by restoring neurotransmitter balance.
|Major Neurotransmitters and How They Affect Behavior|
|Neurotransmitter||Involved in||Potential Effect on Behavior|
|Acetylcholine||Muscle action, memory||Increased arousal, enhanced cognition|
|Beta-endorphin||Pain, pleasure||Decreased anxiety, decreased tension|
|Dopamine||Mood, sleep, learning||Increased pleasure, suppressed appetite|
|Gamma-aminobutyric acid (GABA)||Brain function, sleep||Decreased anxiety, decreased tension|
|Glutamate||Memory, learning||Increased learning, enhanced memory|
|Norepinephrine||Heart, intestines, alertness||Increased arousal, suppressed appetite|
|Serotonin||Mood, sleep||Modulated mood, suppressed appetite|
Psychoactive drugs can act as agonists or antagonists for a given neurotransmitter system. Agonists are chemicals that mimic a neurotransmitter at the receptor site. An antagonist, on the other hand, blocks or impedes the normal activity of a neurotransmitter at the receptor. Agonists and antagonists represent drugs that are prescribed to correct the specific neurotransmitter imbalances underlying a person’s condition. For example, Parkinson’s disease, a progressive nervous system disorder, is associated with low levels of dopamine. Therefore, a common treatment strategy for Parkinson’s disease involves using dopamine agonists, which mimic the effects of dopamine by binding to dopamine receptors.
Certain symptoms of schizophrenia are associated with overactive dopamine neurotransmission. The antipsychotics used to treat these symptoms are antagonists for dopamine—they block dopamine’s effects by binding its receptors without activating them. Thus, they prevent dopamine released by one neuron from signaling information to adjacent neurons.
In contrast to agonists and antagonists, which both operate by binding to receptor sites, reuptake inhibitors prevent unused neurotransmitters from being transported back to the neuron. This allows neurotransmitters to remain active in the synaptic cleft for longer durations, increasing their effectiveness. Depression, which has been consistently linked with reduced serotonin levels, is commonly treated with selective serotonin reuptake inhibitors (SSRIs). By preventing reuptake, SSRIs strengthen the effect of serotonin, giving it more time to interact with serotonin receptors on dendrites. Common SSRIs on the market today include Prozac, Paxil, and Zoloft. The drug LSD is structurally very similar to serotonin, and it affects the same neurons and receptors as serotonin. Psychotropic drugs are not instant solutions for people suffering from psychological disorders. Often, an individual must take a drug for several weeks before seeing improvement, and many psychoactive drugs have significant negative side effects. Furthermore, individuals vary dramatically in how they respond to the drugs. To improve chances for success, it is not uncommon for people receiving pharmacotherapy to undergo psychological and/or behavioral therapies as well. Some research suggests that combining drug therapy with other forms of therapy tends to be more effective than any one treatment alone (for one such example, see March et al., 2007).
By the end of this section, you will be able to:
- Describe the difference between the central and peripheral nervous systems
- Explain the difference between the somatic and autonomic nervous systems
- Differentiate between the sympathetic and parasympathetic divisions of the autonomic nervous system
The nervous system can be divided into two major subdivisions: the central nervous system (CNS) and the peripheral nervous system (PNS), shown in Figure 3.13. The CNS is comprised of the brain and spinal cord; the PNS connects the CNS to the rest of the body. In this section, we focus on the peripheral nervous system; later, we look at the brain and spinal cord.
Peripheral Nervous System
The peripheral nervous system is made up of thick bundles of axons, called nerves, carrying messages back and forth between the CNS and the muscles, organs, and senses in the periphery of the body (i.e., everything outside the CNS). The PNS has two major subdivisions: the somatic nervous system and the autonomic nervous system.
The somatic nervous system is associated with activities traditionally thought of as conscious or voluntary. It is involved in the relay of sensory and motor information to and from the CNS; therefore, it consists of motor neurons and sensory neurons. Motor neurons, carrying instructions from the CNS to the muscles, are efferent fibers (efferent means “moving away from”). Sensory neurons, carrying sensory information to the CNS, are afferent fibers (afferent means “moving toward”). A helpful way to remember this is that efferent = exit and afferent = arrive. Each nerve is basically a bundle of neurons forming a two-way superhighway, containing thousands of axons, both efferent and afferent.
The autonomic nervous system controls our internal organs and glands and is generally considered to be outside the realm of voluntary control. It can be further subdivided into the sympathetic and parasympathetic divisions (Figure 3.14). The sympathetic nervous system is involved in preparing the body for stress-related activities; the parasympathetic nervous system is associated with returning the body to routine, day-to-day operations. The two systems have complementary functions, operating in tandem to maintain the body’s homeostasis. Homeostasis is a state of equilibrium, or balance, in which biological conditions (such as body temperature) are maintained at optimal levels.
The sympathetic nervous system is activated when we are faced with stressful or high-arousal situations. The activity of this system was adaptive for our ancestors, increasing their chances of survival. Imagine, for example, that one of our early ancestors, out hunting small game, suddenly disturbs a large bear with her cubs. At that moment, his body undergoes a series of changes—a direct function of sympathetic activation—preparing him to face the threat. His pupils dilate, his heart rate and blood pressure increase, his bladder relaxes, his liver releases glucose, and adrenaline surges into his bloodstream. This constellation of physiological changes, known as the fight or flight response, allows the body access to energy reserves and heightened sensory capacity so that it might fight off a threat or run away to safety.
While it is clear that such a response would be critical for survival for our ancestors, who lived in a world full of real physical threats, many of the high-arousal situations we face in the modern world are more psychological in nature. For example, think about how you feel when you have to stand up and give a presentation in front of a roomful of people, or right before taking a big test. You are in no real physical danger in those situations, and yet you have evolved to respond to a perceived threat with the fight or flight response. This kind of response is not nearly as adaptive in the modern world; in fact, we suffer negative health consequences when faced constantly with psychological threats that we can neither fight nor flee. Recent research suggests that an increase in susceptibility to heart disease (Chandola, Brunner, & Marmot, 2006) and impaired function of the immune system (Glaser & Kiecolt-Glaser, 2005) are among the many negative consequences of persistent and repeated exposure to stressful situations. Some of this tendency for stress reactivity can be wired by early experiences of trauma.
Once the threat has been resolved, the parasympathetic nervous system takes over and returns bodily functions to a relaxed state. Our hunter’s heart rate and blood pressure return to normal, his pupils constrict, he regains control of his bladder, and the liver begins to store glucose in the form of glycogen for future use. These restorative processes are associated with activation of the parasympathetic nervous system.
By the end of this section, you will be able to:
- Explain the functions of the spinal cord
- Identify the hemispheres and lobes of the brain
- Describe the types of techniques available to clinicians and researchers to image or scan the brain
The brain is a remarkably complex organ comprised of billions of interconnected neurons and glia. It is a bilateral, or two-sided, structure that can be separated into distinct lobes. Each lobe is associated with certain types of functions, but, ultimately, all of the areas of the brain interact with one another to provide the foundation for our thoughts and behaviors. In this section, we discuss the overall organization of the brain and the functions associated with different brain areas, beginning with what can be seen as an extension of the brain, the spinal cord.
The Spinal Cord
It can be said that the spinal cord is what connects the brain to the outside world. Because of it, the brain can act. The spinal cord is like a relay station, but a very smart one. It not only routes messages to and from the brain, but it also has its own system of automatic processes, called reflexes.
The top of the spinal cord is a bundle of nerves that merges with the brain stem, where the basic processes of life are controlled, such as breathing and digestion. In the opposite direction, the spinal cord ends just below the ribs—contrary to what we might expect, it does not extend all the way to the base of the spine.
The spinal cord is functionally organized in 30 segments, corresponding with the vertebrae. Each segment is connected to a specific part of the body through the peripheral nervous system. Nerves branch out from the spine at each vertebra. Sensory nerves bring messages in; motor nerves send messages out to the muscles and organs. Messages travel to and from the brain through every segment.
Some sensory messages are immediately acted on by the spinal cord, without any input from the brain. Withdrawal from a hot object and the knee jerk are two examples. When a sensory message meets certain parameters, the spinal cord initiates an automatic reflex. The signal passes from the sensory nerve to a simple processing center, which initiates a motor command. Seconds are saved, because messages don’t have to go the brain, be processed, and get sent back. In matters of survival, the spinal reflexes allow the body to react extraordinarily fast.
The spinal cord is protected by bony vertebrae and cushioned in cerebrospinal fluid, but injuries still occur. When the spinal cord is damaged in a particular segment, all lower segments are cut off from the brain, causing paralysis. Therefore, the lower on the spine damage occurs, the fewer functions an injured individual will lose.
Bob Woodruff, a reporter for ABC, suffered a traumatic brain injury after a bomb exploded next to the vehicle he was in while covering a news story in Iraq. As a consequence of these injuries, Woodruff experienced many cognitive deficits including difficulties with memory and language. However, over time and with the aid of intensive amounts of cognitive and speech therapy, Woodruff has shown an incredible recovery of function (Fernandez, 2008, October 16).
One of the factors that made this recovery possible was neuroplasticity. Neuroplasticity refers to how the nervous system can change and adapt. Neuroplasticity can occur in a variety of ways including personal experiences, developmental processes, or, as in Woodruff’s case, in response to some sort of damage or injury that has occurred. Neuroplasticity can involve creation of new synapses, pruning of synapses that are no longer used, changes in glial cells, and even the birth of new neurons. Because of neuroplasticity, our brains are constantly changing and adapting, and while our nervous system is most plastic when we are very young, as Woodruff’s case suggests, it is still capable of remarkable changes later in life.
The Two Hemispheres
The surface of the brain, known as the cerebral cortex, is very uneven, characterized by a distinctive pattern of folds or bumps, known as gyri (singular: gyrus), and grooves, known as sulci (singular: sulcus), shown in Figure 3.15. These gyri and sulci form important landmarks that allow us to separate the brain into functional centers. The most prominent sulcus, known as the longitudinal fissure, is the deep groove that separates the brain into two halves or hemispheres: the left hemisphere and the right hemisphere.
There is evidence of specialization of function—referred to as lateralization—in each hemisphere, mainly regarding differences in language functions. The left hemisphere controls the right half of the body, and the right hemisphere controls the left half of the body. Decades of research on lateralization of function by Michael Gazzaniga and his colleagues suggest that a variety of functions ranging from cause-and-effect reasoning to self-recognition may follow patterns that suggest some degree of hemispheric dominance (Gazzaniga, 2005). For example, the left hemisphere has been shown to be superior for forming associations in memory, selective attention, and positive emotions. The right hemisphere, on the other hand, has been shown to be superior in pitch perception, arousal, and negative emotions (Ehret, 2006). However, it should be pointed out that research on which hemisphere is dominant in a variety of different behaviors has produced inconsistent results, and therefore, it is probably better to think of how the two hemispheres interact to produce a given behavior rather than attributing certain behaviors to one hemisphere versus the other (Banich & Heller, 1998).
The two hemispheres are connected by a thick band of neural fibers known as the corpus callosum, consisting of about 200 million axons. The corpus callosum allows the two hemispheres to communicate with each other and allows for information being processed on one side of the brain to be shared with the other side.
Normally, we are not aware of the different roles that our two hemispheres play in day-to-day functions, but there are people who come to know the capabilities and functions of their two hemispheres quite well. In some cases of severe epilepsy, doctors elect to sever the corpus callosum as a means of controlling the spread of seizures (Figure 3.16). While this is an effective treatment option, it results in individuals who have “split brains.” After surgery, these split-brain patients show a variety of interesting behaviors. For instance, a split-brain patient is unable to name a picture that is shown in the patient’s left visual field because the information is only available in the largely nonverbal right hemisphere. However, they are able to recreate the picture with their left hand, which is also controlled by the right hemisphere. When the more verbal left hemisphere sees the picture that the hand drew, the patient is able to name it (assuming the left hemisphere can interpret what was drawn by the left hand).
Much of what we know about the functions of different areas of the brain comes from studying changes in the behavior and ability of individuals who have suffered damage to the brain. For example, researchers study the behavioral changes caused by strokes to learn about the functions of specific brain areas. A stroke, caused by an interruption of blood flow to a region in the brain, causes a loss of brain function in the affected region. The damage can be in a small area, and, if it is, this gives researchers the opportunity to link any resulting behavioral changes to a specific area. The types of deficits displayed after a stroke will be largely dependent on where in the brain the damage occurred.
Consider Theona, an intelligent, self-sufficient woman, who is 62 years old. Recently, she suffered a stroke in the front portion of her right hemisphere. As a result, she has great difficulty moving her left leg. (As you learned earlier, the right hemisphere controls the left side of the body; also, the brain’s main motor centers are located at the front of the head, in the frontal lobe.) Theona has also experienced behavioral changes. For example, while in the produce section of the grocery store, she sometimes eats grapes, strawberries, and apples directly from their bins before paying for them. This behavior—which would have been very embarrassing to her before the stroke—is consistent with damage in another region in the frontal lobe—the prefrontal cortex, which is associated with judgment, reasoning, and impulse control.
The two hemispheres of the cerebral cortex are part of the forebrain (Figure 3.17), which is the largest part of the brain. The forebrain contains the cerebral cortex and a number of other structures that lie beneath the cortex (called subcortical structures): thalamus, hypothalamus, pituitary gland, and the limbic system (a collection of structures). The cerebral cortex, which is the outer surface of the brain, is associated with higher level processes such as consciousness, thought, emotion, reasoning, language, and memory. Each cerebral hemisphere can be subdivided into four lobes, each associated with different functions.
Lobes of the Brain
The four lobes of the brain are the frontal, parietal, temporal, and occipital lobes (Figure 3.18). The frontal lobe is located in the forward part of the brain, extending back to a fissure known as the central sulcus. The frontal lobe is involved in reasoning, motor control, emotion, and language. It contains the motor cortex, which is involved in planning and coordinating movement; the prefrontal cortex, which is responsible for higher-level cognitive functioning; and Broca’s area, which is essential for language production.
People who suffer damage to Broca’s area have great difficulty producing language of any form (Figure 3.18). For example, Padma was an electrical engineer who was socially active and a caring, involved parent. About twenty years ago, she was in a car accident and suffered damage to her Broca’s area. She completely lost the ability to speak and form any kind of meaningful language. There is nothing wrong with her mouth or her vocal cords, but she is unable to produce words. She can follow directions but can’t respond verbally, and she can read but no longer write. She can do routine tasks like running to the market to buy milk, but she could not communicate verbally if a situation called for it.
Probably the most famous case of frontal lobe damage is that of a man by the name of Phineas Gage. On September 13, 1848, Gage (age 25) was working as a railroad foreman in Vermont. He and his crew were using an iron rod to tamp explosives down into a blasting hole to remove rock along the railway’s path. Unfortunately, the iron rod created a spark and caused the rod to explode out of the blasting hole, into Gage’s face, and through his skull (Figure 3.19). Although lying in a pool of his own blood with brain matter emerging from his head, Gage was conscious and able to get up, walk, and speak. But in the months following his accident, people noticed that his personality had changed. Many of his friends described him as no longer being himself. Before the accident, it was said that Gage was a well-mannered, soft-spoken man, but he began to behave in odd and inappropriate ways after the accident. Such changes in personality would be consistent with loss of impulse control—a frontal lobe function.
Beyond the damage to the frontal lobe itself, subsequent investigations into the rod’s path also identified probable damage to pathways between the frontal lobe and other brain structures, including the limbic system. With connections between the planning functions of the frontal lobe and the emotional processes of the limbic system severed, Gage had difficulty controlling his emotional impulses.
However, there is some evidence suggesting that the dramatic changes in Gage’s personality were exaggerated and embellished. Gage’s case occurred in the midst of a 19th century debate over localization—regarding whether certain areas of the brain are associated with particular functions. On the basis of extremely limited information about Gage, the extent of his injury, and his life before and after the accident, scientists tended to find support for their own views, on whichever side of the debate they fell (Macmillan, 1999).
The brain’s parietal lobe is located immediately behind the frontal lobe, and is involved in processing information from the body’s senses. It contains the somatosensory cortex, which is essential for processing sensory information from across the body, such as touch, temperature, and pain. The somatosensory cortex is organized topographically, which means that spatial relationships that exist in the body are generally maintained on the surface of the somatosensory cortex (Figure 3.20). For example, the portion of the cortex that processes sensory information from the hand is adjacent to the portion that processes information from the wrist.
The temporal lobe is located on the side of the head (temporal means “near the temples”), and is associated with hearing, memory, emotion, and some aspects of language. The auditory cortex, the main area responsible for processing auditory information, is located within the temporal lobe. Wernicke’s area, important for speech comprehension, is also located here. Whereas individuals with damage to Broca’s area have difficulty producing language, those with damage to Wernicke’s area can produce sensible language, but they are unable to understand it (Figure 3.21).
The occipital lobe is located at the very back of the brain, and contains the primary visual cortex, which is responsible for interpreting incoming visual information. The occipital cortex is organized retinotopically, which means there is a close relationship between the position of an object in a person’s visual field and the position of that object’s representation on the cortex. You will learn much more about how visual information is processed in the occipital lobe when you study sensation and perception.
Other Areas of the Forebrain
Other areas of the forebrain, located beneath the cerebral cortex, include the thalamus and the limbic system. The thalamus is a sensory relay for the brain. All of our senses, with the exception of smell, are routed through the thalamus before being directed to other areas of the brain for processing (Figure 3.22).
The limbic system is involved in processing both emotion and memory. Interestingly, the sense of smell projects directly to the limbic system; therefore, not surprisingly, smell can evoke emotional responses in ways that other sensory modalities cannot. The limbic system is made up of a number of different structures, but three of the most important are the hippocampus, the amygdala, and the hypothalamus (Figure 3.23). The hippocampus is an essential structure for learning and memory. The amygdala is involved in our experience of emotion and in tying emotional meaning to our memories. The hypothalamus regulates a number of homeostatic processes, including the regulation of body temperature, appetite, and blood pressure. The hypothalamus also serves as an interface between the nervous system and the endocrine system and in the regulation of sexual motivation and behavior.
The Case of Henry Molaison (H.M.)
In 1953, Henry Gustav Molaison (H. M.) was a 27-year-old man who experienced severe seizures. In an attempt to control his seizures, H. M. underwent brain surgery to remove his hippocampus and amygdala. Following the surgery, H.M’s seizures became much less severe, but he also suffered some unexpected—and devastating—consequences of the surgery: he lost his ability to form many types of new memories. For example, he was unable to learn new facts, such as who was president of the United States. He was able to learn new skills, but afterward he had no recollection of learning them. For example, while he might learn to use a computer, he would have no conscious memory of ever having used one. He could not remember new faces, and he was unable to remember events, even immediately after they occurred. Researchers were fascinated by his experience, and he is considered one of the most studied cases in medical and psychological history (Hardt, Einarsson, & Nader, 2010; Squire, 2009). Indeed, his case has provided tremendous insight into the role that the hippocampus plays in the consolidation of new learning into explicit memory.
Midbrain and Hindbrain Structures
The midbrain is comprised of structures located deep within the brain, between the forebrain and the hindbrain. The reticular formation is centered in the midbrain, but it actually extends up into the forebrain and down into the hindbrain. The reticular formation is important in regulating the sleep/wake cycle, arousal, alertness, and motor activity.
The substantia nigra (Latin for “black substance”) and the ventral tegmental area (VTA) are also located in the midbrain (Figure 3.24). Both regions contain cell bodies that produce the neurotransmitter dopamine, and both are critical for movement. Degeneration of the substantia nigra and VTA is involved in Parkinson’s disease. In addition, these structures are involved in mood, reward, and addiction (Berridge & Robinson, 1998; Gardner, 2011; George, Le Moal, & Koob, 2012).
The hindbrain is located at the back of the head and looks like an extension of the spinal cord. It contains the medulla, pons, and cerebellum (Figure 3.25). The medulla controls the automatic processes of the autonomic nervous system, such as breathing, blood pressure, and heart rate. The word pons literally means “bridge,” and as the name suggests, the pons serves to connect the hindbrain to the rest of the brain. It also is involved in regulating brain activity during sleep. The medulla, pons, and various structures are known as the brainstem, and aspects of the brainstem span both the midbrain and the hindbrain.
The cerebellum (Latin for “little brain”) receives messages from muscles, tendons, joints, and structures in our ear to control balance, coordination, movement, and motor skills. The cerebellum is also thought to be an important area for processing some types of memories. In particular, procedural memory, or memory involved in learning and remembering how to perform tasks, is thought to be associated with the cerebellum. Recall that H. M. was unable to form new explicit memories, but he could learn new tasks. This is likely due to the fact that H. M.’s cerebellum remained intact.
You have learned how brain injury can provide information about the functions of different parts of the brain. Increasingly, however, we are able to obtain that information using brain imaging techniques on individuals who have not suffered brain injury. In this section, we take a more in-depth look at some of the techniques that are available for imaging the brain, including techniques that rely on radiation, magnetic fields, or electrical activity within the brain.
Techniques Involving Radiation
A computerized tomography (CT) scan involves taking a number of x-rays of a particular section of a person’s body or brain (Figure 3.26). The x-rays pass through tissues of different densities at different rates, allowing a computer to construct an overall image of the area of the body being scanned. A CT scan is often used to determine whether someone has a tumor or significant brain atrophy.
Positron emission tomography (PET) scans create pictures of the living, active brain (Figure 3.27). An individual receiving a PET scan drinks or is injected with a mildly radioactive substance, called a tracer. Once in the bloodstream, the amount of tracer in any given region of the brain can be monitored. As a brain area becomes more active, more blood flows to that area. A computer monitors the movement of the tracer and creates a rough map of active and inactive areas of the brain during a given behavior. PET scans show little detail, are unable to pinpoint events precisely in time, and require that the brain be exposed to radiation; therefore, this technique has been replaced by the fMRI as an alternative diagnostic tool. However, combined with CT, PET technology is still being used in certain contexts. For example, CT/PET scans allow better imaging of the activity of neurotransmitter receptors and open new avenues in schizophrenia research. In this hybrid CT/PET technology, CT contributes clear images of brain structures, while PET shows the brain’s activity.
Techniques Involving Magnetic Fields
In magnetic resonance imaging (MRI), a person is placed inside a machine that generates a strong magnetic field. The magnetic field causes the hydrogen atoms in the body’s cells to move. When the magnetic field is turned off, the hydrogen atoms emit electromagnetic signals as they return to their original positions. Tissues of different densities give off different signals, which a computer interprets and displays on a monitor. Functional magnetic resonance imaging (fMRI) operates on the same principles, but it shows changes in brain activity over time by tracking blood flow and oxygen levels. The fMRI provides more detailed images of the brain’s structure, as well as better accuracy in time, than is possible in PET scans (Figure 3.28). With their high level of detail, MRI and fMRI are often used to compare the brains of healthy individuals to the brains of individuals diagnosed with psychological disorders. This comparison helps determine what structural and functional differences exist between these populations.
In some situations, it is helpful to gain an understanding of the overall activity of a person’s brain, without needing information on the actual location of the activity. Electroencephalography (EEG) serves this purpose by providing a measure of a brain’s electrical activity. An array of electrodes is placed around a person’s head (Figure 3.29). The signals received by the electrodes result in a printout of the electrical activity of his or her brain, or brainwaves, showing both the frequency (number of waves per second) and amplitude (height) of the recorded brainwaves, with an accuracy within milliseconds. Such information is especially helpful to researchers studying sleep patterns among individuals with sleep disorders.
By the end of this section, you will be able to:
- Identify the major glands of the endocrine system
- Identify the hormones secreted by each gland
- Describe each hormone’s role in regulating bodily functions
The endocrine system consists of a series of glands that produce chemical substances known as hormones (Figure 3.30). Like neurotransmitters, hormones are chemical messengers that must bind to a receptor in order to send their signal. However, unlike neurotransmitters, which are released in close proximity to cells with their receptors, hormones are secreted into the bloodstream and travel throughout the body, affecting any cells that contain receptors for them. Thus, whereas neurotransmitters’ effects are localized, the effects of hormones are widespread. Also, hormones are slower to take effect, and tend to be longer lasting.
Hormones are involved in regulating all sorts of bodily functions, and they are ultimately controlled through interactions between the hypothalamus (in the central nervous system) and the pituitary gland (in the endocrine system). Imbalances in hormones are related to a number of disorders. This section explores some of the major glands that make up the endocrine system and the hormones secreted by these glands (Table 3.2).
The pituitary gland descends from the hypothalamus at the base of the brain, and acts in close association with it. The pituitary is often referred to as the “master gland” because its messenger hormones control all the other glands in the endocrine system, although it mostly carries out instructions from the hypothalamus. In addition to messenger hormones, the pituitary also secretes growth hormone, endorphins for pain relief, and a number of key hormones that regulate fluid levels in the body.
Located in the neck, the thyroid gland releases hormones that regulate growth, metabolism, and appetite. In hyperthyroidism, or Grave’s disease, the thyroid secretes too much of the hormone thyroxine, causing agitation, bulging eyes, and weight loss. In hypothyroidism, reduced hormone levels cause sufferers to experience tiredness, and they often complain of feeling cold. Fortunately, thyroid disorders are often treatable with medications that help reestablish a balance in the hormones secreted by the thyroid.
The adrenal glands sit atop our kidneys and secrete hormones involved in the stress response, such as epinephrine (adrenaline) and norepinephrine (noradrenaline). The pancreas is an internal organ that secretes hormones that regulate blood sugar levels: insulin and glucagon. These pancreatic hormones are essential for maintaining stable levels of blood sugar throughout the day by lowering blood glucose levels (insulin) or raising them (glucagon). People who suffer from diabetes do not produce enough insulin; therefore, they must take medications that stimulate or replace insulin production, and they must closely control the amount of sugars and carbohydrates they consume.
The gonads secrete sexual hormones, which are important in reproduction, and mediate both sexual motivation and behavior. The female gonads are the ovaries; the male gonads are the testes. Ovaries secrete estrogens and progesterone, and the testes secrete androgens, such as testosterone.
|Major Endocrine Glands and Associated Hormone Functions|
|Endocrine Gland||Associated Hormones||Function|
|Hypothalamus||Releasing and inhibiting hormones, such as oxytocin||Regulate hormone release from pituitary gland|
|Pituitary||Growth hormone, releasing and inhibiting hormones (such as thyroid stimulating hormone)||Regulate growth, regulate hormone release|
|Thyroid||Thyroxine, triiodothyronine||Regulate metabolism and appetite|
|Pineal||Melatonin||Regulate some biological rhythms such as sleep cycles|
|Adrenal||Epinephrine, norepinephrine||Stress response, increase metabolic activities|
|Pancreas||Insulin, glucagon||Regulate blood sugar levels|
|Ovaries||Estrogen, progesterone||Mediate sexual motivation and behavior, reproduction|
|Testes||Androgens, such as testosterone||Mediate sexual motivation and behavior, reproduction|