Psychology_ frontiers and applications-85-122.pdf

CHAPTER Biological Foundations of Behaviour THE NEURAL BASES OF BEHAVIOUR Neurons The Electrical Activity of Neurons How Neurons Communicate: Synaptic Transmission Applications: Understanding How Drugs Affect Your Brain The Hierarchical Brain: Structures and Behavioural Functions Research Founda...

CHAPTER Biological Foundations of Behaviour THE NEURAL BASES OF BEHAVIOUR Neurons The Electrical Activity of Neurons How Neurons Communicate: Synaptic Transmission Applications: Understanding How Drugs Affect Your Brain The Hierarchical Brain: Structures and Behavioural Functions Research Foundations: Wilder Penfield and a Cortical Map 3 CHAPTER OUTLINE Frontiers: Human Aggression, Criminal Behaviour, and the Frontal Cortex Focus on Neuroscience: The Neuroscience of Music THE NERVOUS SYSTEM The Peripheral Nervous System The Central Nervous System The brain is the last and grandest biological frontier, the most complex thing we have yet discovered in our universe. It contains hundreds of billions of cells interlinked through trillions of connections. The brain boggles the mind. —James Watson Most people will readily recognize Brad Pitt. The hair, mustache, and goatee are classic features. But if you ever meet Brad Pitt, he will probably not be able to recognize you again. Not because he sees so many people or because he does not pay attention. Brad Pitt cannot remember faces. It is as if the person’s facial features were not committed to memory for him. He does realize that the face belongs to a person and could even tell you if the person is happy or sad. Once he knows who it is, he can remember everything about that individual. He just cannot tell you who the face belongs to. Many people have a similar problem, including primatologist Jane Goodall and neurologist Oliver Sacks. In severe cases of this disorder, individuals cannot even recognize themselves in a mirror. What are the issues here? What do we need to know? Where can we find the information to answer the questions? 66 CHAPTER THREE THE NEURAL BASES OF BEHAVIOUR The brain is a grapefruit-size mass of tissue that feels like jelly and looks like a greyish, gnarled walnut. One of the true marvels of nature, it has been termed “our three-pound universe” (Hooper & Teresi, 1986). To understand how the brain controls our experience and behaviour, we must first understand how its individual cells function and how they communicate with one another. Neurons 1. Name the three main parts of the neuron and describe their functions. 2. Which structural characteristics permit the many possible interconnections among neurons? 3. How do glial cells differ from neurons? What three functions do they have in the nervous system? Specialized cells called neurons are the basic building blocks of the nervous system. These nerve cells are linked together in circuits, not unlike the electrical circuits in a computer. At birth, your brain contained about 100 billion neurons (Bloom, 2000; Kolb & Whishaw, 1989). To put this number in perspective, if each neuron were a centimetre long and they were placed end to end, the resulting chain would circle Earth more than 24 times. Each neuron has three main parts: a cell body, dendrites, and an axon (Figure 3.1). The cell body, or soma, contains the biochemical structures needed to keep the neuron alive, and its nucleus carries the genetic information that determines how the cell develops and functions. Emerging from the cell body are branchlike fibres called dendrites (from the Greek word for tree). These specialized receiving units are like antennas that collect messages from neighbouring neurons and send them on to the cell body. There the incoming information is combined and processed. The many branches of the dendrites can receive input from 1000 or more neighbouring neurons. The surface of the cell body also has receptor areas that can be directly stimulated by other neurons. Extending from one side of the cell body is a single axon, which conducts electrical impulses away from the cell body to other neurons, muscles, or glands. The axon branches out at its end to form a number of axon terminals—as many as several hundred in some cases. Each axon may connect with dendritic branches from numerous neurons, making it possible for a single neuron to pass messages to as many as 50 000 other neurons (Kolb & Whishaw, 2003; Simon, 2007). Given the structure of the dendrites and axons, it is easy to see how there can be trillions of interconnections in the brain, making it capable of performing the complex psychological activities that are of interest to psychologists. Neurons can vary greatly in size and shape. More than 200 different types of neurons have been viewed through electron microscopes (Nolte, 1998). A neuron with its cell body in your spinal cord may have an axon that extends almost a metre to one of your fingertips, equivalent in scale to a basketball attached to a cord 6.5 kilometres long; a neuron in your brain may be less than a millimetre long. Regardless of their shape or size, neurons have been exquisitely sculpted by nature to perform their function of receiving, processing, and sending messages. Neurons are supported in their functions by glial cells (from the Greek word for glue). Glial cells surround neurons and hold them in place. Glial cells also manufacture nutrient chemicals that neurons need, form the myelin sheath around some axons, and absorb toxins and waste materials that might Dendrites Cell membrane Nucleus Myelin sheath Node of Ranvier Soma (cell body) Axon terminals Axon FIGURE 3.1 Structural elements of a typical neuron. Stimulation received by the dendrites or soma (cell body) may trigger a nerve impulse, which travels down the axon to stimulate other neurons, muscles, or glands. Some axons have a fatty myelin sheath interrupted at intervals by the nodes of Ranvier. The myelin sheath helps to increase the speed of nerve conduction. Biological Foundations of Behaviour damage neurons. During prenatal brain development, as new neurons are being formed through cell division, glial cells send out long fibres that guide newly divided neurons to their targeted place in the brain (Fernichel, 2006). Within the nervous system, glial cells outnumber neurons about ten to one. Another function of glial cells is to protect the brain from toxins. Many foreign substances can pass from the circulation into the different organs of the body but cannot pass from the blood into the brain. A specialized barrier, the blood-brain barrier, prevents many substances, including a wide range of toxins, from entering the brain. The walls of the blood vessels within the brain contain smaller gaps than elsewhere in the body, and they are also covered by a specialized type of glial cell (Cserr & Bundgaard, 1986). Together, the smaller gaps and glial cells keep many foreign substances from gaining access to the brain. Recent research has found evidence for much more complex glial function, such as a role in modulating the communication among neurons (Todd, Serrano, Lacaille, & Robitaille, 2006; Zhang & Haydon, 2005). The Electrical Activity of Neurons Neurons do two important things. They generate electricity that creates nerve impulses. They also release chemicals that allow them to communicate with other neurons and with muscles and glands. Let’s first consider how nerve impulses occur. Nerve activation involves three basic steps: 1. At rest, the neuron has an electrical resting potential due to the distribution of positively and negatively charged chemicals (ions) inside and outside the neuron. 2. When stimulated, a flow of ions in and out through the cell membrane reverses the electrical charge of the resting potential, producing an action potential, or nerve impulse. 3. The original distribution of ions is restored, and the neuron is again at rest. Let’s now flesh out the details of this remarkable process. Like other cells, neurons are surrounded by body fluids and separated from this liquid environment by a protective membrane. This cell membrane is a bit like a selective sieve, allowing certain substances to pass through ion channels into the cell while refusing or limiting passage to other substances. An ion channel is quite literally just that, a passageway or channel in the membrane that can open to allow ions to pass through. The chemical environment inside the neuron differs from its external environment in significant ways, and the process whereby a nerve impulse is created involves the exchange of electrically charged atoms called ions. In the salty fluid outside the neuron are positively charged sodium ions (Na1) and negatively charged chloride ions (Cl2). Inside the neuron are large negatively charged protein molecules (anions or A2) and positively charged potassium ions (K1). The high concentration of sodium ions in the fluid outside the cell, together with the negatively charged protein ions inside, results in an uneven distribution of positive and negative ions that makes the interior of the cell negative compared to the outside (Figure 3.2). This internal difference of around 70 millivolts (thousandths of a volt) is called the neuron’s resting potential. At rest, the neuron is said to be in a state of polarization. 4. What causes the negative resting potential of neurons? When is a neuron said to be in a state of polarization? The Action Potential In research that won them the 1963 Nobel Prize, neuroscientists Alan Hodgkin and Andrew Huxley found that if they stimulated the neuron’s axon with a mild electrical stimulus, the interior voltage differential shifted suddenly from 270 millivolts to 140 millivolts. Hodgkin and Huxley had forced the axon to generate a nerve impulse, or action potential. An action potential is a sudden reversal in the neuron’s membrane voltage, during which the membrane voltage momentarily moves from 270 millivolts (inside) to 140 millivolts (Figure 3.2). This shift from negative to positive voltage is called depolarization. What happens in the neuron to cause the action potential? Hodgkin and Huxley found that the key mechanism is the action of sodium and potassium ion channels in the cell membrane. Figure 3.2 shows what happens. In a resting state, the neuron’s sodium and potassium channels are closed, and the concentration of Na1 ions is 10 times higher outside the neuron than inside it (Figure 3.2a). But when a neuron is stimulated sufficiently, nearby sodium channels open up. Attracted by the negative protein ions inside, positively charged sodium ions flood into the axon, creating a state of depolarization (Figure 3.2b). In an instant, the interior now becomes positive (by about 40 millivolts) in relation to the outside, creating the action potential. In a reflex action to restore the resting potential, the cell closes its sodium channels, and positively charged potassium ions flow out through their channels, restoring the negative resting potential (Figure 3.2c). Eventually, the excess sodium ions flow out of the neuron, and the escaped potassium ions are recovered. The resulting voltage changes are shown in Figure 3.2d. Once an action potential occurs at any point on the membrane, its effects spread to adjacent sodium 67 5. What chemical changes cause the process of depolarization that creates graded and action potentials? How do these potentials differ? 68 CHAPTER THREE + + + Na Na+ Na+ Na Na+ Na+ Na+ + Na Na+ Na+ Sodium channel Potassium channel – – –70mV resting potential Potassium channel + + + Sodium ions Sodium channel – + s Stimulu A– K+ + K+ K + A– Na K+ – K+ A + Na+ Action potential produced + Na+ Na+ – – – f Flow o – charge Axon membrane The 10:1 concentration of sodium (Na+) ions outside the neuron and the negative protein (A–) ions inside contribute to a resting potential of –70mV. + Sodium ions + + +40 Resting potential restored (c) – Potassium ions flow out + + + – – – Potassium ions Sodium channels open and sodium ions flood into the axon. Note that the potassium channels are still closed. Action potential K+ K+ K+ (b) – + ++ Na + Na + arge Na of ch Flow – Voltage (millivolts) (a) 0 Sodium ions flow in Return to resting potential Resting potential –70 Refractory period Sodium channels that were open in (b) have now closed and potassium channels behind them are open, allowing potassium ions to exit and restoring the resting potential at that point. Sodium channels are opening at the next point. 1 (d) 2 3 4 5 Time (milliseconds) FIGURE 3.2 From resting potential to action potential. When a neuron is not being stimulated, a difference in electrical charge of about 270 millivolts (mV) exists between the interior and the surface of the neuron. (a) This resting potential is caused by the uneven distribution of positively and negatively charged ions, with a greater concentration of positively charged sodium ions kept outside the cell by closed sodium channels, and the presence of negatively charged protein (A2) ions inside the cell. In addition, the action of sodium-potassium pumps helps to maintain the negative interior by pumping out three sodium (Na1) ions for every two positively charged potassium (K1) ions pumped into the cell. (b) Sufficient stimulation of the neuron causes an action potential. Sodium channels open for an instant, and Na1 ions flood into the axon, reversing the electrical potential from 270 mV to 140 mV. (c) Within a millisecond, the sodium channels close and many K1 ions flow out of the cell through open potassium channels, helping to restore the interior negative potential. As adjacent sodium channels are opened and the sequence in (b) and (c) is repeated, the action potential moves down the length of the neuron. (d) Shown here are the changes in potential that would be recorded from a particular point on the axon. After a brief refractory period during which the neuron cannot be stimulated, another action potential can follow. channels and the action potential flows down the length of the axon to the axon terminals. Immediately after an impulse passes a point along the axon, however, there is a recovery period as K1 ions flow out of the interior. During this absolute refractory period, the membrane is not excitable and cannot generate another action potential. This places an upper limit on the rate at which nerve impulses can occur. In humans, the limit is about 300 impulses per second (Kolb & Whishaw, 2005). It’s all or nothing. One other feature of the action potential is noteworthy. In accordance with the so-called all-or-none law, action potentials occur at a uniform and maximum intensity, or they do not occur at all. Like pressing the shutter release of a camera, which requires a certain amount of pressure, the negative potential inside the axon has to be changed from 270 millivolts to about 250 millivolts (the action potential threshold) by the influx of sodium ions into the axon before the action potential will be triggered. Changes in the negative resting potential that do not reach the 250 millivolts action potential threshold are called graded potentials. Under certain circumstances, graded potentials caused by several neurons can add up Biological Foundations of Behaviour to trigger an action potential in the postsynaptic neuron. For a neuron to function properly, sodium and potassium ions must enter and leave the membrane at just the right rate. Drugs that alter this transit system can decrease or prevent neural functioning. For example, local anaesthetics such as Novocain and Xylocaine attach themselves to the sodium channels, stopping the flow of sodium ions into the neurons. This stops pain impulses from being sent by the neurons (Ray & Ksir, 2004). The Myelin Sheath Many axons that transmit information throughout the brain and spinal cord are covered by a tubelike myelin sheath, a fatty, whitish insulation layer derived from glial cells during development. The myelin sheath is interrupted at regular intervals by the nodes of Ranvier, where the myelin is either extremely thin or absent. The nodes make the myelin sheath look a bit like sausages placed end to end (Figure 3.1). In unmyelinated axons, the action potential travels down the axon length like a burning fuse. In myelinated axons, electrical conduction can skip from node to node, and these “great leaps” from one gap to another account for high conduction speeds of more than 300 kilometres per hour. But even these high-speed fibres are three million times slower than the speed at which electricity courses through an electric wire. This is why your brain, though vastly more complex than any computer, cannot begin to match it in speed of operation. The myelin sheath is most commonly found in the nervous systems of higher animals. In many nerve fibres, the myelin sheath is not completely formed until some time after birth. The increased efficiency of neural transmission that results is partly responsible for the gains that infants exhibit in muscular coordination as they grow older (Cabeza et al., 2005). The tragic effects of damage to the myelin coating can be seen in people who suffer from multiple sclerosis. This progressive disease occurs when the person’s own immune system attacks the myelin sheath. Damage to the myelin sheath disrupts the delicate timing of nerve impulses, resulting in jerky, uncoordinated movements and, in the final stages, paralysis (Toy, 2007). How Neurons Communicate: Synaptic Transmission The nervous system operates as a giant communications network, and its action requires the transmission of nerve impulses from one neuron to another. Early in the history of brain research, scientists thought that the tip of the axon made physical contact with the dendrites or cell bodies of other neurons, passing electricity directly from one neuron to the next. Others, such as famous Spanish anatomist Santiago Ramón y Cajal and British scientist Charles Sherrington, argued that neurons were individual cells that did not make actual physical contact with each other, but communicated at a synapse, a functional (but not physical) connection between a neuron and its target. This idea was controversial: How could a neuron influence the functioning of the heart, or a skeletal muscle, or another neuron within the brain if these cells did not actually touch? What carried the message from one neuron to the next? The controversy persisted until the 1920s, when Otto Loewi, in a series of simple but elegant experiments, demonstrated that neurons released chemicals, and it was these chemicals that carried the message from one neuron to the next cell in the circuit (Loewi, 1935, 1960). Otto Loewi won the Nobel Prize for his discovery of chemical neurotransmission. With the advent of the electron microscope, researchers were able to see that there is indeed a tiny gap or space, called the synaptic cleft, between the axon terminal of one neuron and the dendrite of the next neuron. This discovery raised new and perplexing questions: If the action potential does not cross the synapse, what does? What carries the message and how does it affect the next neuron in the circuit? Neurotransmitters We now know that, in addition to generating electricity, neurons produce neurotransmitters, chemical substances that carry messages across the synapse to either excite other neurons or inhibit their firing. This process of chemical communication involves five steps: synthesis, storage, release, binding, and deactivation. In the synthesis stage, the chemical molecules are formed inside the neuron. The molecules are then stored in chambers called synaptic vesicles within the axon terminals. When an action potential comes down the axon, these vesicles move to the surface of the axon terminal and the molecules are released into the fluid-filled space between the axon of the sending (presynaptic) neuron and the membrane of the receiving (postsynaptic) neuron. The molecules cross the synaptic space and bind (attach themselves) to receptor sites—large protein molecules embedded in the receiving neuron’s cell membrane. These receptor sites, which look a bit like lily pads when viewed through an electron microscope, have a specially shaped surface that fits a specific 69 6. What is the nature and importance of the myelin sheath? Which disorder results from inadequate myelinization? 70 CHAPTER THREE Nerve impulse Transmitter will fit receptor Axon of presynaptic neuron Postsynaptic membrane containing receptors Presynaptic (sending) neuron Axon terminal (b) Ne Receptor molecules al ur Axon Transmitter will not fit receptor u imp lse Synaptic vesicles Synthesis of neurotransmitter Transmitter Approaching Storage in synaptic vesicles Postsynaptic (receiving) neuron Release into synaptic space Postsynaptic membrane containing receptors Synaptic space Binding to receptor sites Dendrites (a) (c) Deactivation through reuptake or breakdown FIGURE 3.3 A synapse between two neurons. The action potential travels to the axon terminals, where it stimulates the release of transmitter molecules from the synaptic vesicles. These molecules travel across the synapse and bind to specially keyed receptor sites on the dendrite of the postsynaptic neuron (a). The lock-and-key nature of neurotransmitters and receptor sites is shown in (b). Only transmitters that fit the receptor will influence membrane potentials. (c) Neurotransmitter activity moves from synthesis to deactivation. If the neurotransmitter has an excitatory effect on the neuron, the chemical reaction creates a graded or an action potential. If the neurotransmitter has an inhibitory effect, the negative potential inside the neuron increases and makes it more difficult to trigger an action potential. transmitter molecule, much like a lock accommodates a single key (Figure 3.3). Excitation, Inhibition, and Deactivation 7. How do neurotransmitters achieve the processes of excitation and inhibition of postsynaptic neurons? The binding of a transmitter molecule to the receptor site produces a chemical reaction that can have one of two effects on the postsynaptic neuron. In some cases, the reaction will depolarize (excite) the postsynaptic cell membrane by stimulating the inflow of sodium or other positively charged ions. Neurotransmitters that create depolarization are called excitatory transmitters. This stimulation, alone or in combination with activity at other excitatory synapses on the dendrites or the cell body, may exceed the action potential threshold and cause the postsynaptic neuron to fire an action potential. In other cases, the chemical reaction created by the docking of a neurotransmitter at its receptor site will hyperpolarize the postsynaptic membrane by stimulating ion channels that allow positively charged potassium ions to flow out of the neuron or negatively charged ions, such as chloride, to flow into the neuron. This makes the membrane potential even more negative (e.g., changing it from 270 millivolts to 272 millivolts). Hyperpolarization makes it more difficult for excitatory transmitters at other receptor sites to depolarize the neuron to its action potential threshold of 255 millivolts. Transmitters that create hyperpolarization are thus inhibitory in their function (Figure 3.4). A given neurotransmitter can have an excitatory effect on some neurons and an inhibitory influence on others. Every neuron is constantly bombarded with excitatory and inhibitory neurotransmitters from other neurons, and the interplay of these influences determines whether the cell fires an action potential. The action of an inhibitory transmitter from one presynaptic neuron may prevent the postsynaptic neuron from reaching the action potential threshold, even if it is receiving excitatory stimulation from several other neurons at the same time. An exquisite balance between excitatory and inhibitory processes must be maintained if the nervous system is to function properly. The process of inhibition allows a fine-tuning of neural activity and prevents an uncoordinated discharge of the nervous system, as occurs in a seizure, when large numbers of neurons fire off action potentials in a runaway fashion. Biological Foundations of Behaviour Excitatory Neurotransmitter Depolarizes neuron’s membrane Increases likelihood of action potential Inhibitory Neurotransmitter Hyperpolarizes neuron’s membrane Decreases likelihood of action potential 71 FIGURE 3.4 Neurotransmitters have either excitatory or inhibitory effects on postsynaptic neurons. Excitatory transmitters depolarize the postsynaptic neuron’s cell membrane, making it less negative and thereby moving it toward the action potential threshold. Inhibitory neurons hyperpolarize the membrane, making it more negative and therefore more difficult to excite to an action potential. Once a neurotransmitter molecule binds to its receptor, it continues to activate or inhibit the neuron until it is shut off, or deactivated. This deactivation occurs in two major ways (Fain, 1999). Some transmitter molecules are deactivated by other chemicals located in the synaptic space that break them down into their chemical components. In other instances, the deactivation mechanism is reuptake, in which the transmitter molecules are reabsorbed into the presynaptic axon terminal. When the receptor molecule is vacant, the postsynaptic neuron returns to its former resting state, awaiting the next chemical stimulation. Most commonly used, and abused, psychoactive drugs influence one of these steps in chemical neurotransmission. Drugs may target the transmitter’s receptor, binding to the receptor in place of the neurotransmitter, or one of the steps in the synthesis or release of the neurotransmitter. Drugs can also alter synaptic transmission by influencing how the transmitter is cleared from the synaptic cleft after it has been released. A drug’s exact psychological TABLE 3.1 effects are determined not by its actions at the synapse, but by which specific chemical transmitter it targets. This chapter’s Applications feature provides information on how some commonly used drugs influence neurotransmission. Specialized Transmitter Systems Through the use of chemical transmitters, nature has found an ingenious way of dividing up the brain into systems that are uniquely sensitive to certain messages. Transmitter molecules can assume many shapes. Because the various systems in the brain recognize only certain chemical messengers, they are protected from “crosstalk” from other systems. At present, 100 to 150 different substances are known or suspected transmitters in the brain, but there may be many more (Fain, 1999; Kolb & Whishaw, 2005). Each substance has a specific excitatory or inhibitory effect on certain neurons. Table 3.1 lists several of the more important neurotransmitters that have been linked to psychological phenomena. Some Neurotransmitters and Their Effects Neurotransmitter Major Function Disorders Associated with Malfunctioning Glutamate (glutamic acid) Excitatory; found throughout the brain; involved in the control of all behaviours, especially important in learning and memory GABA (gammaaminobutyric acid) Inhibitory transmitter; found throughout the brain; involved in controlling all behaviours, especially important in anxiety and motor control Destruction of GABA-producing neurons in Huntington’s disease produces tremors and loss of motor control, as well as personality changes Acetylcholine (ACh) Excitatory at synapses involved in muscular movement and memory Memory loss in Alzheimer’s disease (undersupply) Muscle contractions, convulsions (oversupply) Norepinephrine Excitatory and inhibitory functions at various sites; involved in neural circuits controlling learning, memory, wakefulness, and eating Depression (undersupply) Stress and panic disorders (oversupply) Serotonin Inhibitory at most sites; involved in mood, sleep, eating, and arousal, and may be an important transmitter underlying pleasure and pain Depression, sleeping, and eating disorders (undersupply) Dopamine Can be inhibitory or excitatory; involved in voluntary movement, emotional arousal, learning, motivation, experiencing pleasure Parkinson’s disease and depression (undersupply) Schizophrenia (oversupply) Endorphin Inhibits transmission of pain impulses Insensitivity to pain (oversupply) Pain hypersensitivity, immune problems (undersupply) 72 CHAPTER THREE 8. Describe two methods by which neurotransmitter molecules are deactivated at the synapse. 9. Describe the roles of (a) acetylcholine, (b) dopamine, (c) serotonin, and (d) endorphins in psychological functions. Two widespread neurotransmitters are simple amino acids, glutamate, or glutamic acid, and gamma-aminobutyric acid, or GABA. Both glutamate and GABA are found throughout the central nervous system, and hence have some role in mediating virtually all behaviours. Glutamate is excitatory and has a particularly important role in the mechanisms involved in learning and memory. Improving one’s memory, however, cannot be as simple as enhancing glutamate activity. Since it has a powerful excitatory effect, over-activation of glutamate will induce seizure activity within the brain, especially within the cerebral cortex. Whereas glutmate has a powerful excitatory effect, GABA is an inhibitory neurotransmitter. GABA is especially important for motor control and the control of anxiety. For example, many of the drugs commonly used to treat anxiety disorders, the benzodiazepines, act by enhancing GABA activity. A commonly used drug, alcohol, acts, in part, to make the brain more sensitive to GABA, although in a less specific way than the anti-anxiety benzodiazepines. The symptoms of intoxication reflect the progressive inhibition of brain function with increasing GABAinduced inhibition. Perhaps the best understood neurotransmitter is acetylcholine (ACh), which is involved in memory and muscle activity. Underproduction of ACh is thought to be an important factor in Alzheimer’s disease, a degenerative brain disorder involving profound memory impairment that afflicts between 5 and 10 percent of all people over 65 years of age (Morris & Becker, 2005). Reductions in ACh weaken or deactivate neural circuitry that stores memories. ACh is also an excitatory transmitter at the synapses where neurons activate muscle cells (Sherwood, 1991). Drugs that block the action of ACh, therefore, can prevent muscle activation, resulting in muscular paralysis. One example occurs in botulism, a serious type of food poisoning that can result from improperly canned food. The toxin formed by the botulinum bacteria blocks the release of ACh from the axon terminal, resulting in a potentially fatal paralysis of the muscles, including those of the respiratory system. The opposite effect on ACh occurs with the bite of the black widow spider. The spider’s venom produces a torrent of ACh, resulting in violent muscle contractions, convulsions, and possible death. Thus, although botulism and black widow venom affect ACh synapses in different ways, they can have equally lethal effects. The neurotransmitter dopamine mediates a wide range of functions, including motivation, reward, and feelings of pleasure; voluntary motor control; and control of thought processes. Understanding the neurotransmitter dopamine has also had a profound impact on our understanding of several diseases. In Parkinson’s disease, one group of dopamine-producing neurons degenerate and die. As dopamine is lost in the affected brain areas, there is a concomitant loss of voluntary motor control. The symptoms of Parkinson’s disease are most commonly treated with a drug (L-DOPA) that increases the amount of dopamine within the brain. The treatment of emotionally disturbed people has been revolutionized by the development of psychoactive drugs that operate by either enhancing or inhibiting the actions of transmitters at the synapse. Antipsychotic drugs are one group of drugs that started the so-called “psychiatric revolution” of the 1950s, and they are still widely used today. These drugs attach to dopamine receptors and block dopamine from having its effects. Such blockade of dopamine is effective in treating symptoms of schizophrenia, including disordered thinking, hallucinations, and delusions (LeMoal, 1999; Robinson, 1997). Quite a different mechanism occurs in the treatment of depression. Depression involves abnormal sensitivity to serotonin, a neurotransmitter that influences mood, eating, sleep, and sexual behaviour. Antidepressant drugs increase serotonin activity in several ways. The drug Prozac blocks the reuptake of serotonin from the synaptic space, allowing serotonin molecules to remain active and exert their mood-altering effects on depressed patients. Other antidepressant drugs work on a different deactivating mechanism. They inhibit the activity of enzymes in the synaptic space that deactivate serotonin by breaking it down into simpler chemicals. In so doing, they prolong serotonin activity at the synapse. Endorphins are another important family of neurotransmitters. Endorphins reduce pain and increase feelings of well-being. They bind to the same receptors as the ones activated by opiate drugs, such as opium and morphine, which produce similar psychological effects. The ability of people to continue to function despite severe injury is due in large part to the release of endorphins and their ability to act as analgesics. We discuss the endorphins in greater detail when we discuss pain. Most neurotransmitters have their excitatory or inhibitory effects only on specific neurons that have receptors for them. Others, called neuromodulators, have a more widespread and generalized influence on synaptic transmission. These substances circulate through the brain and either increase or decrease (i.e., modulate) the sensitivity of thousands, perhaps millions, of neurons to their specific transmitters. Neuromodulators play important roles in functions such as eating, sleep, and stress. Thus, some neurotransmitters have very specific effects, whereas others have more general effects on neural activity. Biological Foundations of Behaviour Applications UNDERSTANDING HOW DRUGS AFFECT YOUR BRAIN Drugs affect consciousness and behaviour by influencing the activity of neurons. According to Health Canada, 14 percent of Canadians between ages 15 and 19 smoke tobacco, and that number increases to 21 percent among Canadians aged 20 to 24 (Canadian Tobacco Use Monitoring Survey, Health Canada, 2009). Among Canadians aged 15 to 24, 32.7 percent have used cannabis and 15.4 percent have used some type of illicit drug, such as ecstasy, cocaine/crack, and amphetamines, or hallucinogenic drugs, such as LSD (Health Canada, 2009). Alcohol is present at many university and college parties, in restaurants, at sporting events, and in the refrigerator or cupboard of many Canadian homes. In 2008, 9.3 percent of Canadians were classified as heavy drinkers by Health Canada. Almost all students ingest caffeine in coffee, chocolate, cocoa, and soft drinks. Considering the amount of drugs that we ingest, it is important to have some knowledge of what these drugs are doing within the brain. Most psychoactive drugs produce their effects by either increasing or decreasing the actions of neurotransmitters. An agonist is a drug that increases the activity of a neurotransmitter. Agonists may (1) enhance a neuron’s ability to synthesize, store, or release neurotransmitters; (2) mimic the action of a neurotransmitter by binding with and stimulating postsynaptic receptor sites; or (3) make it more difficult for neurotransmitters to be deactivated, such as by inhibiting reuptake. An antagonist is a drug that inhibits or decreases the action of a neurotransmitter. An antagonist may (1) reduce a neuron’s ability to synthesize, store, or release neurotransmitters; or (2) prevent a neurotransmitter from binding with the postsynaptic neuron by fitting into and blocking the receptor sites on the postsynaptic neuron. With the distinction between agonist and antagonist functions in mind, let’s consider how some commonly used drugs work within the brain. Alcohol is a depressant drug that has both agonist and antagonist effects. Although alcohol can have a wide range of effects, in the concentrations that people consume it, alcohol’s effects are due to its agonist and antagonist actions (Levinthal, 2010). As an agonist, alcohol stimulates the activity of the inhibitory transmitter GABA, thereby depressing neural activity. As an antagonist, it decreases the activity of glutamate, an excitatory transmitter. The effect is a powerful slowing of neural activity that inhibits normal brain functions, including clear thinking, emotional control, and motor coordination. Sedative drugs, including barbiturates and tranquilizers, also increase GABA activity, and taking them with alcohol can be deadly when their depressant effects on neural activity are combined with the alcohol’s effects (Schatzberg et al., 2010). Caffeine is a stimulant drug that increases the activity of neurons and other cells. It is an antagonist for the transmitter adenosine, which inhibits the release of excitatory transmitters. By reducing adenosine activity, caffeine helps produce higher rates of cellular activity. Although caffeine is a stimulant, it is important to note that contrary to popular belief, caffeine does not counteract the effects of alcohol and sober people up. What someone who has been drinking needs is a ride home with a driver who is sober—not a cup of coffee. Nicotine is an agonist for the excitatory transmitter ACh. Its chemical structure is similar enough to ACh to allow it to fit into ACh binding sites and create action potentials. At other receptor sites, nicotine stimulates dopamine activity, which is an important chemical mediator for motivation and reward. This stimulation may help account for nicotine’s powerful addictive properties. Amphetamines are stimulant drugs that boost arousal and mood by increasing the activity of the excitatory neurotransmitters dopamine and norepinephrine. They do so in two major ways. First, they cause neurons to release greater amounts of these neurotransmitters. Second, they inhibit reuptake, allowing dopamine and norepinephrine to keep stimulating postsynaptic neurons (Ksir et al., 2008). Cocaine produces excitation, a sense of increased muscular strength, and euphoria. Like amphetamines, cocaine increases the activity of norepinephrine and dopamine, but it does so in only one major way: It blocks their reuptake. Thus, amphetamines and cocaine have different mechanisms of action FIGURE 3.5 Brain activity is being altered in several ways in this scene. Nicotine from the cigarette smoke is activating acetylcholine and dopamine neurons, increasing neural excitation. The alcohol is stimulating the activity of the inhibitory transmitter GABA and decreasing the activity of an excitatory transmitter, glutamate, thus depressing brain functions. The possibility of a drink having been spiked with one of the powerful and potentially deadly “date rape” sedative drugs could place any of these women at great risk. continued 73 74 CHAPTER THREE on the dopamine and norepinephrine transmitter systems, but both drugs produce highly stimulating effects on mood, thinking, and behaviour. We should comment on two other drugs that, unfortunately, are also found on college campuses. Rohypnol (flunitrazepam, known as roofies or rope) and GHB (gamma hydroxybutyrate, known as easy lay) are so-called “date rape” drugs. Partygoers sometimes add these drugs to punch and other drinks in hopes of lowering drinkers’ inhibitions and facilitating nonconsensual sexual conquest. These drugs are powerful sedatives that suppress general neural activity by enhancing the action of the inhibitory transmitter GABA (Levinthal, 2010). Rohypnol is about 10 times more potent than Valium. At high doses or when mixed with alcohol or other drugs, these substances may lead to respiratory depression, loss of consciousness, coma, and even death. Rohypnol also decreases neurotransmission in areas of the brain involved in memory, producing an amnesia effect that may prevent users from remembering the circumstances under which they ingested the drug or what happened to them afterwards. GHB, which makes its victim appear drunk and helpless, is now a restricted drug, and slipping it into someone’s drink is a criminal act. Increasingly, women are being advised against accepting opened drinks from fellow revellers or leaving their own drinks unattended at parties (Figure 3.5). In Review • Each neuron has dendrites, which receive nerve impulses from other neurons; a cell body (soma), which controls the vital processes of the cell; and an axon, which conducts nerve impulses to adjacent neurons, muscles, and glands. stimulation being received, whereas action potentials obey the all-or-none law, occuring at full intensity if the action potential threshold of stimulation is reached. The myelin sheath increases the speed of neural transmission. • Neural transmission is an electrochemical process. The nerve impulse, or action potential, is a brief reversal in the electrical potential of the cell membrane as sodium ions from the surrounding fluid flow into the cell through sodium ion channels, depolarizing the axon’s membrane. Graded potentials are proportional to the amount of • Passage of the impulse across the synapse is mediated by chemical transmitter substances. Neurons are selective in the neurotransmitters that can stimulate them. Some neurotransmitters excite neurons, whereas others inhibit firing of the postsynaptic neuron. THE NERVOUS SYSTEM 10. What are the three major types of neurons? What are their functions? 11. Differentiate between the central nervous system and the peripheral nervous system. What are the two divisions of the peripheral nervous system? The nervous system is the body’s master control centre. Three major types of neurons carry out the system’s input, output, and integration functions. Sensory neurons carry input messages from the sense organs to the spinal cord and brain. Motor neurons transmit output impulses from the brain and spinal cord to the body’s muscles and organs. Finally, there are neurons that link the input and output functions. Interneurons, which far outnumber sensory and motor neurons, perform connective or associative functions within the nervous system. For example, interneurons allow us to recognize a tune by linking the sensory input from the song we’re hearing with the memory of that song stored elsewhere in the brain. The activity of interneurons makes possible the complexity of our higher mental functions, emotions, and behavioural capabilities. The nervous system can be broken down into several interrelated subsystems (Figure 3.6). The two major divisions are the central nervous system, consisting of all the neurons in the brain and spinal cord, and the peripheral nervous system, composed of all the neurons that connect the central nervous system with the muscles, glands, and sensory receptors. The Peripheral Nervous System The peripheral nervous system contains all the neural structures that lie outside of the brain and spinal cord. Its specialized neurons help to carry out the input and output functions that are necessary for us to sense what is going on inside and outside our bodies and to respond with our muscles and glands. The peripheral nervous system has two major divisions, the somatic nervous system and the autonomic nervous system. Biological Foundations of Behaviour 75 Nervous system Central nervous system (CNS) Brain Peripheral nervous system (PNS) Spinal cord Somatic system (voluntary muscle activation) Forebrain Midbrain Thalamus Hindbrain Hypothalamus Cerebellum Cerebrum (cerebral cortex) Hippocampus Limbic system Amygdala Corpus callosum Nucleus accumbens Brain stem Pons Sympathetic (generally activates) Autonomic system (controls smooth muscle, cardiac muscle, and glands; basically involuntary) Parasympathetic (generally inhibits) Medulla Reticular formation (begins at the level of the medulla and runs up through the midbrain to the forebrain) FIGURE 3.6 Structural organization of the nervous system. The Somatic Nervous System The somatic nervous system consists of the sensory neurons that are specialized to transmit messages from the eyes, ears, and other sensory receptors, and the motor neurons that send messages from the brain and spinal cord to the muscles that control our voluntary movements. The axons of sensory neurons group together like the many strands of a rope to form sensory nerves, and motor neuron axons combine to form motor nerves. (Inside the brain and spinal cord, nerves are called tracts.) As you read this page, sensory neurons located in your eyes are sending impulses into a complex network of specialized visual tracts that course through your brain. At the same time, motor neurons are stimulating the eye movements that allow you to scan the lines of type and turn the pages. The somatic system thus allows you to sense and respond to your environment. The Autonomic Nervous System The body’s internal environment is regulated largely through the activities of the autonomic nervous system, which controls the glands and the smooth (involuntary) muscles that form the heart, the blood vessels, and the lining of the stomach and intestines. The autonomic system is largely concerned with involuntary functions, such as respiration, circulation, and digestion, and it is also involved in many aspects of motivation, emotional behaviour, and stress responses. It consists of two subdivisions, the sympathetic nervous system and the parasympathetic nervous system (Figure 3.7). Typically, these two divisions affect the same organ or gland in opposing ways. The sympathetic nervous system has an activation or arousal function, and it tends to act as a total unit. For example, when you encounter a stressful situation, your sympathetic nervous system simultaneously speeds your heart so it can pump more blood to your muscles, dilates your pupils so more light can enter the eye and improve your vision, slows down your digestive system so that blood can be transferred to the muscles, increases your rate of respiration so your body can get more oxygen, and, in general, mobilizes your body to confront the stressor. This reaction is sometimes called the fightor-flight response. Compared with the sympathetic branch, which tends to act as a unit, the parasympathetic system is far more specific in its opposing actions, affecting one or a few organs at a time. The parasympathetic nervous system slows down body processes and maintains or returns you to a state of rest. Thus, your sympathetic system speeds up your heart rate; your parasympathetic system slows it down. By working 12. Describe the two divisions of the autonomic nervous system, as well as their roles in maintaining homeostasis. 76 CHAPTER THREE Parasympathetic Sympathetic Contracts pupils Dilates pupils (enhanced vision) Constricts bronchi Relaxes bronchi (increased air to lungs) Slows heart beat Accelerates, strengthens heart beat (increased oxygen) Stimulates activity Inhibits activity (blood sent to muscles) Eyes Lungs Heart Stomach, intestines Blood vessels of internal organs Dilates vessels Contracts vessels (increased blood pressure) FIGURE 3.7 The sympathetic branch of the autonomic nervous system arouses the body and speeds up its vital processes, whereas the parasympathetic division slows down body processes. The two divisions work together to maintain equilibrium within the body. together to maintain equilibrium in our internal organs, the two divisions can maintain homeostasis, a delicately balanced or constant internal state. Some acts also require a coordinated sequence of sympathetic and parasympathetic activities. For example, sexual function in the male involves penile erection (through parasympathetic dilation of blood vessels) followed by ejaculation (a primarily sympathetic function; Masters et al., 1988). The Central Nervous System 13. How do spinal reflexes occur? More than any other system in our body, the central nervous system distinguishes us from other creatures. This system contains the spinal cord, which connects most parts of the peripheral nervous system with the brain, and the brain itself. The Spinal Cord Most nerves enter and leave the central nervous system by way of the spinal cord, a structure that in a human adult is 40 to 45 centimetres long and about 2.5 centimetres in diameter. The spinal cord’s neurons are protected by the vertebrae (bones of the spine). When the spinal cord is viewed in crosssection (Figure 3.8), its central portion resembles an H or a butterfly. The H-shaped portion consists largely of grey-coloured neuron cell bodies and their interconnections. Surrounding the grey matter are white-coloured myelinated axons that connect various levels of the spinal cord with each other and with the higher centres of the brain. Entering the back side of the spinal cord along its length are sensory nerves. Motor nerves exit the spinal cord’s front side. Some simple stimulus-response sequences, known as spinal reflexes, can be triggered at the level of the spinal cord without any involvement of the brain. For example, if you touch something hot, sensory receptors in your skin trigger nerve impulses in sensory nerves that flash into your spinal cord and synapse inside with interneurons. The interneurons then excite motor neurons that send impulses to your hand so that it pulls away from the Biological Foundations of Behaviour 77 To the brain Sensory neurons (incoming information) Interneurons Spinal cord Motor neurons (outgoing information) Skin receptors Muscle pulls finger away FIGURE 3.8 A cross-section of the spinal cord shows the organization of sensory and motor nerves. Sensory and motor nerves enter and exit the spinal cord on both sides of the spinal column. Interneurons within the H-shaped spinal grey matter can serve a connective function, as shown here, but in many cases, sensory neurons also can synapse directly with motor neurons. At this level of the nervous system, reflex activity is possible without involving the brain. hot object. Other interneurons simultaneously carry the “Hot!” message up the spinal cord to your brain, but it is a good thing that you don’t have to wait for the brain to tell you what to do in such emergencies. Getting messages to and from the brain takes slightly longer, so the spinal cord reflex system significantly reduces reaction time, and, in this case, potential tissue damage. The Brain The 1.4 kilograms of protein, fat, and fluid that you carry around inside your skull is the real “you.” It is also the most complex structure in the known universe and the only one that can wonder about itself. As befits this biological marvel, your brain is the most active energy consumer of all your body organs. Although the brain accounts for only about 2 percent of your total body weight, it consumes about 20 percent of the oxygen you use in a resting state (Simon, 2007). Moreover, the brain never rests; its rate of energy metabolism is relatively constant day and night. In fact, when you dream, the brain’s metabolic rate actually increases slightly (Simon, 2007). How can this rather nondescript blob of greyish tissue discover the principle of relativity, build the Hubble Telescope, and produce great works of art, music, and literature? Answering such questions requires the ability to study the brain and how it functions. To do so, neuroscientists use a diverse set of tools and procedures. Unlocking the Secrets of the Brain More has been learned in the past three decades about the brain and its role in behaviour than was known in all the preceding ages. This knowledge explosion is due in large part to revolutionary technical advances that have provided scientists with new research tools, as well as to the contributions of psychological research on brain–behaviour relations. Investigators use a variety of methods to study the brain’s structures and activities. Neuropsychological tests. Psychologists have developed a variety of neuropsychological tests to measure verbal and non-verbal behaviours that are known to be affected by particular types of brain damage (Strauss et al., 2006). These tests are used in clinical evaluations of people who may have suffered brain damage through accident or disease. They are also important research tools. For example, Figure 3.9 shows a portion of a Trail Making Test, used to test memory and planning. Scores on the test give an indication of the type and severity of damage the person may have. Neuropsychological tests of this kind have provided much information about brain– behaviour relations. 14. Describe four methods used to study brain– behaviour relations. 78 CHAPTER THREE E F 3 4 B 2 5 D A C 1 6 FIGURE 3.9 The Trail Making Test consists of a randomly scattered set of numbers and letters. On this timed test, the patient must connect the numbers and letters consecutively with a continuous line, or “trail” (i.e., A to 1 to B to 2 to C to 3, and so on). People with certain kinds of brain damage have trouble alternating between the numbers and letters because they cannot retain a plan in memory long enough, and poor test performance reflects this deficit. 15. How are CT scans, PET scans, and MRIs produced, and how is each used in brain research? Destruction and stimulation techniques. Experimental studies are another useful method of learning about the brain (Tatlisumak & Fisher, 2006). Researchers can produce brain damage (lesions) under carefully controlled conditions in which specific nervous tissue is destroyed with electricity, with cold or heat, or with chemicals. They also can surgically remove some portion of the brain and study the consequences. Most experiments of this kind are performed on animals, but humans also can be studied when accident or disease produces a specific lesion or when abnormal brain tissue must be surgically removed. An alternative to destroying neurons is stimulating them, which typically produces opposite effects. A specific region of the brain can be stimulated by a mild electric current or by chemicals that excite neurons. Electrodes can be permanently implanted so that the region of interest can be stimulated repeatedly. Some of these electrodes are so tiny that they can stimulate individual neurons. In chemical stimulation studies, a tiny tube is inserted into the brain so that a small amount of the chemical can be delivered directly to the area to be studied. The neurosurgeon Wilder Penfield, of the Montreal Neurological Institute, pioneered brain surgery with an awake, interacting patient. Penfield stimulated specific points of cortex with a mild electrical current in an attempt to map out the functions of the cerebral cortex (see the Research Foundations feature). Before the advent of modern brain-imaging techniques (which we will discuss shortly), much of our knowledge of the functions of the human cerebral cortex came from the work pioneered by Wilder Penfield, together with the neuropsychological testing we have just discussed. Electrical recording. Because electrodes can record brain activity as well as stimulate it, it is possible to “eavesdrop” on the electrical conversations occurring within the brain. Neurons’ electrical activity can be measured by inserting small electrodes into particular areas of the brain or even into individual neurons. In addition to measuring individual voices, scientists can tune in to “crowd noise” by placing larger electrodes on the scalp to measure the activity of large groups of neurons with the electroencephalogram (EEG) (Figure 3.10a, b). Although the EEG is a rather gross measure that taps the electrical activity of thousands of neurons in many parts of the brain, specific EEG patterns correspond to certain states of consciousness, such as wakefulness and sleep. Clinicians also use the EEG to detect abnormal electrical patterns that signal the presence of brain disorders. Researchers are especially interested in changes in the EEG record that accompany specific psychological events, such as presentation of a sensory stimulus. Changes in the EEG that accompany such events are called event-related potentials (ERPs). Brain imaging. The newest tools of discovery are imaging techniques that permit neuroscientists to peer into the living brain (Figure 3.10c). The most important of these technological “windows” are CT scans, PET scans, and magnetic resonance imaging (MRI). CT scans and MRIs are used to visualize brain structure, whereas PET scans and fMRIs allow scientists to view brain activity (Bremner, 2005). Developed in the 1970s, computerized axial tomography (CT) scans use X-ray technology to study brain structures (Andreason, 1998). A highly focused beam of X-rays takes pictures of narrow slices of the brain. A computer analyzes the X-rayed slices and creates pictures of the brain’s interior from many different angles (Figure 3.10d). Pinpointing where injuries or deterioration have occurred helps to clarify relations between brain damage and psychological functioning. CT scans are 100 times more sensitive than standard X-ray procedures, and the technological advance was so dramatic that its developers, Allan Cormack and Godfrey Hounsfield, were awarded the 1979 Nobel Prize for Medicine. Whereas CT scans provide pictures of brain structures, positron emission tomography (PET) scans measure brain activity, including metabolism, blood flow, and neurotransmitter activity (Hornak, 2000; Ron & David, 1997). PET is based on the fact that glucose, a natural sugar, is the major nutrient of neurons. Thus, when neurons are active, they consume more glucose. To prepare a patient for a Biological Foundations of Behaviour PET scan, a harmless form of radioactive glucose is injected into the bloodstream and travels to the brain, where it circulates in the blood supply. The energy emitted by the radioactive substance is measured by the PET scan, and the data are fed into a computer that uses the readings to produce a colour picture of the brain on a display screen (Figure 79 3.10c, g). Researchers can tell how active particular neurons are by using the PET scan to measure the amount of radioactive glucose that accumulates in them. If a person is performing a mental reasoning task, for example, then a researcher can tell by the glucose concentration pattern which parts of the brain were activated by the task (Raichle, 1994). (b) (a) (c) (d) (e) (f) (g) FIGURE 3.10 Measuring brain activity. (a) The electroencephalogram (EEG) records the activity of large groups of neurons in the brain through a series of electrodes attached to the scalp. (b) The results appear on an EEG readout. (c) Various brain scanning machines, such as the one shown here, produce a number of different images. (d) The CT scan uses narrow beams of X-rays to construct a composite picture of brain structures. (e) MRI scanners produce vivid pictures of brain structures. (f) Functional MRI (fMRI) procedures take images in rapid succession, showing neural activity as it occurs. (g) PET scans record the amount of radioactive substance that collects in various brain regions to assess brain activity. 80 CHAPTER THREE 16. In what sense might the structure of the human brain mirror evolutionary development? Using the PET scan, researchers can study brain activity in relation to cognitive processes, behaviour, and even forms of mental illness. Magnetic resonance imaging (