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Concise Learning and Memory

Concise Learning and Memory (eBook)

The Editor's Selection
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2010 | 1. Auflage
888 Seiten
Elsevier Science (Verlag)
9780080877860 (ISBN)
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The study of learning and memory is a central topic in neuroscience and psychology. Many of the basic research findings are directly applicable in the treatment of diseases and aging phenomena, and have found their way into educational theory and praxis. Concise Learning and Memory represents the best 30 chapters from Learning and Memory: A comprehensive reference (Academic Press March 2008), the most comprehensive source of information about learning and memory ever assembled, selected by one of the most respective scientists in the field, John H. Byrne. This concise version provides a truly authoritative collection of overview articles representing fundamental reviews of our knowledge of this central cognitive function of animal brains. It will be an affordable and accessible reference for scientists and students in all areas of neuroscience and psychology. There is no other single-volume reference with such authority and comprehensive coverage and depth currently available.

* Represents an authoritative selection of the fundamental chapters from the most comprehensive source of information about learning and memory ever assembled, Learning and Memory - A comprehensive reference (Academic Press Mar 2008)
* Representing outstanding scholarship, each chapter is written by a leader in the field and an expert in the topic area
* All topics represent the most up to date research
* Full color throughout, heavily illustrated
* Priced to provide an affordable reference to individuals and workgroups

The study of learning and memory is a central topic in neuroscience and psychology. Many of the basic research findings are directly applicable in the treatment of diseases and aging phenomena, and have found their way into educational theory and praxis.Concise Learning and Memory represents the best 30 chapters from Learning and Memory: A comprehensive reference (Academic Press March 2008), the most comprehensive source of information about learning and memory ever assembled, selected by one of the most respective scientists in the field, John H. Byrne. This concise version provides a truly authoritative collection of overview articles representing fundamental reviews of our knowledge of this central cognitive function of animal brains. It will be an affordable and accessible reference for scientists and students in all areas of neuroscience and psychology. There is no other single-volume reference with such authority and comprehensive coverage and depth currently available. - Represents an authoritative selection of the fundamental chapters from the most comprehensive source of information about learning and memory ever assembled, Learning and Memory - A comprehensive reference (Academic Press Mar 2008)- Representing outstanding scholarship, each chapter is written by a leader in the field and an expert in the topic area- All topics represent the most up to date research- Full color throughout, heavily illustrated- Priced to provide an affordable reference to individuals and workgroups

Front Cover 1
Concise Learning and Memory: The Editor's Selection 4
Copyright Page 5
Table of Contents 6
Contributors 10
Introduction 14
Chapter 1 A Typology of Memory Terms 18
1.1 Introduction 18
1.2 Broad Distinctions 19
1.2.1 Explicit and Implicit Memory 19
1.2.2 Conscious and Unconscious Forms of Memory 20
1.2.3 Voluntary and Involuntary Retention 21
1.2.4 Intentional and Incidental Learning and Retrieval 21
1.2.4.1 Intentional and incidental learning 21
1.2.4.2 Intentional and incidental retrieval 21
1.2.5 Declarative and Nondeclarative Memory 22
1.2.6 Retrospective and Prospective Memory 23
1.3 Types of Short-Term Memory 23
1.3.1 Sensory Memories 23
1.3.2 Short-Term Storage 24
1.3.3 Working Memory 24
1.3.4 Long-Term Working Memory 25
1.4 Varieties of Long-Term Memory 25
1.4.1 Code-Specific Forms of Retention 26
1.4.1.1 Visual–spatial memory 26
1.4.1.2 Imagery 26
1.4.1.3 Olfactory memory 26
1.4.1.4 Skill learning 26
1.4.1.5 Verbal memory 27
1.4.2 Forms of Explicit Memory 27
1.4.2.1 Episodic memory 27
1.4.2.2 Autobiographical memory 27
1.4.2.3 Semantic memory 28
1.4.2.4 Collective memory 29
1.5 Conclusions 30
References 30
Chapter 2 Declarative Memory System: Amnesia 32
2.1 Introduction 32
2.2 Etiology of Neurological Amnesia 33
2.3 Anatomy 33
2.4 The Nature of Amnesia 35
2.4.1 Impairment in Declarative Memory 35
2.4.2 Anterograde Amnesia 35
2.4.3 Remembering versus Knowing and Recollection versus Familiarity 36
2.4.4 Retrograde Amnesia 37
2.4.5 Spatial Memory 38
2.5 Spared Learning and Memory Abilities 38
2.5.1 Immediate and Working Memory 38
2.5.2 Nondeclarative Memory 39
2.5.2.1 Motor skills and perceptual skills 39
2.5.2.2 Artificial grammar learning 40
2.5.2.3 Category learning 40
2.5.2.4 Priming 40
2.5.2.5 Adaptation-level effects 41
2.5.2.6 Classical conditioning 41
2.5.2.7 Habit learning 41
2.6 Functional Amnesia 42
2.7 Summary 42
References 42
Chapter 3 Multiple Memory Systems in the Brain: Cooperation and Competition 44
3.1 Introduction 45
3.2 Inferring Information Type from Learned Behavior 46
3.2.1 The Rigorous Study of Learning 46
3.2.2 Theories of Learning 46
3.2.2.1 Stimulus-response (S-R) associations 46
3.2.2.2 Stimulus-stimulus (S-S) associations 46
3.2.2.3 Stimulus-reinforcer (S-Rf) associations 47
3.2.3 Reinforcers 47
3.2.4 Information Types: Relationships among Elements 48
3.3 Localization of Information Processing 48
3.3.1 Early Localization Attempts 48
3.3.2 HM and the Function of the Hippocampus 48
3.3.2.1 Attempts to replicate HM’s syndrome with animals 49
3.3.3 Contextual Retrieval 49
3.3.4 Spatial Learning 50
3.3.5 Memory and Habit 51
3.3.6 Declarative versus Procedural Memory 51
3.3.7 Double Dissociation of S-S and S-R Learning in Humans 52
3.3.8 Dissociation of Three Information Types in Rats 52
3.3.8.1 Win-shift task – hippocampus-based S-S memory 52
3.3.8.2 Win-stay task – caudate-based S-R memory 53
3.3.8.3 Conditioned cue preference task – amygdala-based S-Rf memory 54
3.3.8.4 Dissociation by damaging brain structures 54
3.3.8.5 Dissociation by reinforcer devaluation 54
3.4 Information Processing Systems 56
3.4.1 Systems Concept 56
3.4.1.1 Systems process incompatible information 57
3.4.1.2 Systems are internally specialized 57
3.4.1.3 Coherence: Some representations are better than others 58
3.4.1.4 The learning-rate parameter 58
3.4.1.5 Cooperation and competition among systems 58
3.4.2 Information Processing and Memory 58
3.4.3 Dissociations of Memory Systems 59
3.5 S-S versus S-R Information Processing 59
3.5.1 Studies with Rats 59
3.5.1.1 Competition on the radial maze 59
3.5.1.2 Cross maze 59
3.5.1.3 Water maze 62
3.5.1.4 Medial versus lateral caudate nucleus 65
3.5.2 Studies with Humans 65
3.5.2.1 Spatial learning 65
3.5.2.2 Probabilistic classification 66
3.5.3 Summary: Competition and Coherence 67
3.6 S-S versus S-Rf Information Processing 67
3.6.1 Studies with Rats 68
3.6.1.1 CCP with spatial cues 68
3.6.1.2 Cooperation and competition in adjacent arms CCP learning 69
3.6.1.3 Path integration versus visual cue conditioning 69
3.6.1.4 Fear conditioning 70
3.6.1.5 Skeletal conditioning 72
3.6.2 Experiments with Humans 72
3.6.2.1 Conditioned preference 72
3.6.2.2 Conditioned fear 73
3.6.2.3 Skeletal responses 73
3.6.3 Summary 73
3.7 S-Rf versus S-R Information Processing 74
3.7.1 Win-Stay and CCP Learning 74
3.8 Summary and Some Outstanding Issues 74
3.8.1 Some Outstanding Issues 76
References 77
Chapter 4 Implicit Memory and Priming 82
4.1 Introduction 82
4.2 Influences of Explicit Versus Implicit Memory 83
4.3 Top-Down Attentional Effects on Priming 85
4.3.1 Priming: Automatic/Independent of Attention? 85
4.3.2 Priming: Modulated by Attention 86
4.3.3 Neural Mechanisms of Top-Down Attentional Modulation 88
4.4 Specificity of Priming 89
4.4.1 Stimulus Specificity 89
4.4.2 Associative Specificity 91
4.4.3 Response Specificity 91
4.5 Priming-Related Increases in Neural Activation 93
4.5.1 Negative Priming 93
4.5.2 Familiar Versus Unfamiliar Stimuli 94
4.5.3 Sensitivity Versus Bias 95
4.6 Correlations between Behavioral and Neural Priming 96
4.7 Summary and Conclusions 99
References 100
Chapter 5 Semantic Memory 104
5.1 Nature of the Representation 105
5.2 Network Approaches 105
5.3 Feature Analytic Approaches 109
5.4 Concept Learning and Categorization 111
5.5 Grounding Semantics 113
5.5.1 Grounding Semantics in Analyses of Large-Scale Databases 113
5.5.2 Grounding Semantics in Perceptual Motor Systems 114
5.6 Measuring Semantic Representations and Processes: Insights from Semantic Priming Studies 115
5.7 The Interplay Between Semantics and Episodic Memory 118
5.8 Representation and Distinctions: Evidence from Neuropsychology 120
5.8.1 Category-Specific Deficits 120
5.8.2 Semantic Dementia 121
5.9 Neuroimaging 122
5.10 Development and Bilingualism 124
5.11 Closing Comments 124
References 124
Chapter 6 Structural Basis of Semantic Memory 128
6.1 Introduction 128
6.2 Semantic Memory and the Medial Temporal Lobe Memory System 129
6.3 Cortical Lesions and the Breakdown of Semantic Memory 130
6.3.1 Object Concepts 130
6.3.2 Semantic Dementia and the General Disorders of Semantic Memory 131
6.3.3 Category-Specific Disorders of Semantic Memory 132
6.3.3.1 Models of category-specific disorders 132
6.3.3.2 Functional neuroanatomy of category-specific disorders 133
6.4 The Organization of Conceptual Knowledge: Neuroimaging Evidence 133
6.4.1 Neuroimaging of Semantic Memory 133
6.4.2 Object Concepts as Sensorimotor Property Circuits 134
6.4.3 Object Categories in the Brain 136
6.4.4 Two Case Studies in Category Representation: Animate Entities and Tools 136
6.4.5 Category-Related Activations in Property Regions Are the Bases of Conceptual Representations of Objects 138
6.4.5.1 Reason #1 to think that property regions are involved in conceptual-level processing: Activity in category regions transcends stimulus features 139
6.4.5.2 Reason #2 to think that property regions are involved in conceptual-level processing: Activations in property areas occur as property inferences 139
6.4.5.3 Reason #3 to think that property regions are involved in conceptual-level processing: Retrieving information from memory depends on reactivating 140
6.4.6 Learning about Objects by Building Property Circuits 141
6.5 Summary 142
References 142
Chapter 7 Episodic Memory: An Evolving Concept 146
7.1 Introduction 146
7.2 Historical Landmarks 146
7.2.1 A Taxonomic Distinction: Episodic and Semantic Memory 146
7.2.2 Subjective Awareness 147
7.2.3 The Remember/Know Paradigm 149
7.2.4 Retrieval Mode 149
7.2.5 Subjective Awareness, Self, and Time 150
7.2.6 The Episodic Memory System 150
7.3 Converging Evidence for the Episodic Memory System 151
7.3.1 Neuropsychology 152
7.3.2 Functional Neuroimaging 153
7.3.3 Development of Episodic Memory: The Magic Number 4 ± 1 155
7.4 Episodic Memory and Mental Time Travel 156
7.4.1 Neuropsychology 157
7.4.2 Functional Neuroimaging 157
7.4.3 Development of Episodic Future Thought 159
7.5 Is Episodic Memory Uniquely Human? 159
7.6 Concluding Remarks 161
References 161
Chapter 8 Working Memory 166
8.1 Introduction 166
8.2 The Working Memory Model 167
8.2.1 The Phonological Loop 167
8.2.1.1 Empirical phenomena 168
8.2.1.2 A computational model of the phonological loop 169
8.2.1.3 The phonological loop and language 170
8.2.1.4 Summary 172
8.2.2 The Visuospatial Sketchpad 172
8.2.2.1 Theory and empirical phenomena 172
8.2.2.2 Summary 174
8.2.3 The Central Executive 174
8.2.3.1 The supervisory attentional system 174
8.2.3.2 Complex memory span 175
8.2.4 The Episodic Buffer 176
8.2.5 Other Models of Working Memory 178
8.2.5.1 Attentional based models 178
8.2.5.2 The resource-sharing model 179
8.2.5.3 Time-based theories 180
8.2.5.4 Summary 180
8.3 Overview 180
References 181
Chapter 9 Prefrontal Cortex and Memory 186
9.1 Introduction 186
9.2 Anatomical Organization of the PFC 186
9.3 PFC and Working Memory 187
9.3.1 PFC Involvement in Working Memory: Short-Term Retention and Cognitive Control 187
9.3.2 Functional Imaging of Working Memory: Evidence for Functional Differentiation within PFC 188
9.4 Effects of Prefrontal Lesions on LTM Encoding and Retrieval 190
9.4.1 Neuropsychological Studies of Patients with Prefrontal Lesions 190
9.4.2 Recollection and Familiarity in Patients with Prefrontal Lesions 190
9.4.3 Theoretical Accounts of Memory Deficits following Prefrontal Lesions 191
9.5 Functional Neuroimaging of LTM Encoding and Retrieval 193
9.5.1 Subsequent Memory Effects and the PFC 193
9.5.2 PFC Activation during LTM Retrieval 196
9.5.3 Laterality of PFC Activation during LTM Encoding and Retrieval 198
9.6 Conclusions and Future Prospects 199
References 200
Chapter 10 Anatomy of the Hippocampus and the Declarative Memory System 206
10.1 Introduction 206
10.1.1 A Short History of the Anatomy of Declarative Memory 206
10.1.2 Overview of the Hippocampal System 206
10.1.2.1 Nomenclature 206
10.1.2.2 Location of the hippocampal system structures 209
10.1.2.3 Cross-species comparisons: Human, monkey, and rodent 210
10.2 The Parahippocampal Region 211
10.2.1 The Postrhinal Cortex 211
10.2.2 The Perirhinal Cortex 212
10.2.3 Entorhinal Cortex 213
10.2.4 Presubiculum 216
10.2.5 The Parasubiculum 217
10.3 The Hippocampal Formation 217
10.3.1 The Dentate Gyrus 218
10.3.2 The Hippocampus Proper 220
10.3.3 The Subiculum 221
10.4 Conclusions 223
10.4.1 The Flow of Sensory Information through the Hippocampal System 223
10.4.2 The Comparative Anatomy of the Hippocampal System 224
References 224
Chapter 11 Long-Term Potentiation: A Candidate Cellular Mechanism for Information Storage in the CNS 226
11.1 Hebb’s Postulate 227
11.2 A Breakthrough Discovery – LTP in the Hippocampus 228
11.2.1 The Hippocampal Circuit and Measuring Synaptic Transmission in the Hippocampal Slice 228
11.2.2 LTP of Synaptic Responses 231
11.2.3 Short-Term Plasticity: PTP and PPF 233
11.3 NMDA Receptor Dependence of LTP 233
11.3.1 Pairing LTP 234
11.3.2 Dendritic Action Potentials 237
11.4 NMDA Receptor-Independent LTP 238
11.4.1 200-Hz LTP 239
11.4.2 TEA LTP 239
11.4.3 Mossy Fiber LTP in Area CA3 239
11.5 A Role for Calcium Influx in NMDA Receptor-Dependent LTP 241
11.6 Presynaptic versus Postsynaptic Mechanisms 241
11.7 LTP Can Include an Increased Action Potential Firing Component 243
11.8 Temporal Integration Is a Key Factor in LTP Induction 246
11.9 LTP Can Be Divided into Phases 247
11.9.1 E-LTP and L-LTP – Types versus Phases 248
11.10 Spine Anatomy and Biochemical Compartmentalization 250
11.11 LTP Outside the Hippocampus 251
11.12 Modulation of LTP Induction 252
11.13 Depotentiation and LTD 252
11.14 Summary 255
References 255
Chapter 12 LTD – Synaptic Depression and Memory Storage 258
12.1 Introduction 258
12.2 LTD of the Hippocampal Schaffer Collateral-CA1 Synapse 259
12.3 Theoretical Framework 260
12.4 NMDAR-Dependent LTD 261
12.4.1 Induction by Calcium 261
12.5 The Role of Calcium-Dependent Enzymatic Reactions 263
12.5.1 Expression Mechanisms 265
12.6 Modulation of LTD 267
12.7 mGluR-Dependent LTD 268
12.7.1 Induction 268
12.7.2 Expression 269
12.8 Depotentiation 270
12.8.1 Time-Sensitive Depotentiation 270
12.8.2 Time-Insensitive Depotentiation 271
12.9 LTD of the Cerebellar Parallel Fiber–Purkinje Cell Synapse 271
12.10 Cerebellar Anatomy and Some Useful Models 272
12.11 The Role of the Cerebellum in Associative Eyeblink Conditioning 274
12.12 Potential Cellular Substrates of Associative Eyeblink Conditioning 275
12.13 Parallel Fiber LTD Induction 276
12.13.1 Parametric Requirements 276
12.13.2 Climbing Fiber Signals 276
12.13.3 Parallel Fiber Signals 278
12.13.4 Second Messengers 279
12.14 Parallel Fiber LTD Expression 280
12.15 Another Type of Cerebellar LTD: Climbing Fiber LTD 281
12.16 Interactions Between LTP and LTD at Parallel Fiber Synapses 282
12.17 Comparison of Bidirectional Plasticity at Hippocampal and Cerebellar Synapses 283
12.18 Is LTD of the Parallel Fiber–Purkinje Cell Synapse Involved in Motor Learning? 284
12.19 Conclusion 286
References 287
Chapter 13 Activity-Dependent Structural Plasticity of Dendritic Spines 298
13.1 Introduction 298
13.2 Brief Historical Perspective 298
13.3 The Structure and Function of Dendritic Spines 299
13.4 The Development of Dendritic Spines 301
13.5 Structural Plasticity of Dendritic Spines Induced by Synaptic Activity: Homeostatic Plasticity, LTP, and LTD 302
13.5.1 Ongoing Synaptic Activity 303
13.5.2 Homeostatic Plasticity 303
13.5.3 Long-Term Potentiation 304
13.5.4 Long-Term Depression 306
13.6 Structural Plasticity of Dendritic Spines Induced by Experience and Behavioral Learning 306
13.7 Structural Plasticity of Dendritic Spines Induced by Neuromodulators: Ovarian Hormones and Neurotrophins 307
13.7.1 Estradiol 308
13.7.2 Brain-Derived Neurotrophic Factor 309
13.8 BDNF, MeCP2, and Dendritic Spine Pathologies in Rett Syndrome 311
13.9 Final Considerations 314
References 314
Chapter 14 Plasticity of Intrinsic Excitability as a Mechanism for Memory Storage 324
14.1 Introduction 324
14.2 Changes in Intrinsic Excitability Produced by Learning and Experience 324
14.2.1 Invertebrate Models 324
14.2.2 Vertebrate Models 326
14.3 Activity-Dependent Modulation of Intrinsic Excitability 328
14.4 Plasticity of Intrinsic Excitability as a Mechanism for Memory Storage: Hypotheses and Lines of Evidence 330
14.5 Summary 331
References 331
Chapter 15 Neural Computation Theories of Learning 334
15.1 Introduction 334
15.2 Hebbian Learning 335
15.3 Unsupervised Hebbian Learning 336
15.4 Supervised Learning 337
15.5 Reinforcement Learning 339
15.6 Spike-Timing Dependent Plasticity 340
15.7 Plasticity of Intrinsic Excitability 342
15.8 Homeostatic Plasticity 343
15.9 Complexity of Learning 343
15.10 Conclusions 345
References 345
Chapter 16 Computational Models of Hippocampal Functions 348
16.1 Introduction 348
16.2 A Theory of Hippocampal Function 349
16.2.1 Systems-Level Functions of the Hippocampus 349
16.2.1.1 Evidence from the effects of damage to the hippocampus 349
16.2.1.2 The necessity to recall information from the hippocampus 349
16.2.1.3 Systems-level neurophysiology of the primate hippocampus 349
16.2.1.4 Systems-level anatomy 351
16.2.2 The Operation of Hippocampal Circuitry as a Memory System 351
16.2.2.1 Hippocampal circuitry 351
16.2.2.2 Dentate granule cells 352
16.2.2.3 CA3 as an autoassociation memory 355
16.2.2.4 CA1 cells 364
16.2.2.5 Backprojections to the neocortex – a hypothesis 365
16.2.2.6 Backprojections to the neocortex – quantitative aspects 366
16.3 Comparison with Other Theories of Hippocampal Function 367
References 369
Chapter 17 Neurobiology of Procedural Learning in Animals 374
17.1 Introduction 374
17.2 The Neural Bases of Procedural Learning: Emergence of the Dorsal Striatal Hypothesis 375
17.3 Dorsal Striatum and Procedural Learning: Dissociation Lesion Experiments 375
17.4 The Dorsal Striatum and Procedural Memory Revisited: Functional Heterogeneity 380
17.5 Dorsal Striatum and Procedural Learning: Pharmacological Experiments 380
17.5.1 Dopamine 381
17.5.2 Glutamate 382
17.5.3 Acetylcholine 383
17.6 Procedural Learning Beyond the Dorsal Striatum: Amygdala and Stimulus-Affect Associations 384
17.7 Conclusions 385
References 385
Chapter 18 Sensitization and Habituation: Invertebrate 390
18.1 Introduction 390
18.2 Habituation and Sensitization in Aplysia 391
18.2.1 Aplysia Withdrawal Reflexes and Underlying Neural Circuits 391
18.2.2 Habituation 392
18.2.2.1 Short-term depression of Aplysia sensorimotor synapses 394
18.2.2.2 Long-term depression of Aplysia sensorimotor synapses 395
18.2.3 Sensitization 396
18.2.3.1 Short-term sensitization 396
18.2.3.2 Long-term sensitization 398
18.2.3.3 Other temporal domains for the memory of sensitization 400
18.3 Habituation and Sensitization in Other Invertebrates 401
18.3.1 Gastropod Molluscs 401
18.3.1.1 Tritonia 401
18.3.1.2 Land snail (Helix) 402
18.3.2 Arthropods 402
18.3.2.1 Crayfish (Procambarus clarkii) 402
18.3.2.2 Honeybee (Apis mellifera) 402
18.3.2.3 Drosophila melanogaster 403
18.3.3 Annelids 403
18.3.3.1 Leech 403
18.3.4 Nematoda 404
18.3.4.1 Caenorhabditis elegans 404
18.4 Emerging Principles 404
References 404
Chapter 19 Cellular Mechanisms of Associative Learning in Aplysia 412
19.1 Aplysia Classical Conditioning and Operant Conditioning 412
19.2 Classical Conditioning 412
19.2.1 Behavioral Studies 412
19.2.2 Neural Mechanisms of Aversive Classical Conditioning in Aplysia 413
19.2.3 Neural Mechanisms of Appetitive Classical Conditioning in Aplysia 414
19.3 Operant Conditioning 416
19.3.1 Behavioral Studies 416
19.3.2 Neural Mechanisms of Appetitive Operant Conditioning in Aplysia 416
19.4 Conclusions 417
References 418
Chapter 20 Procedural Learning: Classical Conditioning 420
20.1 Introduction 421
20.2 Classical Conditioning of the Eyeblink Response 422
20.2.1 The Nature of the Eyeblink Conditioned Response 422
20.2.2 Brain Systems Engaged in Eyeblink Conditioning 423
20.2.3 The Cerebellar System 423
20.2.3.1 Lesions 423
20.2.3.2 Recordings 424
20.2.4 The Pathways 424
20.2.4.1 The UR pathways 424
20.2.4.2 The CR pathway 425
20.2.4.3 The CS pathway 425
20.2.4.4 The US pathway 425
20.2.4.5 Conjoint activation of CS and US pathways 426
20.2.4.6 Reversible inactivation 426
20.2.5 Mechanisms of Memory Storage in the Interpositus Nucleus 427
20.2.6 Cerebellar Cortex 428
20.2.7 Eyeblink Conditioning and the Hippocampus 430
20.2.7.1 Trace conditioning 430
20.3 Classical Fear Conditioning 431
20.3.1 Nature of Conditional Fear 431
20.3.2 Brain Systems Engaged in Fear Conditioning 432
20.3.3 The Amygdalar System 432
20.3.3.1 Lesions 432
20.3.3.2 Measures of neuronal activity 432
20.3.3.3 The pathways 433
20.3.3.4 Reversible inactivation 434
20.3.3.5 Mechanisms of storage in the basolateral amygdala complex 434
20.3.4 Fear Conditioning and the Hippocampus 435
20.3.4.1 Contextual fear conditioning 435
20.3.4.2 Trace fear conditioning 436
20.3.4.3 Recent versus remote fear memories 436
20.4 Interactions Between Conditioned Fear and Eyeblink Conditioning: The Two-Stage Hypothesis 437
20.5 Conclusions 437
References 438
Chapter 21 Neural and Molecular Mechanisms of Fear Memory 446
21.1 An Overview of Pavlovian Fear Conditioning 447
21.2 The Amygdala and Fear Conditioning 447
21.2.1 The Neuroanatomy of Fear 447
21.2.2 Synaptic Plasticity in the Amygdala and Fear Conditioning 448
21.3 LTP as a Mechanism of Fear Learning 448
21.3.1 Why is LTP Important? 448
21.3.2 The ‘Consolidation’ of LTP – E-LTP Versus L-LTP 450
21.4 Biochemical Mechanisms of Fear Memory Formation and Consolidation 450
21.4.1 Short-Term Fear Memory Formation – Glutamatergic Signaling, CaMKII Activation, and AMPAR Trafficking in the Amygdala 451
21.4.1.1 NMDA receptors 451
21.4.1.2 Ca2+/calmodulin-dependent protein kinase 451
21.4.1.3 Metabotropic glutamate receptors and protein kinase C 453
21.4.1.4 AMPA receptor regulation and trafficking 454
21.4.2 Long-Term Fear Memory Formation – Protein Kinase Signaling and Transcriptional Regulation in the Amygdala 454
21.4.2.1 L-VGCCs 454
21.4.2.2 Protein kinase A and mitogen-activated protein kinase 455
21.4.2.3 Neurotrophin signaling 455
21.4.2.4 Transcriptional regulation and macromolecular synthesis 457
21.4.3 A Presynaptic Component to Fear Learning? 458
21.4.3.1 Nitric oxide signaling and fear learning 458
21.5 Is the Lateral Amygdala an Essential Locus of Fear Memory Storage? 459
21.5.1 An Alternative View of the Amygdala and Fear Conditioning 459
21.5.2 A New Strategy for Tracking the Fear Engram 461
21.6 Distributed Versus Local Plasticity in the Amygdala 461
21.6.1 Distributed Plasticity within the LA 461
21.6.2 Distributed Plasticity within Amygdala Nuclei 463
21.7 Summary: A Model of Fear Memory Acquisition and Consolidation in the Amygdala 465
21.8 Beyond ‘Simple’ Fear Conditioning 466
21.8.1 Contextual Fear Conditioning 466
21.8.2 Fear Extinction 467
21.8.3 Retrieval and ‘Reconsolidation’ of Fear Memories 469
21.8.4 Instrumental Fear Learning 470
21.8.5 Memory Modulation by the Amygdala 470
21.9 Fear Learning in Humans 472
21.9.1 The Human Fear Learning System – Lesion and fMRI Studies 472
21.9.2 Instructed Fear – Using the High Road 472
21.9.3 Declarative Memory Formation and the Amygdala 473
21.10 Conclusions 473
References 473
Chapter 22 Conditioned Taste Aversion and Taste Learning: Molecular Mechanisms 482
22.1 Introduction 482
22.2 Measuring Taste Learning, Memory, and Consolidation: The Behavioral Paradigms 483
22.3 Neuroanatomy of Taste and Conditioned Taste Aversion Learning 484
22.4 Long-Term Potentiation in the Insular Cortex 486
22.5 Processing of Taste in the Gustatory Cortex 487
22.6 Molecular Mechanisms of Taste Learning in the Taste Cortex 487
22.7 The Neurotransmitters in the Gustatory Cortex Involved in Taste Learning 488
22.8 The Role of the MAPK/ERK Pathway in the Gustatory Cortex 491
22.9 The Role of Translation Regulation in Taste Memory Consolidation 491
22.10 Modulation of Specific Protein/mRNA Expression During Taste Learning and Consolidation 492
22.11 Temporal Phases in Taste Learning 494
22.12 Summary and New Directions 495
References 497
Chapter 23 Theory of Reward Systems 500
23.1 Introduction 500
23.2 Reward Processes 501
23.2.1 Goal-Directed Actions and Behavioral Control 501
23.2.2 The Effect of Changes in Reward Value 501
23.2.3 Incentive Learning and the Encoding of Reward Value 503
23.2.4 Incentive Learning as an Emotional Process 505
23.2.5 Retrieving Reward Value 506
23.3 Secondary Reward 507
23.3.1 Sensory Versus Secondary Reward 508
23.3.2 Do Secondary Rewards Reward, Reinstate, or Reinforce? 509
23.4 Reward and the Anticipation of Reward 512
23.4.1 Pavlovian-Instrumental Interactions 512
23.4.2 The Two-Process Account of Reward Value 514
23.5 Summary and Conclusions 517
References 518
Chapter 24 The Molecular Mechanisms of Reward 520
24.1 Introduction 520
24.2 Researching Reward Processes: What Do We Mean by Reward and How Do We Measure It? 521
24.3 The Neural Circuitry of Reward 522
24.3.1 The Nucleus Accumbens 522
24.3.2 The Amygdala 524
24.3.3 The Prefrontal Cortex 524
24.3.3.1 The prelimbic cortex 524
24.3.3.2 The orbitofrontal cortex 525
24.4 Dopamine and Reward 526
24.5 Cellular and Molecular Targets of the Dopamine-Reward System: Insights from Drug Addiction 526
24.5.1 The CREB and Fos Families of TFs 528
24.5.2 Clock 531
24.6 The Role of CREB and .FosB in Response to Natural Rewards and Stress 531
24.7 Target Genes of CREB and .FosB 532
24.7.1 Dynorphin in the VTA-NAc Pathway 532
24.7.2 Cyclin-Dependent Kinase 5 534
24.7.3 Nuclear Factor Kappa B 534
24.7.4 Brain-Derived Neurotrophic Factor 534
24.7.4.1 The neurotrophic hypothesis of depression 535
24.7.4.2 BDNF within the VTA-NAc: Reward processing and addiction 535
24.7.5 Glutamate Receptors 536
24.8 Molecular Changes within the PFC 536
24.9 Beyond Corticolimbic Circuitry: A Role for Hypothalamic Feeding Peptides in Reward-Related Learning? 537
24.10 Overview 538
References 539
Chapter 25 Neurophysiology of Motor Skill Learning 544
25.1 Introduction 544
25.2 Definition of Motor Skill Learning 545
25.3 Central Nervous System Structures Involved in Motor Skill Learning 545
25.3.1 Cortical Motor Areas in Nonhuman Primates 545
25.3.2 Cortical Motor Areas in Rodents 546
25.3.3 Role of Somatosensory Cortex in Motor Skill Learning 547
25.4 Organization of Primary Motor Cortex and Its Role in Motor Skill Learning 547
25.4.1 Neurophysiological Changes in M1 Associated with Motor Skill Learning 548
25.4.2 Neuroanatomical Correlates of Motor Skill Training in M1 549
25.5 Secondary Motor Areas and Their Role in Motor Skill Learning 550
25.5.1 Role of the SMA in Motor Skill Learning 550
25.5.2 Two SMAs: Different Roles for SMA and Pre-SMA 551
25.5.2.1 Basic differences in physiology and anatomy of SMA/pre-SMA 551
25.5.2.2 Role of SMA/pre-SMA in learning of motor sequences 552
25.5.2.3 Role of SMA/pre-SMA in self-initiated versus externally guided movements 553
25.5.2.4 Shift-related cells in pre-SMA 554
25.5.2.5 Role of SMA in kinetics and dynamics of movement 554
25.5.3 Lateral Premotor Cortical Areas and Their Role in Motor Skill Learning 554
25.5.3.1 Comparative aspects of lateral premotor areas 554
25.5.3.2 Role of the ventral premotor cortex in motor control 555
25.5.3.3 Role of dorsal premotor cortex in motor control 556
25.5.3.4 Direct comparison of ventral and dorsal premotor cortex response properties 556
25.5.3.5 Role of dorsal and ventral premotor cortex in motor skill learning 556
25.5.3.6 Learning through observation: role of premotor cortex 556
25.5.4 CMAs and Their Role in Motor Behavior 557
25.6 Phases of Motor Learning and Differential Activation of Motor Structures 557
25.7 Summary 558
References 558
Chapter 26 The Role of Sleep in Memory Consolidation 564
26.1 The Role of Sleep in Memory Consolidation 564
26.2 Definitions of Sleep and Memory 565
26.3 Stages of Sleep 565
26.4 Types of Memory 566
26.5 Procedural and Implicit Memory 567
26.5.1 Visual Discrimination Learning 567
26.5.2 Auditory Learning 569
26.5.3 Motor Memory 570
26.6 Episodic Memory 574
26.6.1 Emotional Episodic Memory 579
26.7 Electrophysiological Signatures 579
26.7.1 Sleep Spindles 579
26.7.2 Slow Waves 580
26.7.3 Hippocampal and Cortical Replay 581
26.7.4 Theta Rhythm 581
26.8 Neurohormones and Neurotransmitters 582
26.9 Concluding Comments 583
References 583
Chapter 27 Memory Modulation 588
27.1 Introduction 588
27.2 Endogenous Modulation of Consolidation 589
27.3 Modulating Influences of Adrenal Stress Hormones 589
27.3.1 Epinephrine 590
27.3.2 Glucocorticoids 591
27.3.3 Adrenergic-Glucocorticoid Interactions 591
27.3.4 Other Neuromodulatory Systems 593
27.4 Involvement of the Amygdala in Modulating Memory Consolidation 593
27.4.1 Noradrenergic Influences in the BLA 593
27.4.2 Glucocorticoid Influences in the BLA 596
27.4.3 Cholinergic Influences in the BLA 597
27.4.4 Other Neuromodulatory Influences in the BLA 598
27.5 Involvement of the Amygdala in Modulating Memory Extinction 598
27.6 Amygdala Interactions with Other Brain Systems in Modulating Memory 600
27.6.1 BLA Interactions with the Caudate Nucleus, Hippocampus, and Nucleus Accumbens 600
27.6.2 BLA–Cortical Interactions in Memory Consolidation 603
27.7 Amygdala Activity and Modulation of Human Memory Consolidation 605
27.8 Involvement of the Amygdala in Modulating Memory Retrieval and Working Memory 607
27.8.1 Memory Retrieval 607
27.8.2 Working Memory 609
27.9 Concluding Comments 610
References 611
Chapter 28 Memory-Enhancing Drugs 622
28.1 Background 622
28.1.1 Introduction 622
28.1.2 Early Studies of Drug Enhancement of Learning and Memory 622
28.1.3 The Posttraining Design 623
28.1.4 Posttraining Drug Enhancement of Memory 623
28.1.5 Memory Consolidation versus Memory Modulation 624
28.2 Peripheral Factors 624
28.2.1 Epinephrine 624
28.2.2 Glucose 626
28.2.3 ACTH and Glucocorticoids 629
28.2.4 Estrogen 630
28.3 Neurotransmitters 632
28.3.1 Overview 632
28.3.2 Acetylcholine 632
28.3.3 Norepinephrine 634
28.3.4 Glutamate 635
28.4 Intracellular Factors 635
28.4.1 Calcium Channel Blockers 635
28.4.2 Intracellular Molecular Targets 636
28.5 Conclusions 637
References 637
Chapter 29 Extinction: Behavioral Mechanisms and Their Implications 644
29.1 Six Recovery Effects after Extinction 645
29.1.1 Renewal 645
29.1.2 Spontaneous Recovery 647
29.1.3 Rapid Reacquisition 648
29.1.4 Reinstatement 649
29.1.5 Resurgence 649
29.1.6 Concurrent Recovery 650
29.1.7 Summary 651
29.2 What Causes Extinction? 651
29.2.1 Discrimination of Reinforcement Rate 651
29.2.2 Generalization Decrement 652
29.2.3 Inhibition of the Response 653
29.2.4 Violation of Reinforcer Expectation 654
29.3 Can Extinction Be Made More Permanent? 656
29.3.1 Counterconditioning 656
29.3.2 Other Behavioral Techniques to Optimize Extinction Learning 656
29.3.3 Chemical Adjuncts 657
29.3.4 Summary 659
29.4 Conclusions 659
References 660
Chapter 30 Reconsolidation: Historical Perspective and Theoretical Aspects 666
30.1 Historical Background: Thinking About Memory 666
30.1.1 Reconsolidation: A Hypothetical Construct 667
30.2 The Consolidation Hypothesis 667
30.2.1 Origins and Fate of the Consolidation Hypothesis 667
30.2.2 Challenges to the Consolidation Hypothesis 667
30.2.3 Amnesia and Forgetting as Retrieval Failure 668
30.3 Cue-Dependent Amnesia 669
30.3.1 Seminal Studies by Donald Lewis 669
30.3.2 Behavioral Studies 670
30.4 Cue-Dependent Amnesia: Neurobiological Hypotheses 670
30.4.1 NMDA Receptors in Cue-Dependent Amnesia 671
30.4.2 Role of the Noradrenergic System 671
30.5 Rebirth of Reconsolidation 672
30.6 Neurobiological Substrates and Boundaries of Reconsolidation 672
30.6.1 Neurobiological Substrates 673
30.6.2 Boundaries of Reconsolidation 673
30.6.2.1 A note on the action of anisomycin 673
30.6.2.2 Permanence of cue-dependent amnesia? 673
30.6.2.3 Age and strength of the memory 674
30.6.2.4 Task- and species-related boundaries 674
30.6.2.5 A note on the problem with negative results 675
30.7 Beyond Cue-Dependent Amnesia: Retrieval Strengthens Memory 675
30.7.1 Cue-Dependent Enhancement 675
30.7.1.1 Enhancement by MRF stimulation 675
30.7.1.2 Enhancement by activation of the noradrenergic system 676
30.7.1.3 Enhancement by activation of PKA 677
30.7.2 Clinical Significance of Cue-Dependent Enhancement 677
30.8 New Look at Retrieval and ‘Reconsolidation’ 677
References 678
Chapter 31 Retrieval from Memory 682
31.1 Retrieval from Memory 682
31.2 Empirical Evidence 683
31.2.1 Changes in the Organism’s Internal State 683
31.2.2 Experimentally Induced Amnesias 685
31.2.3 Reconsolidation 686
31.2.4 Cue Competition and Outcome Competition 687
31.2.5 Interference between Cues and Outcomes Trained Apart 688
31.3 Theories of Memory Retrieval 691
31.3.1 Matching of Information as Critical for the Retrieval from Memory 691
31.3.2 The Comparator Hypothesis: A Retrieval-Focused View of Cue Competition 692
31.3.3 Bouton’s Retrieval Model of Outcome Interference 695
31.4 Neurobiology of Retrieval 697
31.5 Concluding Remarks 699
References 700
Chapter 32 False Memories 704
32.1 False Memory for Words: The Deese-Roediger-McDermott Paradigm 705
32.2 Eyewitness Suggestibility: The Misinformation Paradigm 708
32.3 Verbal Overshadowing 710
32.4 Misattributions of Familiarity 711
32.5 Imagination Inflation 713
32.6 Implanted Autobiographical Memories 715
32.7 Connections Across False Memory Paradigms 717
32.8 Conclusions 718
References 719
Chapter 33 Molecular Aspects of Memory Dysfunction in Alzheimer’s Disease 722
33.1 Introduction 723
33.2 Memory Impairment by AD-Related Molecules 723
33.2.1 APP and Aß 723
33.2.1.1 Aß and plaques 725
33.2.1.2 Soluble Aß oligomers 726
33.2.1.3 Neuronal dysfunction versus neuronal death 726
33.2.1.4 Other APP fragments 727
33.2.2 BACE 727
33.2.3 Presenilins 728
33.2.3.1 .-Secretase 728
33.2.3.2 .-Secretase-independent roles of presenilins 728
33.2.4 Tau 729
33.2.4.1 NFTs, neuronal death, and memory loss 729
33.2.4.2 Tangle-independent roles for tau 730
33.2.4.3 Tau phosphorylation and other posttranslational modifications 731
33.2.4.4 Tau and Aß 732
33.2.5 ApoE 732
33.2.5.1 Interactions between Aß and apoE 734
33.2.5.2 Aß-independent mechanisms for apoE4-induced neuronal impairments 734
33.2.6 a-Synuclein 735
33.3 Memory-Related Molecules in AD 735
33.3.1 Neurotransmitter Release 735
33.3.2 Receptors and Channels 737
33.3.2.1 NMDA receptors 737
33.3.2.2 AMPA receptors 738
33.3.2.3 Nicotinic acetylcholine receptors 740
33.3.2.4 Potassium channels 740
33.3.3 Calcium Signaling 741
33.3.3.1 Calcium channels 742
33.3.3.2 Calcium-binding proteins 743
33.3.3.3 Intracellular stores 744
33.3.4 Kinases 745
33.3.4.1 MAPKs 745
33.3.4.2 CaMKII 746
33.3.4.3 PKC 747
33.3.4.4 PKA 748
33.3.4.5 Fyn 749
33.3.4.6 Cdk5 749
33.3.5 Neurotrophic and Neuromodulatory Factors 750
33.3.5.1 BDNF 750
33.3.5.2 Reelin 751
33.3.6 Gene Expression 753
33.3.6.1 CREB 753
33.3.6.2 Arc/Arg3.1 753
33.4 Conclusions 755
References 756
Chapter 34 Developmental Disorders of Learning 772
34.1 Developmental Disorders of Learning: What Do They Actually Mean? 772
34.2 The Concept of Learning Disabilities 773
34.3 Definition 774
34.4 History 774
34.5 Epidemiology 775
34.6 Presentation and Diagnoses 777
34.7 Etiology 779
34.8 Relevant Theoretical Models and Considerations 780
34.9 Manifestation and Life Course 781
34.10 Treatment, Remediation, Intervention, and Prevention 782
34.11 Conclusion 783
References 783
Chapter 35 Angelman Syndrome 786
35.1 Introduction 786
35.2 Understanding the Genetics of AS 786
35.2.1 The Prevalence of AS 786
35.2.2 Maternal Imprinting and AS 787
35.2.3 The Ubiquitin Ligase Pathway 788
35.3 Modeling AS in a Mouse 788
35.3.1 Production of the AS Mouse Model 788
35.3.2 Characterization of the AS Mouse Model 789
35.3.2.1 Physical Similarities of AS and the Maternal Deficient Ube3a-Null Mouse 789
35.3.2.2 Cognitive Similarities of AS and the Maternal Deficient Ube3a-Null Mouse 790
35.3.2.3 Physiologic Similarities of AS and the Maternal Deficient Ube3a-Null Mouse 790
35.3.3 AS Mouse Hippocampal Physiology 790
35.4 Molecular Changes in the AS Mouse 791
35.5 CaMKII in Synaptic Plasticity and Memory Formation 791
35.5.1 Activation and Regulation of CaMKII 791
35.5.2 Regulation of CaMKII Activity in Synaptic Plasticity and Memory Formation 793
35.6 Genetic Rescue of the AS Phenotype 794
35.7 Proposed Mechanisms Underlying CaMKII Misregulation 794
35.8 Concluding Remarks 796
References 796
Chapter 36 Epigenetics – Chromatin Structure and Rett Syndrome 798
36.1 Introduction 798
36.2 Mechanisms of Epigenetic Marking 799
36.2.1 Epigenetic Marking of Histones 799
36.2.2 Histone Acetylation 800
36.2.3 Histone Methylation 801
36.2.4 Histone Ubiquitination 801
36.2.5 Histone Sumoylation 801
36.2.6 Histone Phosphorylation 801
36.2.7 Other Histone Modifications 801
36.2.8 DNA (Cytosine-5) Methylation 801
36.2.9 Epigenetic Modulation of Transcription 802
36.3 Epigenetic Mechanisms in Synaptic Plasticity 802
36.3.1 Transcription and Chromatin Structure 803
36.3.2 Chromatin Remodeling Enzymes and Synaptic Plasticity 803
36.3.3 Histone Acetylation and Synaptic Plasticity 805
36.3.4 Histone Acetylation and Seizure 805
36.3.5 Epigenetics in Plasticity and Seizure – Conclusions 806
36.4 Epigenetics in Memory Formation 806
36.4.1 Chromatin Remodeling Enzymes and Memory Storage 807
36.4.2 Histone Acetylation and Memory Storage 807
36.4.3 Factor Acetylation and Memory Storage 808
36.4.4 DNA Methylation and ‘Lifetime’ Memory Storage 809
36.4.5 Epigenetics in Memory Formation – Conclusions 809
36.5 Epigenetics in Cognition: Rett Syndrome 809
36.6 Conclusions 812
References 812
Chapter 37 Neurogenesis 818
37.1 Introduction 818
37.2 Stem Cells in the Adult Brain 819
37.2.1 Neural Stem Cells in vitro 819
37.2.1.1 Culturing of neural stem cells 819
37.2.1.2 Proliferation and differentiation of NSCs 820
37.2.2 Neural Stem Cells in vitro 820
37.2.2.1 The hippocampal neurogenic niche 820
37.2.3 Neurogenesis in Nonneurogenic Areas Following Manipulation 822
37.3 Maturation of Adult-Born Granule Cells 822
37.3.1 Molecular Maturation and Identification of Adult-Born Granule Cells 822
37.3.2 Electrophysiology of Maturing AGCs 823
37.3.2.1 Techniques used in characterizing maturation stages of AGCs 824
37.3.2.2 Depolarizing GABA input 824
37.3.2.3 Spine formation and the onset of glutamatergic inputs 825
37.3.2.4 Timeline of projections to CA3 825
37.3.2.5 Regulation of maturation process 826
37.4 Systems Regulation of Adult Neurogenesis 826
37.4.1 Physiological Regulators of Adult Neurogenesis 826
37.4.1.1 Natural variation in adult neurogenesis 826
37.4.1.2 Environmental enrichment 827
37.4.1.3 Physical exercise 827
37.4.1.4 Learning 827
37.4.1.5 Aging 828
37.4.1.6 Neurotransmitters 828
37.4.1.7 Additional regulators of adult neurogenesis 828
37.4.2 Pathological Regulators of Adult Neurogenesis 829
37.4.2.1 Stress and depression 829
37.4.2.2 Seizures 829
37.4.2.3 Ischemia 830
37.4.2.4 Irradiation and inflammation 830
37.4.2.5 Neurodegenerative diseases and drugs 830
37.5 Function of Neurogenesis 830
37.5.1 Hippocampal Circuit Function and the Role of the DG 831
37.5.2 Theoretical Functions of Adult Neurogenesis 831
37.5.3 Experimental Evidence for Functional Significance of Adult Neurogenesis 832
37.5.3.1 Correlational evidence 832
37.5.3.2 ‘Causal’ evidence 833
37.6 Conclusions 834
References 834
Index 838

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