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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, the biology of sex and gender,… and other contents.
Brain & Behavior Fifth Edition To Duejean taken from her family and friends by Alzheimer’s disease —Bob Garrett To my father You were the smartest man I’ve ever known I miss you every day —Gerald Hough Brain & Behavior An Introduction to Behavioral Neuroscience Fifth Edition Bob Garrett California Polytechnic State University, San Luis Obispo Gerald Hough Rowan University Contributions by Meghan C Kahn Indiana University Southeast Joshua S Rodefer Valdosta State University FOR INFORMATION: SAGE Publications, Inc 2455 Teller Road Thousand Oaks, California 91320 E-mail: order@sagepub.com SAGE Publications Ltd 1 Oliver’s Yard 55 City Road London EC1Y 1SP United Kingdom SAGE Publications India Pvt Ltd B 1/I 1 Mohan Cooperative Industrial Area Mathura Road, New Delhi 110 044 India SAGE Publications Asia-Pacific Pte Ltd 3 Church Street #10-04 Samsung Hub Singapore 049483 Copyright © 2018 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 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 5 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) How can we treat symptoms of Parkinson’s disease? Parkinson’s disease is typically treated by administering levodopa (L-dopa), which is the precursor for dopamine Parkinson’s tends to be more severe in men than in women, presumably because estrogen indirectly raises dopamine levels (Haaxma et al., 2007) Dopamine will not cross the blood-brain barrier but L-dopa will, and the brain converts it to dopamine Dopamine agonists can also be helpful, and even placebos increase dopamine release (de la FuenteFernández 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 L-dopa 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 Early attempts showed that implanted embryonic neural cells could survive in the striatum and produce dopamine (Figure 11.23; 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 three years but had disappeared at the end of five 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 3 level that could establish its effectiveness sufficiently for approval by the U.S Food and Drug Administration (FDA) (Denyer & Douglas, 2012) To avoid previous disappointments, the British company Oxford Biomedica has used a procedure called ProSavin to deliver a combination of three genes into the striatum to increase dopamine production there; all 15 drug-resistant patients improved in motor capability and maintained improvement for the full year of this phase 1/phase 2 safety and dosage trial (Palfi et al., 2014) These procedures are still in their infancy; we need to remember that the first several heart transplant operations failed, but they are almost routine today Figure 11.23 Transplanted Embryonic Cells in the Brain of a Parkinson’s Patient 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 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 11.21), have provided some improvement for patients who have difficulty using dopaminergic drugs (Cosgrove & Eskandar) Michael J Fox had such lesions, and they vastly improved his ability to control his movement (M J Fox, 2002) These two structures produce a rhythmic bursting activity like the rhythmic 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 More recently, physicians are turning to a less drastic procedure known as deep brain stimulation (DBS), in which electrical stimulation through implanted electrodes is used to trigger dopamine release in areas deprived of that neurotransmitter While effective, there is a higher risk of weight gain and sensitivity to the pleasurable aspects of food seen in some dopamine-increasing drugs (see the accompanying Application) 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 mild, infrequent 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.” The patient loses the ability to carry out daily activities Death usually follows within 15–30 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, whereas defective or degenerated neurons in the cortex probably account for the psychological symptoms (Figure 11.24; J B Martin, 1987; Tabrizi et al., 1999) 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 Application: Deep Brain Stimulation and Parkinson’s Disease Source: ALFRED PASIEKA/Science Photo Library/Getty Although almost 30 years old, an effective treatment for the motor tremors and repetitive movements seen in Parkinson’s disease patients continues to be a procedure called deep brain stimulation (DBS) The mechanism by which DBS works is to block electrical signals that are responsible for the tremors associated with Parkinson’s In this technique, neurosurgeons implant electrodes into the brain and run insulated wires under the skin down the neck into the upper chest area There, the wires are attached to a pacemaker-like device that is also implanted into the patient’s chest In this way, a precise set of electrical pulses can be sent to the target area (usually the basal ganglia) to “reset” activity in the brain area(s) and restore normal function After a set of stimulations, tremor usually dissipates within seconds (Blahak et al., 2009), whereas effective treatment for dystonia (uncontrollable repetitive muscle contractions) may take additional months of treatment So what does DBS do in the brain? There’s a lot of debate as to what exactly the stimulation does to improve motor function Early research concluded the stimulation temporarily knocked out neurons in the stimulation site (like a reversible lesion; Wichmann, Bergman, & DeLong, 1994), but later teams suggested the added electrical charges made dendritic inputs stronger (McIntyre, Grill, Sherman, & Thakor, 2004) Other findings suggest an increase in chemical neurotransmitters such as adenosine (Bekar et al., 2008) and dopamine (Gale et al., 2013) Improved motor functioning, allowing L-dopa reduction, has been reported for as long as 10 years (reviewed in Fasano, Daniele, & Albanese, 2012) Results are mixed regarding reducing 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%–16% of patients affected, possibly due to L-dopa reduction This improvement does carry some risk: Some studies have reported the onset of pathological gambling, hypersexuality, and compulsive eating Recent work has suggested that side effects of DBS of the subthalamic nucleus include increased impulsivity and sensitivity to food rewards, resulting in undesired weight gain, which indicates that the neurons and circuits play a role in multiple behaviors In addition, there is some loss of verbal fluency after DBS, and apathy increases in some patients 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 less than 26 repetitions of the bases cytosine, adenine, and guanine (CAG repeats; see Chapter 1) The more repeats the person has beyond 26, the earlier in life the person will succumb to the disease (F O Walker, 2007) 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 Numerous drugs are used to treat the various symptoms, including antidepressants and antipsychotics, but only one (Tetrabenazine) has been approved specifically for Huntington’s disease by the FDA 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 nine-month duration of the study and significantly reduced huntingtin protein levels for eight 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), but a recent method using human stem cells overexpressing neural growth factors has shown some promise in improving function in a mouse model (Pollock et al., 2016) Autoimmune Diseases Myasthenia gravis (MG) 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 MG was about 33%; now few patients die from the disease, thanks to improved treatment (Rowland, 2000a) Figure 11.24 Loss of Brain Tissue in Huntington’s Disease Source: Courtesy of Robert E Schmidt, Washington University 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 MG patients turned out to have 70%–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 11.25; Rowland, Hoefer, & Aranow, 1960) Remember from Chapter 2 that acetylcholinesterase breaks down acetylcholine at the synapse; these inhibitors increase the amount of available neurotransmitter at the neuronmuscle junction Although immune system therapy has sometimes been used (Shah & Lisak, 1993), removal of the thymus (thymectomy) has now become a standard treatment for MG (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%–17% (Ashour et al., 1995; Jaretzki et al., 1988) Multiple sclerosis (MS) 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 11.26) As a result, the person experiences muscular weakness, tremor, pain, 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 Effect of an Acetylcholinesterase Inhibitor on Myasthenia Gravis 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, 38, pp 547–560 Like myasthenia gravis, multiple sclerosis is an autoimmune disease Injecting foreign myelin protein into the brains of animals produces symptoms like those of MS (Wekerle, 1993), and T cells that are reactive to myelin proteins (see Chapter 8) have been found in the blood of MS patients (Allegretta, Nicklas, Sriram, & Albertini, 1990) A genome-wide study has implicated various immune system genes in MS (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 MS patients (H J Wagner et al., 2000), and patients more often had mumps or measles during adolescence (Hernán et al., 2001) Figure 11.26 The Brain of a Deceased Multiple Sclerosis Patient Source: Science Source Although many drugs are available to treat the various symptoms of the disease, only a few drugs modify the problematic immune activity in MS patients; these immune-suppressing drugs slow the progression but do not repair the harm already done A drug that blocks voltage-gated potassium channels, dalfampridine, helps demyelinated axons transmit signals by increasing the strength of action potentials; it improves motor performance, particularly walking (Jeffrey, 2010), but it can increase the risk of seizures (U.S Food and Drug Administration, 2012) In a multicenter stem cell study, 281 patients with progressive MS were treated by harvesting stem cells from their bone marrow, wiping out their immune systems using chemotherapy, and then injecting the stem cells back; 46% of the patients had no additional symptoms five years afterwards (Muraro et al., 2017) 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 330 What are the genetic and environmental causes of the movement disorders described in this chapter? In Perspective Unless we have a disorder like Michael J Fox does (described in the chapter introduction), 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 do 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 And when the system becomes damaged, even the easiest behaviors become quite difficult 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 Chapter 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 Several 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? Test 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 occurring 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 conditions at the surface of our skin conditions in the internal organs the position and movement of our limbs and body balance and the head’s position and movement The skin senses include touch, warmth, and cold touch, temperature, and pain touch, temperature, movement, and pain touch, warmth, cold, and pain Sharp pain and dull pain are due primarily to different kinds of injury pain neurons with different characteristics the passage of time the person’s attention to the pain According to Melzack and Wall, pressing the skin near a wound reduces pain by triggering inhibition in the pain pathway triggering pain messages from nearby areas releasing endorphins into the brain releasing histamine into the wound area Endorphins activate the same receptors as opiate drugs occupy receptors for pain neurotransmitters block reuptake of pain neurotransmitters inhibit brain centers that process pain emotion Both congenital pain insensitivity and chronic pain involve developmental alterations of brain areas responsible for the emotion of pain alterations in the myelination of pain fibers gene-mediated alterations of pain sensitivity variations in the amount of substance P available Research suggests phantom pain is due to the patient’s anxiety over the limb loss memory of the pain of injury or disease that prompted the amputation activity in severed nerve endings in the stump neural reorganization in the somatosensory area Without a posterior parietal cortex, we would be most impaired in moving making smooth movements orienting movements to objects in space awareness of spontaneously occurring movements If the nerves providing sensory feedback from the legs were cut, we would be able to walk but not run have trouble standing upright lose strength in our legs quickly lose muscle mass in our legs not be able to move our legs 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 prepares for the movement initiates the movement executes the movement all of these 11 Cells in the premotor cortex would be particularly involved when you remember a visual stimulus during a delay period catch a fly ball start to play a series of notes on the piano execute a movement 12 The primary motor cortex is most involved in combining sensory inputs planning movements preparing movements executing movements 13 The basal ganglia and the cerebellum produce no movements movements requiring extra force reflexive movements sequences of movements 14 Parkinson’s disease is characterized most by deterioration of the myelin sheath dancelike involuntary movements deterioration of dopamine-releasing neurons immune system attack on acetylcholine receptors 15 Results of removing the thymus gland suggest that myasthenia gravis is a(n) disease genetic autoimmune virus-caused degenerative Answers: c, 2 d, 3 b, 4 a, 5 a, 6 c, 7 d, 8 c, 9 b, 10 a, 11 b, 12 d, 13 a, 14 c, 15 b On the Web The following websites are coordinated with this chapter’s content You can access these websites from the SAGE edge Student Resources site; select this chapter and then click on Web Resources (Bold items are links.) C-Span archived a recording of Michael J Fox’s 1999 testimony before Congress In this video, he has not taken his daily L-dopa dose and, therefore, is exhibiting “off his L-dopa” symptoms 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 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 Todd Kuiken is now testing a prosthetic arm that includes sensors and stimulators to provide sensation of touch A new type of brain-controlled limb replacement, designed in collaboration between Johns Hopkins Medical School and the U.S Department of Defense DARPA, has been mounted directly to an amputee’s skeleton and can be controlled simply by thought Finally, Hugh Herr is using bioengineering techniques to design prosthetic limbs that are more natural in design and function For Further Reading Lucky Man, by Michael J Fox (Hyperion, 2002), details the actor’s initial diagnosis, struggle to balance life and work, and how he decided that helping others was more important than helping himself 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 (HarperPerennial, 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 and in current use at the hospital (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 327 basal ganglia 332 body integrity identity disorder 319 cardiac muscles 325 central pattern generator (CPG) 328 chronic pain 323 deep brain stimulation (DBS) 335 dermatome 317 endorphins 321 familial 333 gate control theory 322 Golgi tendon organs 328 Huntington’s disease 335 inflammatory soup 320 levodopa (L-dopa) 334 Lewy bodies 334 multiple sclerosis 337 muscle spindles 327 myasthenia gravis 337 out-of-body experience 319 Parkinson’s disease 333 periaqueductal gray (PAG) 322 phantom pain 324 posterior parietal cortex 318 premotor cortex 330 primary motor cortex 331 primary somatosensory cortex 317 proprioception 314 secondary somatosensory cortex 318 skeletal muscles 325 skin senses 314 smooth muscles 325 somatosensory cortex 332 somatotopic map 317 striatum 333 substance P 320 substantia nigra 333 supplementary motor area 331 vestibular sense 315 edge.sagepub.com/garrett5e SAGE edge offers a robust online environment featuring an impressive array of free tools and resources for review, study, and further exploration, keeping both instructors and students on the cutting edge of teaching and learning ... Chapter 7 • 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... Chapter 11 • 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... Chapter 1 • What Is Behavioral Neuroscience? The Origins of Behavioral Neuroscience Prescientific Psychology and the Mind -Brain Problem Descartes and the Physical Model of Behavior Helmholtz and the Electrical Brain