Mechanisms of Memory

Mechanisms of Memory

von: J. David Sweatt

Elsevier Trade Monographs, 2003

ISBN: 9780080521961 , 350 Seiten

Format: PDF

Kopierschutz: DRM

Windows PC,Mac OSX Apple iPad, Android Tablet PC's

Preis: 78,95 EUR

Mehr zum Inhalt

Mechanisms of Memory


 

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„ Alzheimers 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