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(BQ) Part 1 book “Brain and behavior” has contents: Communication within the nervous system, the organization and functions of the nervous system, the methods and ethics of research, motivation and the regulation of internal states, emotion and health,… and other contents.
ENGAGING, RELEVANT, ACCESSIBLE APPLIED FEATURES OUTSTANDING PEDAGOGY Resources That Give Instructors and Students an Edge! To Duejean She walks in beauty, like the night Of cloudless climes and starry skies; And all that’s best of dark and bright Meet in her aspect and her eyes And on that cheek, and o’er that brow, So soft, so calm, yet eloquent, The smiles that win, the tints that glow, But tell of days in goodness spent, A mind at peace with all below, A heart whose love is innocent! —Lord Byron Copyright © 2015 by SAGE Publications, Inc All rights reserved No part of this book may be reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, or by any information storage and retrieval system, without permission in writing from the publisher Printed in Canada Library of Congress Cataloging-in-Publication Data Garrett, Bob Brain & behavior : an introduction to biological psychology / Bob Garrett ; contributions by Gerald Hough and John Agnew.—Fourth edition pages cm Includes bibliographical references and index ISBN 978-1-4522-6095–2 (pbk : alk paper) ISBN 978-1-4833-1241-5 (web pdf) Psychobiology—Textbooks I Title II Title: Brain and behavior QP360.G375 2014 612.8—dc23 2014007564 14 15 16 17 18 10 9 8 7 6 5 4 3 2 1 deficits and depression that often accompany Parkinson’s disease; they may represent the brain’s attempt to remove proteins that have been damaged by toxins The patient’s complement of genes helps determine age of onset, rate of progression, and whether cognitive loss will be a part of the disease FIGURE 11.21 Lewy Bodies in a Brain With Parkinson’s Disease A neuron containing two stained Lewy bodies, abnormal clumps of protein SOURCE: From “α-Synuclein in Lewy Bodies,” by M G Spillantini et al., 1997, Nature 8/28/1997 Copyright © 1997 Used with permission Several environmental influences have been implicated in Parkinson’s disease One cause is subtle brain injury; being knocked unconscious once increases the risk by 32%, and the risk rises by 174% for those knocked out several times Other research points to a variety of toxins, including industrial chemicals, carbon monoxide, herbicides, and pesticides (Olanow & Tatton, 1999) Numerous studies show an association between pesticide use and Parkinson’s, but the human studies are correlational, and establishing a causal relationship has been difficult (reviewed in Moretto & Colosio, 2013) Pesticide exposure produces some of the symptoms of Parkinson’s in animals, though with very high dosages Animal studies also suggest that some genes increase sensitivity to the toxic effects, providing another example of the interaction between hereditary and environmental effects While firm conclusions have eluded us, a study in California’s highly agricultural Central Valley that found a tripling of risk with occupational exposure to the pesticides ziram, maneb, and paraquat (Wang et al., 2011) suggests extreme caution while we try to sort things out FIGURE 11.22 Transplanted Embryonic Cells in the Brain of a Parkinson’s Patient The patient died in a car accident 7 months after her surgery (a) Her right putamen (part of the striatum) was removed and placed on a photograph of the magnetic resonance image of her brain made at the time of surgery The red lines indicate the angle at which the needles were inserted into the brain to inject the fetal cells (right side of the brain) and as a control procedure (left side) The dark area on the putamen along the needle track is due to the staining of new dopamine cells and shows that the axons had grown 2 to 3 millimeters from the cell bodies The image in (b) is an enlargement of the putamen SOURCE: From “Transplantation of Embryonic Dopamine Neurons for Severe Parkinson’s Disease,” by C R Freed et al., 2001, New England Journal of Medicine, 334, pp 710–719, fig 3a and b, p 717 Interestingly, the risk of Parkinson’s disease is reduced as much as 80% in coffee drinkers (G W Ross et al., 2000) The risk also drops by 50% in smokers (Fratiglioni & Wang, 2000), but of course no benefit of smoking outweighs its dangers Rat studies indicate that cigarette smoke may prevent the accumulation of neurotoxins (Soto-Otero, Méndez-Alvarez, Sánchez-Sellero, Cruz-Landeira, & López-Rivadulla, 2001) and that caffeine reduces the effect of neurotoxins by blocking adenosine receptors, which we saw in Chapter results in increased dopamine and acetylcholine release (J.-F Chen et al., 2001) In heavy coffee drinkers, a variant of the glutamate receptor gene GRIN2A reduces Parkinson’s risk by 59% (Hamza et al., 2011) There has been some clinical success in treating Parkinson’s with adenosine and glutamate receptor antagonists (Gasparini, Di Paolo, & Gomez-Mancilla, 2013; Hickey & Stacy, 2012) Parkinson’s disease is typically treated by administering levodopa (L-dopa), which is the precursor for dopamine Dopamine will not cross the blood-brain barrier but L-dopa will, and in the brain it is converted to dopamine Dopamine agonists can also be helpful, and even placebos increase dopamine release (de la Fuente-Fernández et al., 2001) But these treatments increase dopamine throughout the brain, which causes side effects ranging from restlessness and involuntary movements to hallucinations Also, as more neurons die, more drug is required, increasing the side effects While levodopa remains the standard, its side effects mean that some patients are forced to use other drugs Unfortunately, these drugs also treat only some of the symptoms and with limited benefit However, researchers in the United Kingdom are experimenting with a novel way of screening potential drugs (see accompanying In the News) Early attempts showed that implanted embryonic neural cells could survive in the striatum and produce dopamine (Figure 11.22; C R Freed et al., 2001; Greene & Fahu, 2002) However, behavioral improvement was not clinically significant, and some of the patients developed involuntary movements, apparently due to excess dopamine More recent work using adult neural stem cells resulted in more than 80% improvement in motor behavior ratings; the improvement held up for years but had disappeared at the end of years (Lévesque, Neuman, & Rezak, 2009) Clinical application is hampered by immune reactions to stem cells and by the development of tumors at the implant site Recent work indicates that immune response is minimal with stem cells taken from the individual (Morizane et al., 2013), and tumor development can be avoided by allowing the stem cells to mature into an early form of neural cell before implanting (Doi et al., 2012) Gene therapy has also been tried experimentally, with the intent of increasing dopamine levels or reducing excess activity in affected brain areas Results have been mixed in the handful of clinical trials conducted at the phase 1 and phase 2 levels; so far, no procedure has reached the critical phase level that could establish its effectiveness sufficiently for approval by the U.S Food and Drug Administration (FDA) (Denyer & Douglas, 2012) In an attempt to avoid previous disappointments, the British company Oxford Biomedica has treated 15 drug-resistant patients with a combination of three genes; all patients improved in motor capability and maintained improvement for the full year of this phase 1/2 safety and dosage trial (Palfi et al., 2014) These procedures are in their infancy, and we need to remember that the first several heart transplant operations failed but they are almost routine today Curing Parkinson’s in a Dish A team of scientists at the Sheffield Institute for Translational Neuroscience is searching for a drug that will rescue dying cells, not just reduce the symptoms of Parkinson’s disease To speed the process of sifting through numerous possible drugs, they tested the effects of compounds on cells obtained from patients Five years and 2,000 drugs later, they have found one that worked Ursodeoxycholic acid (UDCA) preserved the function of the cells’ mitochondria, which supply energy to cells Because UDCA is already licensed for other uses, the researchers can proceed directly to a phase 1 clinical trial to determine safety and optimum dosage 5 Screening Parkinson’s Drugs Frustration with therapeutic alternatives is creating something of a revival in surgical treatments, which were largely abandoned when drugs for Parkinson’s disease became available (Cosgrove & Eskandar, 1998) Strategically placed lesions in the subthalamic nucleus and the globus pallidus, both in the basal ganglia (see Figure 11.20 again), have provided some improvement for patients who have difficulty using dopaminergic drugs (Cosgrove & Eskandar) These two structures produce a rhythmic bursting activity similar to the rhythm of activity in Parkinsonian tremors, which apparently explains why destroying them reduces this symptom (Perkel & Farries, 2000) But the surgery can damage adjacent structures, resulting in other deficits, such as weakness in a part of the body A less drastic procedure is deep brain stimulation (DBS), electrical stimulation through implanted electrodes Improved motor functioning, allowing levodopa reduction, has been reported for as long as 10 years (reviewed in Fasano, Daniele, & Albanese, 2012) Results are mixed with regard to cognitive deficits, which often are more disabling and resistant to treatment than the motor symptoms DBS usually improves or eliminates impulse control problems in the 13% to 16% of patients affected, possibly due to levodopa reduction; however, some studies have reported onset of pathological gambling, hypersexuality, and compulsive eating In addition, there is some loss of verbal fluency after DBS, and apathy increases in some patients “ This is a scary thing There is a test available, but I haven’t had the guts to take it yet —Shana Martin, at risk for Huntington’s disease ” Huntington’s Disease Like Parkinson’s disease, Huntington’s disease is a degenerative disorder of the motor system involving cell loss in the striatum and cortex Years before a diagnosis, Huntington’s disease begins with jerky movements that result from impaired error correction (M A Smith, Brandt, & Shadmehr, 2000) Later, involuntary movements appear, first as fidgeting and then as movements of the limbs and, finally, writhing of the body and facial grimacing Because these movements sometimes resemble a dance, Huntington’s disease is also called Huntington’s chorea, from the Greek word choreia, which means “dance.” Needless to say, the patient loses the ability to carry out daily activities Death usually follows within 15 to 30 years after the onset of the disease Unlike Parkinson’s disease, cognitive and emotional deficits are a universal characteristic of Huntington’s disease These deficits include impaired judgment, difficulty with a variety of cognitive tasks, depression, and personality changes The motor symptoms are due to the degeneration of inhibitory GABA-releasing neurons in the striatum, while defective or degenerated neurons in the cortex probably account for the psychological symptoms (Figure 11.23; J B Martin, 1987; Tabrizi et al., 1999) Huntington’s disease results from a mutated form of the huntingtin gene (Huntington’s Disease Collaborative Research Group, 1993) The loss of neurons is probably due to the accumulation of the gene’s protein, also known as huntingtin, whose function is unknown (DiFiglia et al., 1997) In normal individuals, the gene has between 10 and 34 repetitions of the bases cytosine, adenine, and guanine (see Chapter 1) The more repeats the person has beyond 37, the earlier in life the person will succumb to the disease (R R Brinkman, Mezei, Theilmann, Almqvist, & Hayden, 1997) Because the gene is dominant, a person who has a parent with Huntington’s has a 50% chance of developing the disease This is an unusual example of a human disorder resulting from a single gene FIGURE 11.23 Loss of Brain Tissue in Huntington’s Disease Left, a section from a normal brain; right, a section from a person with Huntington’s disease The enlarged lateral ventricle in the diseased brain is due to loss of neurons in the caudate nuclei (arrows) SOURCE: Courtesy of Robert E Schmidt, Washington University A number of drugs are used to treat the various symptoms, including antidepressants and antipsychotics, but only one has been approved specifically for Huntington’s disease by the FDA (“FDA Approves,” 2008) It reduces the excess dopamine that causes the abnormal movements Drugs that silence the huntingtin gene are showing promise in animals; a single injection of one of these drugs normalized movement in mice for the 9-month duration of the study and significantly reduced huntingtin protein levels for weeks in monkeys (Kordasiewicz et al., 2012) Grafting of fetal striatal cells has so far produced only modest and temporary improvement (Cicchetti et al., 2009), and stem cell studies have only reached the point of demonstrating that the transplanted cells survive and mature (Maucksch, Vazey, Gordon, & Connor, 2013) Autoimmune Diseases Myasthenia gravis is a disorder of muscular weakness caused by reduced numbers or sensitivity of acetylcholine receptors The muscle weakness can be so extreme that the patient has to be maintained on a respirator In fact, 25 years ago the mortality rate from myesthenia gravis was about 33%; now few patients die from the disease, thanks to improved treatment (Rowland, 2000a) The loss of receptors was demonstrated in an interesting way The venom of the many-banded Formosan krait, a very poisonous snake from Taiwan, paralyzes prey by binding to the acetylcholine receptor When the venom’s toxin is labeled with radioactive iodine and applied to a sample of muscle tissue, it allows researchers to identify and count the acetylcholine receptors The patients turned out to have 70% to 90% fewer receptors than normal individuals (Fambrough, Drachman, & Satyamurti, 1973) Drugs that inhibit the action of acetylcholinesterase give temporary relief from the symptoms of myesthenia gravis (Figure 11.24; Rowland, Hoefer, & Aranow, 1960) Remember that acetylcholinesterase breaks down acetylcholine at the synapse; these inhibitors increase the amount of available neurotransmitter at the neuron-muscle junction FIGURE 11.24 Effect of an Acetylcholinesterase Inhibitor on Myasthenia Gravis (a) Patients often have drooping eyelids, as shown here This patient also could not move his eyes to look to the side (b) The same patient 1 min after injection of an acetylcholinesterase inhibitor The eyes are open and able to move freely SOURCE: From “Mysathenic Syndromes,” by L P Rowland, P F A Hoefer, and H Aranow, Jr., 1960, Research Publications—Association for Research in Nervous and Mental Disease, pp 38, pp 547–560 Although immune system therapy has sometimes been used (Shah & Lisak, 1993), removal of the thymus (thymectomy) has become a standard treatment for myasthenia gravis (Rowland, 2000a) The thymus is the major source of lymphocytes that produce antibodies Improvement can take years, but thymectomy eliminates symptoms completely in almost 80% of patients and reduces them in another 13% to 17% (Ashour et al., 1995; Jaretzki et al., 1988) Multiple sclerosis is a motor disorder with many varied symptoms, caused by deterioration of myelin (demyelination) and neuron loss in the central nervous system In Chapter 2, you saw that demyelination causes slowing or elimination of neural impulses Demyelination thus reduces the speed and strength of movements Even before that happens, impulses traveling in adjacent neurons, which should arrive simultaneously, become desynchronized because of differential loss of myelin An early sign of the disorder is impairment of functions that require synchronous bursts of neural activity, like tendon reflexes and vibratory sensation (Rowland, 2000b) As the disease progresses, unmyelinated neurons die, leaving areas of sclerosis, or hardened scar tissue (Figure 11.25) As a result, the person experiences muscular weakness, tremor, impaired coordination, urinary incontinence, and visual problems Studies indicate that neuron loss is more important than previously thought and suggest that the loss results from a degenerative process in addition to the demyelination (DeLuca, Ebers, & Esiri, 2004; De Stefano et al., 2003) FIGURE 11.25 The Brain of a Deceased Multiple Sclerosis Patient The arrows indicate areas of sclerosis, or hardened scar tissue (dark areas) SOURCE: Science Source Like myasthenia gravis, multiple sclerosis is an autoimmune disease Injecting foreign myelin protein into the brains of animals produces symptoms very similar to those of multiple sclerosis (Wekerle, 1993), and T cells that are reactive to myelin proteins (see Chapter 8) have been found in the blood of multiple sclerosis patients (Allegretta, Nicklas, Sriram, & Albertini, 1990) A genome-wide study has implicated various immune system genes in multiple sclerosis (International Multiple Sclerosis Genetics Consortium, 2007), but some environmental condition may be needed to trigger the immune attack on myelin One possibility is that the immune system has been sensitized by an earlier viral infection; for example, studies have found antibodies for Epstein-Barr virus in multiple sclerosis patients (H J Wagner et al., 2000), and patients more often had mumps or measles during adolescence (Hernán, Zhang, Lipworth, Olek, & Ascherio, 2001) Several drugs are available that modify immune activity in multiple sclerosis patients; they slow the progress of the disease but do not repair the harm already done A new direction may be indicated by a potassium channel blocker, dalfampridine; it improves motor performance, particularly walking (Jeffrey, 2010), but it has the disadvantage of increasing seizure risk (“FDA Drug Safety Communication,” 2012) On the stem cell front, the FDA has approved a phase 1 safety trial using cells harvested from patients’ bone marrow; in preclinical testing, the procedure reduced brain inflammation, repaired myelin, and improved brain function (“Ground Breaking Multiple Sclerosis Stem Cell Trial,” 2013) Concept Check Take a Minute to Check Your Knowledge and Understanding Explain how antagonistic muscles and spinal reflexes maintain posture What contribution does each of the cortical motor areas make to movement? Make a diagram showing how you think the neurons would be interconnected to carry out the target and arm selection task described in the Hoshi & Tanji study on page 358 What are the genetic and environmental causes of the movement disorders described here? In Perspective Unless we have a disorder, we usually take our body senses and our capability for movement for granted And yet just standing upright is a remarkable feat Granted, a mechanical robot could do it easily, but only if it had a rigid body like R2D2’s If the robot had our flexibility of movement and posture, it would have to devote a fair amount of its computer brain to making split-millisecond adjustments to avoid toppling over Then another chunk of its computer would be required just to locate a visual object in space, to reach out smoothly and quickly for the object, and to shape its hand for grasping, deciding whether to use the whole hand or the finger and thumb and how much pressure to apply, and so on You get the idea Better let a human it, because all that fancy equipment comes standard on the basic model Now you see why so much of the brain is concerned with the sensory and motor components of movement It is a wonder that we have enough left over for the demands of learning, intelligence, and consciousness, but as you will see in the remaining chapters, we do Summary The Body Senses • The body senses include proprioception, which tells us about the position and movement of our limbs and body; the skin senses, which inform us about the conditions in the periphery of our body; and the vestibular sense, which contributes information about head position and movement and helps us maintain balance • The skin senses—touch, warmth, cold, and pain—tell us about conditions at the body surface and about objects in contact with our body • The body senses are processed in a series of structures in the primary and secondary somatosensory cortex and in the posterior parietal cortex, with several similarities to visual processing Pain processing also extends into additional areas • In their quest to find better ways of relieving pain, researchers have learned how the nervous system detects painful stimulation and found that the body has its own ways of relieving pain Chronic pain presents particularly difficult challenges Movement • There are three types of muscles: cardiac (heart); smooth (internal organs); and skeletal muscles, which move the body by tugging against their attachments to bones • Spinal reflexes produce quick responses and provide postural adjustments Central pattern generators provide routines such as rhythmic walking movements • Cortical motor areas assess spatial and body information and construct movements by passing information through a succession of brain areas • The basal ganglia and cerebellum refine movements produced by the motor cortex • A number of diseases attack the motor system at various points of vulnerability Major causes that have been implicated are heredity, toxins, and autoimmune disorders ■ Study Resources For Further Thought • Of proprioception, the vestibular sense, pain, and the other skin senses, which do you think you could most afford to give up? Why? • If pain is beneficial, why does the body have pain relief mechanisms? • Imagine a robot with a humanlike body It is programmed to walk, reach, grasp, and so on It has visual and auditory capabilities, but no body senses What would its movement be like? • Judging by the examples given of movement disorders, what are the points of vulnerability in the motor system? Quiz: Testing Your Understanding Explain how endorphins relieve pain, describing the receptors and the pathway from the periaqueductal gray; include how we determine whether pain relief is endorphin based Walking barefoot, you step on a sharp rock You reflexively withdraw your foot, plant it firmly on the ground again, and regain your posture Describe these behaviors in terms of the sensory/pain mechanisms and reflexes involved Trace the progress of a movement through the parietal and frontal lobes, giving the names of the structures and a general idea of the processing in each Compare the symptoms, causes, and treatment options for Parkinson’s and Huntington’s diseases Select the best answer: Proprioception gives us information about a conditions at the surface of our skin b conditions in the internal organs c the position and movement of our limbs and body d balance and the head’s position and movement The skin senses include a touch, warmth, and cold b touch, temperature, and pain c touch, temperature, movement, and pain d touch, warmth, cold, and pain Sharp pain and dull pain are due primarily to a different kinds of injury b pain neurons with different characteristics c the passage of time d the person’s attention to the pain According to Melzack and Wall, pressing the skin near a wound reduces pain by a creating inhibition in the pain pathway b distracting attention from the injury c releasing endorphins d releasing histamine into the wound area Endorphins a activate the same receptors as opiate drugs b occupy receptors for pain neurotransmitters c block reuptake of pain neurotransmitter d inhibit brain centers that process pain emotion Both congenital pain insensitivity and chronic pain involve a developmental alterations of brain areas responsible for the emotion of pain b alterations in the myelination of pain fibers c gene-mediated alterations of pain sensitivity d variations in the amount of substance P available Research suggests phantom pain is due to a the patient’s anxiety over the limb loss b memory of the pain of injury or disease that prompted the amputation c activity in severed nerve endings in the stump d neural reorganization in the somatosensory area Without a posterior parietal cortex we would be most impaired in a moving b making smooth movements c orienting movements to objects in space d awareness of spontaneously occurring movements If the nerves providing sensory feedback from the legs were cut, we would a have to use vision to guide our leg movements b have trouble standing upright c lose strength in our legs d a and b e b and c 10 A monkey is presented a stimulus, and then must wait a few seconds before it can reach to the correct stimulus Activity in the secondary motor area during the delay suggests that this area a prepares for the movement b initiates the movement c executes the movement d all of these 11 Cells in the premotor cortex would be particularly involved when you a remember a visual stimulus during a delay period b catch a fly ball c start to play a series of notes on the piano d execute a movement 12 The primary motor cortex is most involved in a combining sensory inputs b planning movements c preparing movements d executing movements 13 The basal ganglia and the cerebellum produce a no movements b movements requiring extra force c reflexive movements d sequences of movements 14 Parkinson’s disease is characterized most by a deterioration of the myelin sheath b dancelike involuntary movements c deterioration of dopamine-releasing neurons d immune system attack on acetylcholine receptors 15 Results of removing the thymus gland suggest that myasthenia gravis is a(n) disease a genetic b autoimmune c virus-caused d degenerative Answers: c, 2 d, 3 b, 4 a, 5 a, 6 c, 7 d, 8 c, 9 d, 10 a, 11 b, 12 d, 13 a, 14 c, 15 b Online Resources The following resources are available at edge.sagepub.com/garrett4e Select your country, click on Student Resources, then Chapter Resources; then select this chapter Chapter Resources • Quiz • Flashcards • Animations • Web links from the text • Web resources On the Web You can access these websites from the Chapter Resources page; select this chapter and then click on Web links from the text (Bold items are links.) The Vestibular Disorders Association has information about vestibular problems and provides additional resources such as newsletters, books, and videotapes The American Pain Foundation offers information for pain patients, testimonials from people suffering pain from an assortment of causes, and links to numerous other pain sites The International Association for the Study of Pain has links to more technical resources on pain The In the News feature about monkeys learning to coordinate both hands of a computer avatar with their brains came from a ScienceNOW news article In BrainFacts.org’s Searching for Answers videos, patients and their families describe what it is like to live with Huntington’s disease, Parkinson’s disease, and amyotrophic lateral sclerosis (ALS, or Lou Gehrig’s disease) You can get information about a variety of movement disorders from the Neuromuscular Disease Center, National Parkinson Foundation, Huntington’s Disease Association, and National Multiple Sclerosis Society In an interview with Katie Couric, actor Michael J Fox talks about living with Parkinson’s disease and about his views on stem cell research A University of Sheffield news release describes the groundbreaking study that screened 2,000 potential drugs for Parkinson’s disease Chapter Updates and Biopsychology News For Further Reading Awakenings, by Oliver Sacks (Vintage Books, 1999), describes Dr Sacks’s early experiments in using L-dopa to treat the symptom of parkinsonism in patients with sleeping sickness The movie with Robin Williams was based on this book Phantoms in the Brain, by V S Ramachandran and Sandra Blakeslee (Harper Perennial, 1999), called “enthralling” by the New York Times and “splendid” by Francis Crick, uses numerous (often strange) cases to explain people’s perception of their bodies Wall and Melzack’s Textbook of Pain, edited by Stephen McMahon, Martin Koltzenburg, Irene Tracey, and Dennis Turk (Saunders, 6th ed., 2013), and The Massachusetts General Hospital Handbook of Pain Management, edited by Jane Ballantyne (Lippincott Williams and Wilkins, 3rd ed., 2005) are technical references on pain and pain management Oxford Textbook of Movement Disorders, by David Burn (Oxford University Press, 2013), covers the science of movement disorders, along with their diagnosis and treatment Key Terms antagonistic muscles basal ganglia body integrity identity disorder cardiac muscles central pattern generator (CPG) chronic pain deep brain stimulation (DBS) dermatome endorphins familial gate control theory Golgi tendon organs Huntington’s disease levodopa (L-dopa) Lewy bodies multiple sclerosis muscle spindles myasthenia gravis out-of-body experience Parkinson’s disease periaqueductal gray (PAG) phantom pain posterior parietal cortex premotor cortex primary motor cortex primary somatosensory cortex proprioception secondary somatosensory cortex skeletal muscles skin senses smooth muscles somatosensory cortex somatotopic map striatum substance P substantia nigra supplementary motor area vestibular sense ... Title: Brain and behavior QP360.G375 2 014 612 .8—dc23 2 014 007564 14 15 16 17 18 10 9 8 7 6 5 4 3 2 1 FOR INFORMATION: SAGE Publications, Inc 2455 Teller Road Thousand Oaks, California 913 20 E-mail: order@sagepub.com... The Biology of Sex and Gender CHAPTER 8 Emotion and Health PART III Interacting With the World CHAPTER 9 Hearing and Language CHAPTER 10 Vision and Visual Perception CHAPTER 11 The Body Senses and Movement PART IV... The Body Senses and Movement PART IV Complex Behavior CHAPTER 12 Learning and Memory CHAPTER 13 Intelligence and Cognitive Functioning CHAPTER 14 Psychological Disorders CHAPTER 15 Sleep and Consciousness Glossary