Neuropsychopharmacology: A Tribute to Joseph T. Coyle

 
 
Academic Press
  • 1. Auflage
  • |
  • erschienen am 7. Juni 2016
  • |
  • 414 Seiten
 
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978-0-12-809820-2 (ISBN)
 

Neuropsychopharmacology: A Tribute to Joseph T. Coyle is a new volume from Advances in Pharmacology presenting reviews of recent breakthroughs in glutamate pharmacology and a tribute to one of the most influential neuroscientists of our times. With a variety of chapters and the best authors in the field, the volume is an essential resource for pharmacologists, immunologists, and biochemists alike.


  • Features contributions from the best authors in the field
  • Provides an essential resource for pharmacologists, immunologists, and biochemists
  • Includes new approaches for diagnosing and treating major neurological and psychiatric diseases
  • Features a tribute to one of the most influential neuroscientists of our times
1054-3589
  • Englisch
  • San Diego
  • |
  • USA
Elsevier Science
  • 20,51 MB
978-0-12-809820-2 (9780128098202)
0128098201 (0128098201)
weitere Ausgaben werden ermittelt
  • Front Cover
  • Neuropsychopharmacology: A Tribute to Joseph T. Coyle
  • Copyright
  • Contents
  • Contributors
  • Foreword
  • References
  • Preface
  • Chapter One: My Life in Clinical Neuroscience: The Beginning
  • 1. Introduction
  • 2. The Early Years
  • 3. Medical School
  • 4. Postgraduate Training
  • 5. Getting Started at Hopkins
  • 6. Conclusion
  • References
  • Chapter Two: Kynurenines and Glutamate: Multiple Links and Therapeutic Implications
  • 1. Introduction
  • 2. Neurobiology of Kynurenines: The Early Years
  • 3. Kynurenergic Modulation of Glutamate Function: Several Distinct Mechanisms
  • 4. Targeting Kynurenines to Target Glutamate
  • 5. Functional Implications and Clinical Relevance
  • 6. Conclusion
  • Conflict of Interest
  • Acknowledgments
  • References
  • Chapter Three: The Therapeutic Role of d-Cycloserine in Schizophrenia
  • 1. Introduction
  • 2. A Brief Review of NMDA Receptor Structure and Function
  • 3. History of the Glutamate Model of Schizophrenia
  • 4. Glycine-Site Agonists
  • 5. Early Trials with DCS
  • 6. DCS Added to Second-Generation Antipsychotics
  • 7. Glycine Reuptake Inhibitors
  • 8. D-Serine as a Therapeutic Target
  • 9. Inhibitors of Glutamate Release
  • 10. DCS Pharmacology and NMDA Receptor Subunit Composition
  • 11. DCS Memory Enhancing Effects
  • 12. DCS Effects on Memory in Humans
  • 13. NMDA Receptors and Neuroplasticity
  • 14. DCS and Plasticity
  • 15. DCS and Plasticity in Schizophrenia
  • 16. Conclusion
  • Conflict of Interest
  • References
  • Chapter Four: Impulsivity, Stimulant Abuse, and Dopamine Receptor Signaling
  • 1. Introduction
  • 2. Impulsivity as a Therapeutic Target in Stimulant-Use Disorder
  • 3. Dopamine Receptor Signaling and Inhibitory Control
  • 4. Dopamine D2-Type Receptor Deficits and Impulsivity in Stimulant-Use Disorder
  • 5. Augmenting Dopamine Function in Stimulant Users
  • 6. Conclusion
  • Conflict of Interest
  • References
  • Chapter Five: Excitotoxicity as a Common Mechanism for Fetal Neuronal Injury with Hypoxia and Intrauterine Inflammation
  • 1. Introduction
  • 2. Excitotoxicity Mechanisms
  • 3. Hypoxia and Intrauterine Inflammation as a Function of Excitotoxicity in Animal Models
  • 4. Clinical Studies
  • 5. Conclusion
  • Conflict of Interest
  • Acknowledgments
  • References
  • Chapter Six: Transcriptional Regulation of Glutamate Transporters: From Extracellular Signals to Transcription Factors
  • 1. Introduction
  • 2. Differential Localization of Glutamate Transporters
  • 3. Why Study Transcriptional Regulation of Glutamate Transporters?
  • 3.1. Transcriptional Regulation of SLC1A3/GLAST/EAAT1
  • 3.2. Transcriptional Regulation of SLC1A2/GLT-1/EAAT2
  • 3.3. Transcriptional Regulation of SLC1A1/EAAC1/EAAT3
  • 3.4. Transcriptional Regulation of SLC1A6/EAAT4 and SLC1A7/EAAT5
  • 3.5. Epigenetic Regulation
  • 4. Conclusion
  • Conflict of Interest
  • Acknowledgments
  • References
  • Chapter Seven: The Long and Winding Road: From the High-Affinity Choline Uptake Site to Clinical Trials for Malignant Bra ...
  • 1. Baltimore, Hopkins, The Coyle Lab, and All that Jazz ...
  • 2. Toward Gene Therapy for Brain Tumors: Reengineering the Brain Immune System
  • 2.1. Malignant Brain Tumors: Glioblastoma Multiforme, WHO Grade IV
  • 2.2. Endogenous Immunotherapy: Reengineering the Brain Immune System to Treat Malignant Brain Tumors
  • 2.3. The Brain Immune System
  • 2.4. Gene Immunotherapy for Brain Tumors
  • 2.5. Reengineering the Brain Immune System to Treat Malignant Brain Tumors
  • 2.6. The Holy Grail: Endogenous Immunotherapy Trials in Human Patients Suffering from GBM
  • 3. Conclusions
  • Conflict of Interest
  • References
  • Chapter Eight: Choline on the Move: Perspectives on the Molecular Physiology and Pharmacology of the Presynaptic Choline T ...
  • 1. Introduction
  • 2. ACh, HACU, and the Birth of CHT
  • 2.1. An Overview of the Mechanics of ACh Synapses
  • 2.2. From ACh to HACU
  • 2.3. HC-3: Key Reagent in the Definition of HACU
  • 2.4. HC-3-Binding Sites: HACU Enters the Molecular Era
  • 3. CHT Molecular Biology and Regulation
  • 3.1. Early Efforts to Identify CHT Proteins
  • 3.2. Cloning and Characterization of CHT cDNAs and Genes
  • 3.3. Molecular Mechanisms of CHT Regulation
  • 4. CHT Contributions to Cholinergic Function and Dysfunction In Vivo
  • 4.1. CHT Genetic Animal Models
  • 4.2. CHT Gene Contributions to Human Disorders
  • 5. Advances in CHT Pharmacology
  • 5.1. The Search for Novel CHT Modulators: MKC-231
  • 5.2. The Search for Novel CHT Modulators: ML352
  • 6. Conclusion
  • Conflict of Interest
  • Acknowledgments
  • References
  • Chapter Nine: Still NAAG'ing After All These Years: The Continuing Pursuit of GCPII Inhibitors
  • 1. Introduction
  • 1.1. NAAG Is a Widely Distributed Cotransmitter
  • 1.2. NAAG Is Produced by NAAG Synthetase and Packaged in Vesicles by Sialin
  • 1.3. NAAG Is Released from Synapses and Axons
  • 1.4. The Answer to the Nagging Question: GCPII Controls the Dual Function of NAAG
  • 1.5. Under Basal Conditions, NAAG Provides Negative Presynaptic Feedback and Glial Trophic Effects via mGlu3 Receptors an ...
  • 1.6. Under High Levels of Synaptic Activity, NAAG Release and GCPII Activity Are Enhanced Resulting in Excess Glutamate R ...
  • 1.7. NAAG's Role in Glutamate Supply and Energy Metabolism
  • 2. Design of GCPII Inhibitors
  • 2.1. First Potent and Selective GCPII Inhibitor Discovered
  • 2.2. Second-Generation Phosphinic Acid-Based GCPII Inhibitors
  • 2.3. Thiol-Based GCPII Inhibitors
  • 2.4. Urea-Based GCPII Inhibitors
  • 2.5. Hydroxamic Acid-Based GCPII Inhibitors
  • 2.6. GCPII Structural Studies
  • 2.7. Other Classes of GCPII Inhibitors
  • 2.8. Strategies for Improving the Pharmacokinetic Properties of GCPII Inhibitors
  • 2.9. Intranasal Delivery for Enhancing Brain Penetration of GCPII Inhibitors
  • 3. Therapeutic Utility of GCPII Inhibitors in CNS and PNS Disorders
  • 3.1. Stroke and TBI
  • 3.2. Amyotrophic Lateral Sclerosis
  • 3.3. Schizophrenia
  • 3.4. Multiple Sclerosis
  • 3.5. Drug Addiction
  • 3.6. Alzheimer´s Disease
  • 3.7. Pain
  • 3.8. Peripheral Neuropathy
  • 4. Conclusion
  • Conflict of Interest
  • Acknowledgments
  • References
  • Chapter Ten: Ultimate Translation: Developing Therapeutics Targeting on N-Methyl-d-Aspartate Receptor
  • 1. Introduction
  • 2. Neurotransmitters for NMDAR
  • 3. Presynaptic Regulation
  • 3.1. Glycine Transporter-1
  • 3.2. Alanine, Serine, and Cysteine Transporter
  • 3.3. Serine Racemase
  • 4. Postsynaptic Regulation
  • 4.1. Channel Ionophore
  • 4.2. Agonist and Partial Agonist of the Co-agonist Site
  • 5. Termination of the Action by D-Amino Acid Oxidase
  • 6. Experiences in CNS Disorders
  • 6.1. Anti-NMDAR Encephalitis
  • 6.2. Schizophrenia
  • 6.3. Depression
  • 6.4. Obsessive-Compulsive Disorder
  • 6.5. Alzheimer´s Disease
  • 6.6. Amyotrophic Lateral Sclerosis
  • 7. Conclusion
  • Conflict of Interest
  • Acknowledgments
  • References
  • Chapter Eleven: The Good and Bad Sides of NAAG
  • 1. Introduction
  • 2. The History of NAAG
  • 2.1. Biochemistry of NAAG
  • 2.2. Metabolism of NAAG
  • 3. NAAG and the Glutamatergic System
  • 3.1. NAAG and mGluRs
  • 3.2. NAAG and NMDA Receptors
  • 4. NMDA Receptors
  • 4.1. NMDA Receptor Subunit Distribution, Development, and Subcellular Localization
  • 4.2. Intracellular Signaling of Synaptic and Extrasynaptic NMDA Receptors
  • 4.3. NMDA Receptors and Protons
  • 5. Clinical Implications of NAAG
  • 5.1. Schizophrenia
  • 5.2. Ischemic Stroke
  • 6. Why is There so Much Controversy Regarding the Effect of NAAG on NMDA Receptors?
  • 7. The Effect of NAAG on NMDA Receptors is Subunit and pH Dependent
  • 8. Possible Mechanism of Action of NAAG on NMDA Receptors
  • 9. Putative Mechanism for NAAG-Mediated Neuroprotection
  • Conflict of Interest
  • References
  • Chapter Twelve: The NMDA Receptor and Schizophrenia: From Pathophysiology to Treatment
  • 1. Introduction
  • 2. NMDA Receptor: Structure and Function
  • 3. Glycine Modulatory Site
  • 3.1. Serine Racemase and D-Serine
  • 3.1.1. Cellular Localization of Serine Racemase and D-Serine
  • 3.2. Glycine and Kynurenic Acid
  • 4. NMDA Receptor Hypofunction and Schizophrenia
  • 4.1. Circuit-Based Framework for Reduced NMDAR Function in Schizophrenia
  • 5. Augmenting NMDA Receptor Function to Treat Schizophrenia
  • 5.1. The Glycine Modulatory Site
  • 5.2. Allosteric Modulation of the NMDA Receptor
  • 5.3. Metabotropic Glutamate Receptors 2 and 3
  • 5.4. Metabotropic Glutamate Receptor 5
  • 5.5. Cholinergic Receptors
  • 6. Conclusion
  • Conflict of Interest
  • Acknowledgments
  • References
  • Index
  • Back Cover

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