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Mechanisms of memory / J. David Sweatt.

Van Pelt Library QP406 .S884 2003
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Holman Biotech Commons QP406 .S884 2003
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Format:
Book
Author/Creator:
Sweatt, J. David.
Language:
English
Subjects (All):
Memory--Physiological aspects.
Memory.
Memory--physiology.
Medical Subjects:
Memory--physiology.
Physical Description:
xvii, 400 pages : illustrations (some color) ; 24 cm
Place of Publication:
Amsterdam ; Boston : Academic, [2003]
Summary:
This book is the first comprehensive overview of the cellular and molecular mechanisms underlying higher-order learning and memory. Focusing on mechanisms relevant to hippocampus-dependent memory formation, the book progresses systematically from behavior to cellular physiology to the molecular and genetic levels. Moreover, it integrates modern discoveries concerning learning and memory disorders, such as mental retardation syndromes and Alzheimer's Disease. Written in a readable and engaging style, the book emphasizes results from the cutting edge of contemporary methodologies, such as genetic engineering, molecular biology, complex behavioral characterization, cellular physiology, proteomics, and molecular structure.
The book draws numerous examples from the recent experimental literature, and has as a unifying theme the modern hypothesis-testing approach to basic research. As such, the book provides a foundation of experimental design that should be useful to all students pursuing an interest in laboratory research. In addition, active researchers in the learning and memory field will benefit from its extensive review of recent publications in the area and from the cross-disciplinary approach used in writing the book.
Mechanisms of Memory should serve as an enlightening and valuable resource for students new to the learning and memory field. More established investigators looking to expand their breadth of knowledge, particularly in the molecular and biochemical aspects of memory and memory disorders, will similarly benefit from the multidisciplinary approach used throughout the book, and from the detailed presentation of the material covered.
Contents:
1. Introduction
The Basics of Psychological Learning and Memory Theory
A. Categories of Learning and Memory 6
B. Memory Exhibits Long-Term and Short-Term Forms 9
II. Unconscious Learning 12
A. Simple Forms of Learning 12
B. Unconscious Learning and Unconscious Recall 16
C. Unconscious Learning and Subject to Conscious Recall 17
D. Operant Conditioning 20
E. Currently Popular Associative Learning Paradigms 21
III. Conscious Learning
Subject to Conscious and Unconscious Recall 23
A. Declarative Learning 23
B. Spatial Learning 25
IV. Final Note
Will Molecular Studies Change the Way We Think about Learning Behavior? 26
2. Rodent Behavioral Learning and Memory Models
II. Behavioral Assessments in Rodents 30
A. Fear Conditioning 30
B. Avoidance Conditioning 35
C. Simple Maze Learning 35
D. Spatial Learning 37
E. Taste Learning 41
III. Modern Experimental Uses of Rodent Behavioral Models 44
A. The Four Basic Types of Experiments 44
B. Using Behavioral Paradigms in Block and Measure Experiments 46
IV. Control Experiments 53
A. Open Field Analysis and Elevated Plus Maze Performance 53
B. Rotating-Rod Performance
Coordination and Motor Learning 53
C. Acoustic Startle and Pre-Pulse Inhibition 54
D. Nociception 55
E. Vision Tests
Light-Dark Exploration and Visual Cliff 56
3. The Hippocampus Serves a Role in Multimodal Information Processing, and Memory Consolidation
II. Studying the Hippocampus 62
A. The Hippocampus Serves a Role in Information Processing
Space, Time, and Relationships 63
III. Hippocampal Function in Cognition 65
A. Space 65
B. Time 72
C. Multimodal Associations
The Hippocampus as a Generalized Association Machine and Multimodal Sensory Integrator 77
D. The Hippocampus also is Required for Memory Consolidation 84
4. Long-Term Potentiation as a Physiological Phenomenon
I. Synapses in the Hippocampus
The Hippocampal Circuit 93
II. A Breakthrough Discovery
LTP in the Hippocampus 94
A. The Hippocampal Slice Preparation 97
B. Measuring Synaptic Transmission in the Hippocampal Slice 99
III. NMDA Receptor-Dependence of LTP 102
A. Pairing LTP 104
B. Dendritic Action Potentials 106
IV. NMDA Receptor-Independent LTP 110
A. 200-Hz LTP 110
B. TEA LTP 110
C. Mossy Fiber LTP in Area CA3 111
V. A Role for Calcium Influx in NMDA Receptor-Dependent LTP 112
5. Complexities of Long-Term Potentiation
II. Presynaptic Versus Postsynaptic Mechanisms 118
III. LTP Can Include an Increased AP Firing Component 127
IV. Temporal Integration in LTP Induction 130
V. LTP Can Be Divided into Phases 131
A. E-LTP and L-LTP
Types Versus Phases 134
VI. Spine Anatomy and Biochemical Compartmentalization 142
6. The Biochemistry of LTP Induction
II. LTP Induction Component 1
Mechanisms Upstream of the NMDA Receptor That Directly Regulate NMDA Receptor Function 150
A. The Structure of the NMDA Receptor 151
B. Kinase Regulation of the NMDA Receptor 151
C. Redox Regulation of the NMDA Receptor 154
D. Polyamine Regulation of the NMDA Receptor 154
III. LTP Induction Component 2
Mechanisms Upstream of the NMDA Receptor That Control Membrane Depolarization 154
A. Dendritic Potassium Channels 155
B. Voltage-Dependent Sodium Channels (and Calcium Channels?) 160
C. AMPA Receptor Function 160
D. GABA Receptors 161
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 163
A. Cell Adhesion Molecules and the Actin Matrix 164
B. Presynaptic Processes 167
C. Anchoring and Interacting Proteins of the Postsynaptic Compartment 167
V. LTP Induction Component 4
Feed-Forward and Feedback Mechanisms That Regulate the Level of Calcium Attained 174
A. VDCCs 175
B. The Spine Apparatus 176
C. Mitochondrial Calcium-Handling 176
VI. LTP Induction Component 5
Extrinsic Signals That Regulate the Response to the Calcium Influx 177
A. The cAMP Gate for LTP Induction 177
B. The PLC/PKC/Neurogranin System 179
VII. LTP Induction Component 6
The Mechanisms for the Generation of the Actual Persisting Biochemical Signals 181
VIII. Summary
Models for Biochemical Information Processing in LTP Induction 182
A. Four-Way Coincidence Detection 182
7. Biochemical Mechanisms for Short-Term Information Storage at the Cellular Level
I. Targets of the Calcium Trigger 192
A. CaMKII in E-LTP 194
B. A Second Target of Calcium: PKC 198
C. A Final Potential Target of Calcium
Phospholipases 210
D. Section Summary: Mechanisms for Generating Persisting Signals in E-LTP 211
II. Targets of the Persisting Signals 212
A. AMPA Receptors in E-LTP 212
B. Direct Phosphorylation of the AMPA Receptor 215
C. Regulation of Steady-State Levels of AMPA Receptors 216
D. Silent Synapses 218
E. Proteolysis 218
F. Presynaptic Changes
Increased Release 218
G. Postsynaptic Changes in Excitability 221
III. Dendritic Protein Synthesis 221
8. Biochemical Mechanisms for Long-Term Information Storage at the Cellular Level
I. The Case for Altered Gene Expression in L-LTP 235
II. Signaling Mechanisms 240
A. A Core Signal Transduction Cascade Linking Calcium to the Transcription Factor CREB 241
B. Modulatory Influences That Impinge Upon This Cascade 244
C. Additional Transcription Factors Besides CREB That May Be Involved in L-LTP Induction 245
D. Gene Targets in L-LTP 245
E. mRNA Targeting and Transport 251
F. Effects of the Gene Products on Synaptic Structure 253
III. Summary
Altered Genes and Altered Circuits 257
9. LTP Does Not Equal Memory
I. LTP Does Not Equal Memory 264
A. The Block Experiment 265
B. The Mimic Experiment 271
C. The Measure Experiment 274
II. Roles for LTP 285
A. Hippocampal Information Processing 285
B. Short-Term Information Storage in the Hippocampus 288
C. Consolidation Storage of Information Within the Hippocampus for Downloading to the Cortex 290
10. Inherited Disorders of Human Memory
Mental Retardation Syndromes
I. Neurofibromatosis, Coffin-Lowry Syndrome, and the ras/ERK Cascade 308
II. Angelman Syndrome 316
III. Fragile X Syndromes 325
A. Fragile X Mental Retardation Syndrome Type 1 325
B. Fragile X Mental Retardation Type 2 327
11. Aging-Related Memory Disorders
Alzheimer's Disease
I. Aging-Related Memory Decline 338
II. What Is AD? 339
A. Stages of AD 339
B. Pathological Hallmarks of AD 342
C. A[beta]42 as the Cause of AD 349
III. Genes
Familial and Late-Onset AD 352
A. APP Mutations 352
B. Presenilin Mutations 354
C. ApoE4 Alleles in AD 354
IV. Apolipoprotein E in the Nervous System 355
V. Mouse models for AD 355
A. The Tg2576 Mouse 356
12. The Chemistry of Perpetual Memory
I. Short-, Long-, and Ultralong-Term Forms of Learning 372
II. Use of Invertebrate Preparations to Study Simple Forms of Learning 373
III. Short-Term Facilitation in Aplysia is Mediated by Changes in the Levels of Intracellular Second Messenger 377
Thus, Reaction Category 1: Altered Levels of Second Messengers 377
IV. Intermediate-Term Facilitation in Aplysia Involves Altered Gene Expression and Persistent Protein Kinase Activation
A Second Category of Reaction 378
Thus, We Have Reaction Category 2: Generation of Long Half-Life Molecules 379
V. Long-Term Synaptic Facilitation in Aplysia Involves Changes in Gene Expression and Resulting Anatomical Changes 379
VI. Three Attributes of Chemical Reactions Mediating Memory 384
A. Long-Term Memory in Mammals 384
B. Long Half-Life Reactions 385
C. Ultralong-Term Memory: Mnemogenic Chemical Reactions 386
VII. Summary: A General Chemical Model for Memory 388.
Notes:
Includes bibliographical references and index.
ISBN:
0126789576
OCLC:
52919375

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