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Cover
1
Contents
8
Foreword
12
Preface
14
Acknowledgments
18
Chapter 1. Introduction„The Basics of Psychological Learning and Memory Theory
22
I. Introduction
22
II. Unconscious Learning
31
III. Conscious Learning„Subject to Conscious and Unconscious Recall
42
IV. Final Note„Will Molecular Studies Change the Way We Think about Learning Behavior?
45
References
46
Chapter 2. Rodent Behavioral Learning and Memory Models
48
I. Introduction
48
II. Behavioral Assessments in Rodents
49
III. Modern Experimental Uses of Rodent Behavioral Models
63
IV. Control Experiments
72
V. Summary
77
References
77
Chapter 3. The Hippocampus Serves a Role in Multimodal Information Processing, and Memory Consolidation
80
I. Introduction
80
II. Studying the Hippocampus
81
III. Hippocampal Function in Cognition
84
IV. Summary
106
References
106
Chapter 4. Long-Term Potentiation as a Physiological Phenomenon
110
I. Synapses in the Hippocampus„The Hippocampal Circuit
112
II. A Breakthrough Discovery„LTP in the Hippocampus
113
III. NMDA Receptor-Dependence of LTP
121
IV. NMDA Receptor-Independent LTP
129
V. A Role for Calcium Influx in NMDA Receptor-Dependent LTP
131
VI. Summary
133
References
133
Chapter 5. Complexities of Long-Term Potentiation
136
I. Introduction
136
II. Presynaptic Versus Postsynaptic Mechanisms
137
III. LTP Can Include an Increased AP Firing Component
146
IV. Temporal Integration in LTP Induction
149
V. LTP Can Be Divided into Phases
150
VI. Spine Anatomy and Biochemical Compartmentalization
161
VII. Summary
163
References
163
Chapter 6. The Biochemistry of LTP Induction
166
I. Introduction
167
II. LTP Induction Component 1„ Mechanisms Upstream of the NMDA Receptor That Directly Regulate NMDA Receptor Function
169
III. LTP Induction Component 2„ Mechanisms Upstream of the NMDA Receptor That Control Membrane Depolarization
173
IV. LTP Induction Component 3„The Components of the Synaptic Infrastructure That Are Necessary for the NMDA Receptor and the Synaptic Signal Transduction Machinery to Function Normally
182
V. LTP Induction Component 4„ Feed-Forward and Feedback Mechanisms That Regulate the Level of Calcium Attained
193
VI. LTP Induction Component 5„Extrinsic Signals That Regulate the Response to the Calcium Influx
196
VII. LTP Induction Component 6„The Mechanisms for the Generation of the Actual Persisting Biochemical Signals
200
VIII. Summary„Models for Biochemical Information Processing in LTP Induction
201
References
203
Chapter 7. Biochemical Mechanisms for Short-Term Information Storage at the Cellular Level
208
Chapter Overview
208
I. Targets of the Calcium Trigger
211
II. Targets of the Persisting Signals
231
III. Dendritic Protein Synthesis
240
IV. Chapter Summary
245
References
245
Chapter 8. Biochemical Mechanisms for Long-Term Information Storage at the Cellular Level
252
Introduction
252
I. The Case for Altered Gene Expression in L-LTP
254
II. Signaling Mechanisms
259
III. Summary„Altered Genes and Altered Circuits
276
References
277
Chapter 9. LTP Does Not Equal Memory
282
I. LTP Does Not Equal Memory
283
II. Roles for LTP
304
III. Summary
317
References
317
Chapter 10. Inherited Disorders of Human Memory„Mental Retardation Syndromes
326
I. Neurofibromatosis, Coffin-Lowry Syndrome, and the ras/ERK Cascade
327
II. Angelman Syndrome
335
III. Fragile X Syndromes
344
IV. Summary
351
References
352
Chapter 11. Aging-Related Memory Disorders„ Alzheimers Disease
356
I. Aging-Related Memory Decline
357
II. What Is AD?
358
III. Genes„Familial and Late-Onset AD
371
IV. Apolipoprotein E in the Nervous System
374
V. Mouse models for AD
374
VI. Summary
379
References
379
Chapter 12. The Chemistry of Perpetual Memory
386
I. Short-, Long-, and Ultralong-Term Forms of Learning
391
II. Use of Invertebrate Preparations to Study Simple Forms of Learning
392
III. Short-Term Facilitation in Aplysia is Mediated by Changes in the Levels of Intracellular Second Messenger
396
IV. Intermediate-Term Facilitation in Aplysia Involves Altered Gene Expression and Persistent Protein Kinase Activation„A Second Category of Reaction 378
397
V. Long-Term Synaptic Facilitation in Aplysia Involves Changes in Gene Expression and Resulting Anatomical Changes
398
VI. Three Attributes of Chemical Reactions Mediating Memory
403
VII. Summary: A General Chemical Model for Memory
407
References
408
Index
410
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