(BQ) Part 2 book “Brain and behavior” has contents: Learning and memory, intelligence and cognitive functioning, psychological disorders, sleep and consciousness.
Part IV Complex Behavior Chapter 12 Learning and Memory Chapter 13 Intelligence and Cognitive Functioning Chapter 14 Psychological Disorders Chapter 15 Sleep and Consciousness 12 Learning and Memory In this chapter you will learn • How and where memories are stored in the brain • What changes occur in the brain during learning • How aging and two major disorders impair learning Learning as the Storage of Memories Amnesia: The Failure of Storage and Retrieval APPLICATION: THE LEGACY OF HM Mechanisms of Consolidation and Retrieval Where Memories Are Stored Two Kinds of Learning Working Memory CONCEPT CHECK Brain Changes in Learning Long-Term Potentiation How LTP Happens Neural Growth in Learning Consolidation Revisited Changing Our Memories APPLICATION: TOTAL RECALL IN THE NEWS: RECALLING IT NOW HELPS YOU REMEMBER IT LATER CONCEPT CHECK Learning Deficiencies and Disorders Effects of Aging on Memory Alzheimer’s Disease IN THE NEWS: NATIONAL INSTITUTES OF HEALTH TEAMS WITH DRUG COMPANIES Korsakoff’s Syndrome CONCEPT CHECK In Perspective Summary Study Resources the age of 7, Henry Molaison’s life was forever changed by a seemingly A t minor incident: He was knocked down by a bicycle and was unconscious for 5 minutes Three years later, he began to have minor seizures, and his first major seizure occurred on his 16th birthday Still, Henry had a reasonably normal adolescence, taken up with high school, science club, hunting, and rollerskating, except for a 2-year furlough from school because the other boys teased him about his seizures “ Discovering the physical basis of learning in humans and other mammals is among the greatest remaining challenges facing the neurosciences —Brown, Chapman,Kairiss, & Keenan, 1988 ” After high school, he took a job in a factory, but eventually the seizures made it impossible for him to work He was averaging 10 small seizures a day and 1 major seizure per week Because anticonvulsant medications were unable to control the seizures, Henry and his family decided on an experimental operation that held some promise In 1953, when he was 27, a surgeon removed much of both of his temporal lobes, where the seizure activity was originating The surgery worked, for the most part: With the help of medication, the petit mal seizures were mild enough not to be disturbing, and major seizures were reduced to about one a year Henry returned to living with his parents He helped with household chores, mowed the lawn, and spent his spare time doing difficult crossword puzzles Later, he worked at a rehabilitation center, doing routine tasks like mounting cigarette lighters on cardboard displays Henry’s intelligence was not impaired by the operation; his IQ test performance even went up, probably because he was freed from the interference of the abnormal brain activity However, there was one important and unexpected effect of the surgery Although he could recall personal and public events and remember songs from his earlier life, Henry had difficulty learning and retaining new information He could hold new information in memory for a short while, but if he were distracted or if a few minutes passed, he could no longer recall the information When he worked at the rehabilitation center, he could not describe the work he did He did not remember moving into a nursing home in 1980, or even what he ate for his last meal And although he watched television news every night, he could not remember the day’s news events later or even recall the name of the president (Corkin, 1984; B Milner, Corkin, & Teuber, 1968) Henry’s inability to form new memories was not absolute Although he could not find his way back to the new home his family moved to after his surgery if he was more than two or three blocks away, he was able to draw a floor plan of the house, which he had navigated many times daily (Corkin, 2002) Over the years he became aware of his condition, and he was very insightful about it In his own words, Every day is alone in itself, whatever enjoyment I’ve had, and whatever sorrow I’ve had Right now, I’m wondering Have I done or said anything amiss? You see, at this moment everything looks clear to me, but what happened just before? That’s what worries me It’s like waking from a dream; I just don’t remember (B Milner, 1970, p 37) Over a period of 55 years, Henry would be the subject of a hundred scientific studies that he could not remember; he was known to the world as patient HM to protect his privacy In the next several pages, you will see why many consider HM’s surgery the most significant single event in the study of learning Learning as the Storage of Memories Some one-celled animals “learn” surprisingly well, for example, to avoid swimming toward a light where they have received an electric shock before I have placed the term learn in quotation marks because such simple organisms lack a nervous system; their behavior changes briefly, but if you take a lunch break during your subject’s training, when you return, you will have to start all over again Such a temporary form of learning may help an organism avoid an unsafe area long enough for the danger to pass or linger in a place where food is more abundant But without the ability to make a more or less permanent record, you could not learn a skill, and experience would not help shape who you are We will introduce the topic of learning by examining the problem of storage How does studying amnesia help us understand memory? Amnesia: The Failure of Storage and Retrieval HM’s symptoms are referred to as anterograde amnesia, an impairment in forming new memories (Anterograde means “moving forward.”) This was not HM’s only memory deficit; the surgery also caused retrograde amnesia, the inability to remember events prior to impairment His retrograde amnesia extended from the time of surgery back to about the age of 16; he had a few memories from that period, but he did not remember the end of World War II or his own graduation, and when he returned for his 35th high school reunion, he recognized none of his classmates Better memory for earlier events than for recent ones may seem implausible, but it is typical of patients who have brain damage similar to HM’s How far back the retrograde amnesia extends depends on how much damage there is and which specific structures are damaged FIGURE 12.1 Temporal Lobe Structures Involved in Amnesia (a) HM’s brain (top left) and a normal brain (below) You can see that the amygdala (A), hippocampus (H), and other structures labeled in the normal brain are partly or completely missing in HM’s brain (b) Structures of the medial temporal lobe, which are important in learning (The frontal lobe is to the left.) SOURCES: (a) From “HM’s Medial Temporal Lobe Lesion: Findings From Magnetic Resonance Imaging,” by S Corkin, D G Amaral, R G González, K A Johnson, and B T Hyman, 1997, Journal of Neurosicence, 17, pp 3964– 3979 Copyright © 1997 by the Society for Neuroscience Used with permission (b) Adapted with permission from “Remembrance of Things Past,” by D L Schacter and A D Wagner, Science, 285, pp 1503–1504 Illustration: K Sutliff © 1999 American Association for the Advancement of Science Reprinted with permission from AAAS HM’s surgery damaged or destroyed the hippocampus, nearby structures that along with the hippocampus make up the hippocampal formation, and the amygdala Figure 12.1 shows the location of these structures; because they are on or near the inside surface of the temporal lobe, they form part of what is known as the medial temporal lobe (remember that medial means “toward the middle”) Because HM’s surgery was so extensive, it is impossible to tell which structures are responsible for the memory functions that were lost Studies of patients with varying degrees of temporal lobe damage have helped determine which structures are involved in amnesia and, therefore, in memory Henry died in 2008 at the age of 82, but he continues to make a contribution, as the accompanying Application explains APPLICATION The Legacy of HM SOURCE: Wikimedia Commons Not only did Henry Moliason devote much of his life to numerous scientific investigations, but his brain will continue to be the subject of study for many years to come (Lafee, 2009) Soon after his death, Henry’s preserved brain was in a plastic cooler strapped in a seat on a flight from Boston to San Diego; in the next seat was Jacopo Annese, director of the Brain Observatory at the University of California at San Diego After several months of preparation, Annese and his colleagues dissected Henry’s brain into slices as thin as the width of a hair Each slice was microscopically photographed with such resolution that the data from each slice would fill 200 DVDs The data were then combined into a three-dimensional reconstruction of the brain, which is available online Scientists can navigate through it to the area of their interest and then zoom in to the level of individual neurons Ironically, the man who could not remember will never be forgotten 1 HM and His Brain The hippocampus consists of several substructures with different functions The part known as CA1 provides the primary output from the hippocampus to other brain areas; damage in that part of both hippocampi results in moderate anterograde amnesia and only minimal retrograde amnesia If the damage includes the rest of the hippocampus, anterograde amnesia is severe Damage to the entire hippocampal formation results in retrograde amnesia extending back 15 years or more (J J Reed & Squire, 1998; Rempel-Clower, Zola, Squire, & Amaral, 1996; Zola-Morgan, Squire, & Amaral, 1986) More extensive retrograde impairment occurs with broader damage or deterioration, like that seen in Alzheimer’s disease, Huntington’s disease, and Parkinson’s disease, apparently because memory storage areas in the cortex are compromised (Squire & Alvarez, 1995) “ Most memories, like humans and wines, do not mature instantly Instead they are gradually stabilized in a process referred to as consolidation —Yadin Dudai ” Mechanisms of Consolidation and Retrieval HM’s memory impairment consisted of two problems: consolidation of new memories and, to a lesser extent, retrieval of older memories Consolidation is the process in which the brain forms a more or less permanent physical representation of a memory Retrieval is the process of accessing stored memories—in other words, the act of remembering When a rat presses a lever to receive a food pellet or a child is bitten by a dog or you skim through the headings in this chapter, the experience is held in memory at least for a brief time But just like the phone number that is forgotten when you get a busy signal the first time you dial, an experience does not necessarily become a permanent memory; and if it does, the transition takes time Until the memory is consolidated, it is particularly fragile New memories may be disrupted just by engaging in another activity, and even older memories are vulnerable to intense experiences such as emotional trauma or electroconvulsive shock treatment (a means of inducing convulsions, usually in treating depression) Researchers divide memory into two stages, short-term memory and long-term memory Long-term memory, at least for some kinds of learning, can be divided into two stages that have different durations and occur in different locations (see Figure 12.2), as we will see later (McGaugh, 2000) FIGURE 12.2 Stages of Consolidation Making a memory permanent involves multiple stages and different processes SOURCE: From “Memory—A Century of Consolidation,” by J L McGaugh, Science, 287, pp 248–251 Reprinted with permission from AAAS An animal study clearly demonstrates that the hippocampus participates in consolidation Rats were trained in a water maze, a tank of murky water from which they could escape quickly by learning the location of a platform submerged just under the water’s surface (Figure 12.3; Riedel et al., 1999) Then, for 7 days the rats’ hippocampi were temporarily disabled by a drug that blocks receptors for the neurotransmitter glutamate Eleven days later—plenty of time for the drug to clear the rats’ systems—they performed poorly compared with control subjects (Riedel et al.) Researchers have been able to “watch” the consolidation happening in humans, using brain scans and event-related potentials Presenting words or pictures activated the hippocampus and adjacent cortex; how well the material was remembered later could be predicted from how much activation occurred in those areas during stimulus presentation (Figure 12.4; Alkire, Haier, Fallon, & Cahill, 1998; Brewer, Zhao, Desmond, Glover, & Gabrieli, 1998; Fernández et al., 1999) FIGURE 12.3 A Water Maze The rat learns to escape the murky water by finding the platform hidden just below the surface FIGURE 12.4 Hippocampal Activity Related to Consolidation The arrow is pointing to the hippocampal region Reds and yellows indicate positive correlations of activity at the time of learning with later recall; blues indicate negative correlations SOURCE: From “PET Imaging of Conscious and Unconscious Memory,” by M T Alkire, R J Haier, J H Fallon, and S J Barker, 1996, Journal of Consciousness Studies, 3, pp 448–462 Animals that were given the glutamate-blocking drug at the time of testing instead of immediately after training also had impaired recall in the water maze, indicating that the hippocampus has a role in retrieval as well as consolidation Researchers have used PET scans to confirm that the hippocampus also retrieves memories in humans (D L Schacter, Alpert, Savage, Rauch, & Albert, 1996; Squire et al., 1992) Figure 12.5 shows increased activity in the hippocampi while the research participants recalled words learned during an experiment The involvement of the hippocampus in retrieval seems inconsistent with HM’s ability to recall earlier memories But the memories that patients with hippocampal damage can recall are of events that occurred at least 2 years before their brain damage Many researchers have concluded that the hippocampal mechanism plays a time-limited role in consolidation and retrieval, a point we will examine shortly This diminishing role of the hippocampus would explain why older memories suffer less than recent memories after hippocampal damage FIGURE 12.5 Hippocampal Activity in the Human Brain During Retrieval (a) As participants tried to recall visually presented words that had been Pharmacological treatment of drug addiction, 150 Phase difference, 278 Phencyclidine (PCP), 139 Phenotype, 9 Phenylketonuria, 422 Pheromones, 204, 204–205 Phobia, 467 Phonological hypothesis, 287 Photopigments, 306 Photoreceptors, 306 Phototherapy, 462 Phrenology, 6, 7 (figure) Physical model of behavior, 4–5 Physiological psychology See Biopsychology Pigment mixing, 312 Pineal gland, 66, 67 (figure), 69 (figure) Pinel, Philippe, 442 (figure) Pinker, Steven, 290 Pinna, 266, 267 (figure) Pi-Sunyer, Xavier, 174 Pitch, 265 Pitt, Brad, 328 Pituitary gland, 66, 67 (figure), 162 (figure) Place cells, 379, 379 (figure) Place theory, 272–275 Plagiarism, in research, 116 Planum temporale, 287 Plaques, 391 Plasticity, 78 Plateau phase, 199 Pluripotent, 86 Polarization, 28 Polygenic, 9 Pons, 67 (figure), 69, 69 (figure), 162 (figure), 350 (figure) Positive symptoms, 445 Positron emission tomography (PET), 108, 109 (figure), 249 (figure), 286 (figure) Postcentral gyrus, 60 (figure) Posterior, 61–62, 69 (figure) Posterior parietal cortex, 65, 325 (figure), 343–346, 344 (figure), 357 (figure) Postsynaptic integration, 39–40 Postsynaptic neuron, 36, 36 (figure) Posttraumatic stress disorder (PTSD), 467–468 Prader-Willi syndrome, 160, 173 Precentral gyrus, 60 (figure), 62 Predator control, through learned taste aversion, 167 Predatory aggression, 250 Prefrontal cortex, 60 (figure), 62–63 emotion and, 237–238, 239 movement and, 357–358 Prefrontal parietal network, 500 Premotor cortex, 356, 357 (figure), 358, 359 (figure) Prenatal hormones, and the brain, 209–210 Prenatal influences, and sexual orientation, 221–223 Preoptic area, 162, 162 (figure) Prescientific psychology, and biopsychology, 3–4 Presynaptic neurons, 36, 36 (figure), 45 presynaptic axon, 36 (figure) presynaptic excitation, 41 presynaptic inhibition, 41 presynaptic terminal, 38 (figure) Price, Jill, 388 Primary auditory cortex, 284 (figure) Primary motor area, 357 (figure) Primary motor cortex, 62, 344 (figure), 356, 357 (figure), 360–361 Primary somatosensory cortex, 65, 344 (figure), 345, 357 (figure) Primary visual cortex, 282 (figure), 284 (figure), 325 (figure) Processing efficiency (brain), and intelligence, 410 Processing speed (brain), and intelligence, 409 Projection areas, 65 Proliferation, of the nervous system, 76 Proprioception, 340 Prosody, 289 Prosopagnosia, 327, 328 (figure) Prosthesis, 353, 360 Protein kinase M zeta, 386 Psilocin, 138 Psilocybin, 138 Psychedelic drugs, 138–139 Psychoactive drugs, 130–141 depressants, 132–134 marijuana, 140–141 opiates, 131–132 psychedelics, 138–139 stimulants, 134–138 See also Addiction Psychobiology See Biopsychology Psychological dependence, 141 Psychological disorders, 439–478 ability to cope with, 440 (figure) affective disorders, 454–467 anxiety disorders, 467–470 obsessive-compulsive disorder (OCD), 470–474 schizophrenia, 441–454 Psychology, prescientific, and biopsychology, 3–4 Psychomotor stimulant, 139 Psychosis, 441 Psychosurgery, 63 PTSD (posttraumatic stress disorder), 467–468 Pupil, 306 (figure) Pure sounds/tones, 266, 266 (figure) Putamen, 361 (figure) Raderscheidt, Anton, 331 Radial arm maze, 381 (figure) Radial glial cells, 76 Raine, Adrian, 252 Raphé nuclei, 492, 493 (figure) Rapid eye movement (REM) sleep, 461, 488 Rate law, 33 Raven Progressive Matrices, 405, 417 Reading, impairment of, 286–288 Recall, 379 (figure), 389 Receptive aphasia, 283 Receptive field, 307, 315 (figure), 319 (figure), 359 (figure) Receptors, 264, 306 (figure), 341 (figure) Recessive allele, 9 Reconsolidation, of memories, 388–389 Rectum, 169 (figure) Reeve, Christopher, 85–86, 85 (figure) Reflex, 71 Refractory periods, 33 Refractory phase, 199 Regeneration, 82 Reimer, David, 217, 217 (figure) Relational memory, 381 Relationship studies, comparison of, 114 (table) Relative refractory period, 33 REM sleep behavior disorder, 498 functions of, 488–489 Reorganization, 80, 84–85 Research, 95–126 addiction, 153 correlational studies, 97, 97–98 experimental studies, 97, 97–98 science and, 96–99 theory and, 96–99 See also Research ethics; Research techniques Research ethics, 115–121 animal research and, 117–120 gene therapy, 115, 120 human research and, 117 plagiarism and fabrication, 116 research participants, protecting welfare of, 116–120 stem cell therapy, 120–121 See also Research Research techniques, 99–115 brain activity, measuring and manipulating, 102–107 brain imaging techniques, 107–115 heredity, investigating, 112–115 light and electron microscopy, 102 neurons, staining and imaging, 99–101 See also Research Reserve hypothesis, 396 Resolution, 199 Resonance, 272 Resting potential, 28–29, 31 Restrictors, 187 Reticular formation, 69 Retina, 306–308, 306 (figure), 307 (figure), 309 (figure) Retinohypothalamic pathway, 486 Retinotopic map, 317 Retrieval, of memories, 376–378, 378 (figure), 389 Retrograde amnesia, 375 Reuptake, 41 Reverse-learning hypothesis, 491 Reward, 142 dopamine and, 143–146 neural basis of addiction and, 142–143 See also Addiction Reward dependent, 239 Rhodopsin, 306 Rhythms affective disorders and, 461–463 during waking and sleeping, 486–488 Rolls, Barbara, 166 Rolls, Edmund, 166 Round window, 267, 267 (figure) Rumbaugh, Duane, 293 Rushton, Philippe, 415 Russell, Bertrand, 444 Rutherford, William, 271 Ryan, Anna, 497 Sacks, Oliver, 65, 328, 474, 506 Sagittal plane, 61 (figure) Salience network, 470 Saltatory conduction, 34 Sapap3 gene, and excessive grooming, 472 (figure) Satiety, 164, 166–167 Satisfaction, sexual, 199 Savage-Rumbaugh, Sue, 293 Savant, 424, 425 (figure) Scanning electron microscope, 102, 103 (figure) Schacter, Stanley, 234 Schavan, Annette, 116 Schiff, Nicholas, 513 Schiller, Daniela, 468 Schizophrenia, 441–454 brain anomalies in, 448–454 characteristics of, 441–442 dopamine hypothesis for, 446–448 genes, search for, 444 heredity and, 443–445 pregnancy and, 452–453 two kinds of, 445–446 vulnerability model, 445 Schwann cells, 34, 34 (figure) Science experimental versus correlational studies, 97–98 research and, 96–99 theory and tentativeness in, 96–97 See also Research Sclera, 306 (figure) Seasonal affective disorder (SAD), 462–463 Secondary motor areas, and movement, 358–360 Secondary somatosensory cortex, 344 (figure), 345 Sedaris, David, 471 Sedative, 132 Selective serotonin reuptake inhibitors, 457 Self See Sense of self Semantic memory, 380 Semenya, Caster, 216 Semicircular canals, 267 (figure) Sensation, 265 Sensation seeking, 161 Sense of self, 500, 503–510 body image and, 505–506 disorders of self, 507–510 dissociative identity disorder, 507–510 memory and, 506 mirror neurons, 507 split brains, 507–510 theory of mind, 507 Senses See Body senses; Movement Sensorimotor system, 340 Sensory neurons, 25, 26 (figure) Sensory-specific satiety, 166–167 Septal nuclei, 235 (figure) Serotonin eating disorders and, 189–190 inhibition of aggressio, and, 253–254 levels of, and suicide, 466 (figure) Seth, Ankil, 500 Set point, 162 Severe combined immunodeficiency (SCID), 96 Sex, 198–205, 207 arousal and satisfaction, 199 biological determination of, 207–210 brain structures and neurotransmitters, 201–204 chromosomes and hormones, 207–209 odors, pheromones, and sexual attraction, 204–205 prenatal hormones and the brain, 209–210 testosterone, role of, 200–201 See also Biology of sex and gender; Sexual orientation Sexual development, 46 XY differences in, 213–214 Sexuality-at-birth hypothesis, 215 Sexually dimorphic nucleus (SDN), 202, 202 (figure) Sexual orientation, 218–224 biological model, social implications of the, 224 genetic and epigenetic influences, 219–221 prenatal influences on brain structure and function, 221–223 social influence hypothesis, 219 See also Biology of sex and gender; Sex Shapiro, Ehud, 10 Sharp pain, 347 Short-term memory, 377 Simner, Julia, 332 Simple cells, 320, 321 (figure) Simulation theory, 424 Singer, Jerome, 234 Sizemore, Chris, 508, 509 (figure) Skeletal muscles, 354 Skin conductance response (SCR), 238 Skin senses, 340–342 Sleep, 481–517 as a form of consciousness, 498–499 brain structures, of sleep and waking, 491–494 circadian rhythms, 484–486, 495 (figure) controls, 491–492 disorders, 494–498 disruption, and health, 244 memory and, 490–491 REM and non-REM, 488–489 rhythms, during waking and sleeping, 486–488 slow-wave, 487–488 waking and arousal, 492–494 See also Consciousness Sleep spindles, 487 Sleepwalking, 496 Slow-wave sleep, 487–488 Small intestine, 169 (figure) Smith, Christine, 378 Smooth muscles, 354 Snyder, Allan, 424 Sociability molecule, 427 Social factors, and stress, 247–248 Social impairment, and autism, 423–424 Social influence hypothesis, of sexual orientation, 219 Sodium-potassium pump, 24, 29 Soma (cell body), 24, 25 (figure), 26 (figure), 39 (figure) Somatic nervous system, 73 Somatosensory cortex, 65, 343–346, 352 (figure) Somatotopic map, 345 Sound localization, 278–281, 278 (figure), 279 (figure) Sowell, Elizabeth, 431 Spaced restudy, 389 Spatial frequency theory, of form vision, 322–323 Spatial memory, 380 Spatial resolution, 103 Spatial rotation task, 210 (figure) Spatial summation, 39, 40 (figure) Speciesism, 118 Specific nerve energies, doctrine of, 80 Spinal cord, 57 (figure), 67 (figure), 69–71, 71 (figure), 350 (figure), 355–356 Spinal nerves, 73 Split brains, 507–510 Splitters, 405 Sporadic autism, 429 Sports gender and, 216 head injuries and, 83 Squire, Larry, 378 SRY gene, 208 Staining and imaging neurons, 99–101 Stapes (stirrup), 266, 267 (figure) State-dependent learning, 509 Stem cells, 86, 86 (figure), 112 Stem cell therapy, 120–121 Stereotaxic techniques, 105–106, 106 (figure), 107 (figure) Sternberg, Robert, 405 Stimulants, 134–138 amphetamines, 136–137 caffeine, 138 cocaine, 135–136 nicotine, 137–138 Stirrup, 267 (figure), 268 (figure) Stomach, 169 (figure) Stress, 242–249 as an adaptive response, 242–243 definition, 242 negative effects of, 243–246 pain and, 248–249 social, personality, and genetic factors, 247–248 See also Emotion Stress-diathesis model, 466 Stretch reflex, 355 (figure) Striated muscles, 354 Striatum, 362, 380 Stroke, 82 Studies, experimental versus correlational, 97–98 Subfornical organ (SFO), 163, 164 (figure) Subgenual prefrontal cortex, 464 Substance P, 347 Substantia nigra, 68, 361 (figure), 362 Subthalamic nucleus, 361 (figure) Sudden cardiac death, 245 Suicide, and affective disorders, 466–467 Sulcus, 58, 58 (figure) Summation, spatial and temporal, 40 (figure) Superior, 61–62 Superior colliculi, 67 (figure), 68, 69 (figure) Supplementary motor area, 356, 357 (figure), 359 Suprachiasmatic nucleus (SCN), 162 (figure), 223, 484 (figure) Sweet taste, and obesity, 182 Sylvester, Chad, 469 Sympathetic ganglion chain, 74 Sympathetic nervous system, 73, 75 (figure) Synapse, 36–41, 36 (figure), 42 (figure) Synaptic activity regulating, 41 terminating, 40–41 Synaptic cleft, 36, 36 (figure) Syndactyly, 80, 81 (figure) Synesthesia, 304, 332 Tardive dyskinesia, 446 Taste aversion, learned, 167–168 hunger and, 165–168 obesity and, 182 preference, learned, 168 Taub, Edward, 118 T cells, 242 Tectorial membrane, 267, 268 (figure), 269 (figure) Telephone theory, 271 Temperature regulation, 162–163 Temporal lobe, 60 (figure), 65, 375 (figure) Temporal resolution, 103 Temporal summation, 39, 40 (figure) Terminals, 25, 25 (figure), 26 (figure) Testes, 208 Testosterone, 200–201, 250 (figure) Thalamus, 66, 67 (figure), 69 (figure), 164 (figure), 361 (figure), 493 (figure) Theory, 97 research and, 96–99 science and, 96–97 See also Research Theory of mind, 423, 424, 425, 507 Theory theory, 424 Theta waves, 487 Thiamine (B1), 397 Third interstitial nucleus of the anterior hypothalamus (INAH3), 223 Third ventricle, 68, 164 (figure) Thirst, 163–164 Three Faces of Eve, The, 508 Time differences, brain circuit for detecting, 279–280 Tirrell, Albert, 496 Tolerance, 130 Tononi, Giulio, 491 Tonotopic map, 272, 274 (figure) Tools, use of, 412 Topographically organized, 269 Total recall, 388 Tourette’s syndrome, 473, 474 (figure) Tower of Hanoi problem, 380, 380 (figure) Tracts, 56, 73 Transcranial direct current stimulation, 107 Transcranial magnetic stimulation (TMS), 98, 107, 107 (figure), 460 Transient receptor potential (TRP), 341 Transsexual, 211–212 Traumatic brain injury (TBI), 82 Trichromatic theory, of color vision, 311 Tricyclic antidepressants, 457 Tsai, Guochuan, 509 Tuberomamillary nucleus, 492, 493 (figure) Tuning curves, 273, 274 (figure) Twin studies, 16 (figure), 113, 443–444 Two-photon microscope, 102 Tympanic canal, 267, 268 (figure) Tympanic membrane, 266, 267 (figure), 268 (figure) Ultradian rhythms, 486 Unipolar depression, 455 Unipolar neuron, 26 (figure) Vaccines antidrug, 148 childhood, and autism, 428 Vagus nerve, 164 (figure) Ventral, 61 (figure) Ventral attention network, 469 Ventral horns, 71 Ventral prefrontal cortex, 464 Ventral root, 71 Ventral stream, 270, 325, 325 (figure) Ventral tegmental area, 68, 143 Ventricles, 68, 68 (figure), 448, 449 (figure) Ventrolateral preoptic nucleus, 492 Ventromedial hypothalamus, 162 (figure), 174, 202 Vesicles, 37 Vestibular canal, 268 (figure) Vestibular organs, 343 (figure) Vestibular sense, 342–343 Virtual reality, as treatment for anxiety disorders, 468 Visible spectrum, 304–305 Vision, 303–337 color vision, 311–316 form vision, 316–323 light, and the visual apparatus, 304–310 perception of objects, color, and movement, 323–333 restoring, 310 See also Visual perception, disorders of Visual acuity, 307 Visual analysis, pathways of, 324–326 Visual cortex, 60 (figure), 66, 317 (figure) Visual field, 308 Visual perception, disorders of, 326–331 color agnosia, 329 movement agnosia, 330 neglect and the role of attention in vision, 330–331 object and face agnosia, 326–329 See also Vision Visual word form area (VWFA), 328 Voineagu, Irene, 429 Volleying, 272, 272 (figure) Volley theory, 271 Voltage, 28 Vomeronasal organ (VNO), 205, 205 (figure) von Békésy, Georg, 272 von Helmholtz, Hermann, 6, 6 (figure), 272, 311 Voodoo death, 245 vos Savant, Marilyn, 404 Vulnerability, 14–16 Vulnerability model, and schizophrenia, 445 Wada technique, 289 Wakefield, Andrew, 116, 428 Waking arousal and, 492–493 rhythms during, 486–488 Wall, Patrick, 349 Water maze, 377 (figure) Wavelength coded, 329 Wechsler Adult Intelligence Scale, 406 Wernicke, Carl, 282 Wernicke-Geschwind model, of language, 284–286, 284 (figure) Wernicke’s aphasia, 283 Wernicke’s area, 60 (figure), 65, 282 (figure), 283–284, 284 (figure) Wever, Ernest, 270–271 White matter, 47 (figure), 58, 70 See also Cerebral cortex Whitestone, Heather, 264, 264 (figure), 275, 277 Wiesel, Thorsten, 319 Williams, Brad, 388 Winter birth effect, 451 Wisconsin Card Sorting Test, 448, 450 Withdrawal, 130 Wolffian ducts, 208 Word salad, 284 Working memory, 381–382 Writing, impairment of, 286–288 Wundt, Wilhelm, 3, 3 (figure) X-linked, 9 y Cajal, Santiago Ramón, 99 Yehuda, Rachel, 245 Young-Helmholtz theory, 311 Zeitgebers, 484 Zimmerman, Luke, and Down chromosomes, 421 (figure) Zygote, 9 ... (a) HM’s brain (top left) and a normal brain (below) You can see that the amygdala (A), hippocampus (H), and other structures labeled in the normal brain are partly or completely missing in HM’s brain. .. 12 Learning and Memory In this chapter you will learn • How and where memories are stored in the brain • What changes occur in the brain during learning • How aging and two major disorders impair learning... dendrites into the spines (Lisman et al., 20 02; Shi et al., 1999) In addition, an increase in dopamine unmasks previously silent synapses and, 12 to 18 hours later, initiates the growth of new synapses (C H Bailey, Kandel, & Si, 20 04)