Mechanisms of Memory
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This fully revised second edition provides the only unified synthesis of available information concerning the mechanisms of higher-order memory formation. It spans the range from learning theory, to human and animal behavioral learning models, to cellular physiology and biochemistry. It is unique in its incorporation of chapters on memory disorders, tying in these clinically important syndromes with the basic science of synaptic plasticity and memory mechanisms. It also covers cutting-edge approaches such as the use of genetically engineered animals in studies of memory and memory diseases. Written in an engaging and easily readable style and extensively illustrated with many new, full-color figures to help explain key concepts, this book demystifies the complexities of memory and deepens the reader’s understanding.
Key Features
- More than 25% new content, particularly expanding the scope to include new findings in translational research.
- Unique in its depth of coverage of molecular and cellular mechanisms
- Extensive cross-referencing to Comprehensive Learning and Memory
- Discusses clinically relevant memory disorders in the context of modern molecular research and includes numerous practical examples
Readership
Senior undergraduates and graduate students studying memory, as well as those interested in the medical professions and in translational aspects of basic memory research.
Table of Contents
Foreword to First Edition
Preface to First Edition
Preface to Second Edition
Acknowledgments
1. Introduction: The Basics of Psychological Learning and Memory Theory
I. Introduction
A. Categories of Learning and Memory
B. Memory Exhibits Long-Term and Short-Term Forms
II . Short-Term Memory
A. Sensory Memory and Short-Term Storage
B. Working Memory
C. The Prefrontal Cortex and Working Memory
D. Reverberating Circuit Mechanisms Contrast with Molecular Storage Mechanisms for Long- Term Memory
III. Unconscious Learning
A. Simple Forms of Learning
B. Unconscious Learning and Unconscious Recall
C. Unconscious Learning and Subject to Conscious Recall
D. Operant Conditioning
E. Currently Popular Associative Learning Paradigms
IV . Conscious Learning — Subject to Conscious and Unconscious Recall
A. Declarative Learning
B. Spatial Learning
V . Summary
Further Reading
Journal Club Articles
References
2. Studies of Human Learning and Memory
I. Introduction — Historical Precedents with Studies of Human Subjects
A. Amnesias
B. Memory Consolidation
II . The Hippocampus in Human Declarative, Episodic, and Spatial Memory
A. Anatomy of the Hippocampal Formation
B. Lesion Studies in Human Memory Formation
C. Imaging Studies
III . Motor Learning
A. Anatomy
B. Habits
C. Stereotyped Movements
D. Sequence Learning
IV . Prodigious Memory
A. Mnemonists
B. Savant Syndrome
C. You are a Prodigy
V. Summary
Further Reading
Journal Club Articles
References
3. Non-Associative Learning and Memory
I. Introduction — The Rapid Turnover of Biomolecules
II. Short-Term, Long-Term, and Ultralong-Term Forms of Learning
III. Use of Invertebrate Preparations to Study Simple Forms of Learning
A. The Cellular Basis of Synaptic Facilitation in Aplysia
IV. Short-Term Facilitation in Aplysia is Mediated by Changes in the Levels of Intracellular Second Messengers
V. Long-Term Facilitation in Aplysia Involves Altered Gene Expression and Persistent Protein Kinase Activation — A Second Category of Reaction
VI. Long-Term Synaptic Facilitation in Aplysia Involves Changes in Gene Expression and Resulting Anatomical Changes
VII. Attributes of Chemical Reactions Mediating Memory
VIII. Sensitization in Mammals
IX. Summary — A General Biochemical Model for Memory
Further Reading
Journal Club Articles
References
4. Rodent Behavioral Learning and Memory Models
I. Introduction
II. Behavioral Assessments in Rodents
A. Assessing General Activity and Sensory Perception
B. Fear Conditioning
C. Avoidance Conditioning
D. Eye-Blink Conditioning
E. Simple Maze Learning
F. Spatial Learning
G. Taste Learning
H. Novel Object Recognition
I. Studying Memory Reconsolidation Using a Fear Conditioning Protocol
III . Modern Experimental Uses of Rodent Behavioral Models
A. The Four Basic Types of Experiments
B. Use of Behavioral Paradigms in Block and Measure Experiments
IV . Summary
Further Reading
Journal Club Articles
References
5. Associative Learning and Unlearning
I. Introduction
A. Classical Associative Conditioning
II. Fear Conditioning and the Amygdala
A. Long-Term Potentiation in Cued Fear Conditioning
III. Eye-Blink Conditioning and the Cerebellum
IV. Positive Reinforcement Learning
A. Reward and Human Psychopathology
B. Positive Reinforcement Learning
C. Operant Conditioning of Positive Reinforcement
V. Memory Suppression — Forgetting Versus Extinction, and Latent Inhibition
VI. Summary
Further Reading
Journal Club Articles
References
6. Hippocampal Function in Cognition
I. Introduction
II. Studying the Hippocampus
A. Hippocampal Anatomy
III. Hippocampal Function in Cognition
A. Space
B. Timing
C. Multimodal Associations — The Hippocampus as a Generalized Association Machine and Multimodal Sensory Integrator
D. The Hippocampus is also Required for Memory Consolidation
IV. Summary
Further Reading
Journal Club Articles
References
7. Long-Term Potentiation — A Candidate Cellular Mechanism for Information Storage in the Central Nervous System
I. Hebb’s Postulate
II. A Breakthrough Discovery — Long-Term Potentiation in the Hippocampus
A. The Hippocampal Circuit and Measuring Synaptic Transmission in the Hippocampal Slice
B. Long-Term Potentiation of Synaptic Responses
C. Short-Term Plasticity — Paired-Pulse Facilitation and Post-Tetanic Potentiation
III. NMDA Receptor-Dependence of Long-Term Potentiation
A. Pairing Long-Term Potentiation
B. Dendritic Action Potentials
IV. NMDA Receptor-Independent Long-Term Potentiation
A. 200 Hz Long-Term Potentiation
B. Tetra-Ethyl Ammonium Long-Term Potentiation
C. Mossy Fiber Long-Term Potentiation in Area CA3
V . A Role for Calcium Infl ux in NMDA Receptor- Dependent Long-Term Potentiation
VI . Pre-Synaptic Versus Post-Synaptic Mechanisms
VII. Long-Term Potentiation can Include an Increased Action Potential Firing Component
VIII. Long-Term Potentiation can be Divided into Phases
A. Early-Long-Term Potentiation and Late-Long- Term Potentiation — Types Versus Phases
IX. Modulation of Long-Term Potentiation Induction
X. Depotentiation and Long-Term Depression
XI. A Role for Long-Term Potentiation in Hippocampal Information Processing, Hippocampus-Dependent Timing, and Consolidation of Long-Term Memory
A. Long-Term Potentiation in Hippocampal Information Processing
B. Timing-Dependent Information Storage in the Hippocampus
C. Consolidation — Storage of Information within the Hippocampus for Down-Loading to the Cortex
D. A Model for Long-Term Potentiation in Consolidation of Long-Term Memory
XII. Summary
Further Reading
Journal Club Articles
References
8. The NMDA Receptor
I. Introduction
A.Structure of the NMDA Receptor
II. NMDA Receptor Regulatory Component 1 — Mechanisms Upstream of the NMDA Receptor that Directly Regulate NMDA Receptor Function
A. Kinase Regulation of the NMDA Receptor
B. Redox Regulation of the NMDA Receptor 198
C. Polyamine Regulation of the NMDA Receptor
III. NMDA Receptor Regulatory Component 2 — Mechanisms Upstream of the NMDA Receptor that Control Membrane Depolarization
A. Dendritic Potassium Channels — A-type Currents
B. Voltage-Dependent Sodium Channels
C. AMPA Receptor Function
D. GABA Receptors
IV. NMDA Receptor Regulatory Component 3 — The Components of the Synaptic Infrastructure that are Necessary for the NMDA Receptor and the Synaptic Signal Transduction Machinery to Function Normally
A. Cell Adhesion Molecules and the Actin Matrix
B. Pre-Synaptic Processes
C. Anchoring and Interacting Proteins of the Post- Synaptic Compartment — Post-Synaptic Density Proteins
D. AMPA Receptors 204
E. CaMKII — the Calcium/Calmodulin-Dependent Protein Kinase II
V. Summary
Further Reading
Journal Club Articles
References
9. Biochemical Mechanisms for Information Storage at the Cellular Level
I. Targets of the Calcium Trigger
A. CaMKII
B. Two Additional Targets of CaM — Adenylyl Cyclase and Nitric Oxide Synthase
C. Another Major Target of Calcium — PKC
D. Section Summary — Mechanisms for Generating Persisting Signals in Long-Term Potentiation and Memory
II. Targets of the Persisting Signals
A. AMPA Receptors in E-LTP
B. Direct Phosphorylation of the AMPA Receptor
C. Regulation of Steady-State Levels of AMPA Receptors
D. Silent Synapses
E. Pre-Synaptic Changes — Increased Release
F. Post-Synaptic Changes in Excitability?
III. Dendritic Protein Synthesis
IV. An Overview of the Role of Protein Synthesis in Memory
V. Summary
Further Reading
Journal Club Articles
References
10. Molecular Genetic Mechanisms for Long-Term Information Storage at the Cellular Level
I. Introduction 237
II. Altered Gene Expression in Late-Long-Term Potentiation and Long-Term Memory
III. Signaling Mechanisms
A. A Core Signal Transduction Cascade Linking Calcium to the Transcription Factor CREB
B. Modulatory Influences that Impinge on this Cascade
C. Additional Transcription Factors besides CREB that are Involved in Memory Formation
D. Gene Targets in Late-Long-Term Potentiation
E. mRNA Targeting and Transport
F. Effects of the Gene Products on Synaptic Structure
IV. Experience-Dependent Epigenetic Modifi cations in the Central Nervous System
A. What is Epigenetics?
B. What are Epigenetic Marks and What do they do?
C. Epigenetic Tagging of Histones
D. Signaling Systems that Control Histone Modifications
E. Epigenetic Mechanisms in Learning and Memory
F. Environmental Enrichment and Recovery of Lost Memories
G. Section Summary
V. Neurogenesis in the Adult Central Nervous System
VI. Summary
Further Reading
Journal Club Articles
References
11. Inherited Disorders of Human Memory — Mental Retardation Syndromes
I. Neurofi bromatosis, Coffi n-Lowry Syndrome, and the ras/ERK Cascade
II. Angelman Syndrome
III. Fragile X Syndromes
A. Fragile X Mental Retardation Syndrome Type 1
B. Fragile X Mental Retardation Type 2
IV. Summary
Further Reading
Journal Club Articles
References
12. Aging-Related Memory Disorders — Alzheimer’s Disease
I. Aging-Related Memory Decline
A. Mild Cognitive Impairment
B. Age-Related Dementias
II . What is Alzheimer’s Disease?
A. Stages of Alzheimer’s Disease
B. Pathological Hallmarks of Alzheimer’s Disease
C. A β 42 as the Cause of Alzheimer’s Disease
III. Genes — Familial and Late-Onset Alzheimer’s Disease
A. APP Mutations
B. Presenilin Mutations
C. ApoE4 Alleles in Alzheimer’s Disease
IV. Apolipoprotein E in the Nervous System
V. Mouse Models for Alzheimer’s Disease
A. The Tg2576 Mouse
VI. Summary
Further Reading
Journal Club Articles
References
Appendix
I. Introduction
II. Introduction to Hypothesis Testing
A. Theories
B. Models
C. Hypotheses
III. The Four Basic Types of Experiments
IV. An Example of a Hypothesis and How to Test it
A. Some Real-life Examples of Hypothesis Testing
V. Some Additional Terminology of Hypothesis Testing
A. Hypothesis Versus Prediction
B. Accuracy, Precision, and Reproducibility
C. Type I and Type II Errors
VI. Summary
References
Index
Product details
- No. of pages: 362
- Language: English
- Copyright: © Academic Press 2009
- Published: September 28, 2009
- Imprint: Academic Press
- Hardcover ISBN: 9780123749512
- eBook ISBN: 9780080959191
About the Editor
J. David Sweatt
David Sweatt received a PhD in Pharmacology from Vanderbilt University for studies of intracellular signaling mechanisms. He then did a post-doctoral Fellowship at the Columbia University Center for Neurobiology and Behavior, working on memory mechanisms in the laboratory of Nobel laureate Eric Kandel. From 1989 to 2006 he was a member of the Neuroscience faculty at Baylor College of Medicine in Houston, Texas, rising through the ranks there to Professor and Director of the Neuroscience PhD program. In 2006 he moved to the University of Alabama at Birmingham where he served for ten years as the Evelyn F. McKnight endowed Chairman of the Department of Neurobiology at UAB Medical School, and the Director of the Evelyn F. McKnight Brain Institute at UAB. Dr. Sweatt’s laboratory studies biochemical mechanisms of learning and memory, most recently focusing on the role of epigenetic mechanisms in memory formation. In addition, his research program also investigates mechanisms of learning and memory disorders, such as intellectual disabilities, Alzheimer’s Disease, and aging-related memory dysfunction. He is currently the Allan D. Bass endowed Chairman of the Department of Pharmacology at Vanderbilt University Medical School, and has expanded his research program to include developing PharmacoEpigenetic approaches to enable new treatments for cognitive dysfunction. Dr. Sweatt has won numerous awards and honors, including an Ellison Medical Foundation Senior Scholar Award and election as a Fellow of the American Association for the Advancement of Science. In 2013 he won the Ipsen Foundation International Prize in Neural Plasticity, one of the most prestigious awards in his scientific field. In 2014 he was the recipient of the PROSE Award for the most outstanding reference volume published in 2013, for his book Epigenetic Mechanisms in the Nervous System. The book was also one of five finalists for the 2014 Dawkins Award for the most outstanding academic book published in 2013. In 2014, 2015, 2016, and 2017 Thomson-Reuters named him as a “Highly Cited Researcher” and as one of the “World’s Most Influential Scientific Minds.”
Affiliations and Expertise
McKnight Brain Institute, Department of Neurobiology, University of Alabama at Birmingham, Birmingham, Alabama, USA
About the Author
J. David Sweatt
David Sweatt received a PhD in Pharmacology from Vanderbilt University for studies of intracellular signaling mechanisms. He then did a post-doctoral Fellowship at the Columbia University Center for Neurobiology and Behavior, working on memory mechanisms in the laboratory of Nobel laureate Eric Kandel. From 1989 to 2006 he was a member of the Neuroscience faculty at Baylor College of Medicine in Houston, Texas, rising through the ranks there to Professor and Director of the Neuroscience PhD program. In 2006 he moved to the University of Alabama at Birmingham where he served for ten years as the Evelyn F. McKnight endowed Chairman of the Department of Neurobiology at UAB Medical School, and the Director of the Evelyn F. McKnight Brain Institute at UAB. Dr. Sweatt’s laboratory studies biochemical mechanisms of learning and memory, most recently focusing on the role of epigenetic mechanisms in memory formation. In addition, his research program also investigates mechanisms of learning and memory disorders, such as intellectual disabilities, Alzheimer’s Disease, and aging-related memory dysfunction. He is currently the Allan D. Bass endowed Chairman of the Department of Pharmacology at Vanderbilt University Medical School, and has expanded his research program to include developing PharmacoEpigenetic approaches to enable new treatments for cognitive dysfunction. Dr. Sweatt has won numerous awards and honors, including an Ellison Medical Foundation Senior Scholar Award and election as a Fellow of the American Association for the Advancement of Science. In 2013 he won the Ipsen Foundation International Prize in Neural Plasticity, one of the most prestigious awards in his scientific field. In 2014 he was the recipient of the PROSE Award for the most outstanding reference volume published in 2013, for his book Epigenetic Mechanisms in the Nervous System. The book was also one of five finalists for the 2014 Dawkins Award for the most outstanding academic book published in 2013. In 2014, 2015, 2016, and 2017 Thomson-Reuters named him as a “Highly Cited Researcher” and as one of the “World’s Most Influential Scientific Minds.”
Affiliations and Expertise
McKnight Brain Institute, Department of Neurobiology, University of Alabama at Birmingham, Birmingham, Alabama, USA