Front Cover

International Review of Neurobiology

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Contents

Contributors

Preface

Chapter 1: Effects of Psychostimulants on Neurotrophins: Implications for Psychostimulant-Induced Neurotoxicity

I. Introduction

II. Psychostimulants

III. Neurotrophins

IV. Neurotrophins and Psychostimulants

V. Psychostimulants, Neurotoxicity, and Neurotrophins

VI. Psychostimulants, Neurotrophins, and Psychosis

VII. Conclusions

References

Chapter 2: Dosing Time-Dependent Actions of Psychostimulants

I. Introduction: The Concept of the Dosing Time-Dependent Actions of Drugs

II. Diurnal Variations in the Behavioral Actions of Psychostimulants

III. Diurnal Variations in the CNS Systems

IV. Diurnal Variations and Melatonin

V. Possible Clinical Implications

VI. Conclusions

References

Chapter 3: Dopamine-Induced Behavioral Changes and Oxidative Stress in Methamphetamine-Induced Neurotoxicity

I. Background: Neuronal Damage Caused by Amphetamines

II. Dopamine Quinone Formation as a Dopaminergic Neuron-Specific Neurotoxic Factor in Methamphetamine-Induced Neurotoxicity

III. Methamphetamine-Induced Behavioral Changes: Relation to Neuronal Damage

IV. Conclusion

References

Chapter 4: Acute Methamphetamine Intoxication: Brain Hyperthermia, Blood-Brain Barrier, Brain Edema, and morphological cell abnormalities

I. Introduction

II. Basic Terminology and Major Topics of This Study

III. Brain Temperature Responses to METH are Dose-Dependent and Modulated by Activity State and Environmental Conditions

IV. Acute METH Intoxication Results in BBB Leakage, Acute Glial Activation, and Morphological Alterations of Brain Cells: Role of Brain Temperature

V. Conclusions

Acknowledgments

References

Chapter 5: Molecular Bases of Methamphetamine-Induced Neurodegeneration

I. Epidemiology of Methamphetamine Abuse

II. Clinical Toxicology of METH Abuse

III. Role of Oxidative Stress in METH Toxicity

IV. Involvement of AP-1-Related Transcription Factors in METH-Induced Neurotoxicity

V. Role of DNA Damage in METH-Induced Toxicity

VI. METH Toxicity and Excitotoxicity

VII. Role of Blood-Brain Barrier Dysfunction in METH Toxicity

VIII. Involvement of Mitochondrial Death Pathway in METH-Induced Apoptosis

IX. Involvement of the Endoplasmic Reticulum-Dependent Death Pathway in METH-Induced Apoptosis

X. Microglial Reactions and METH Toxicity

XI. Neuroprotective Mechanisms and METH Toxicity

Acknowledgments

References

Chapter 6: Involvement of Nicotinic Receptors in Methamphetamine- and Mdma-Induced Neurotoxicity: Pharmacological Implications

I. Long-Term Effects of Amphetamine Derivatives on CNS

II. The Role of Reactive Species in Amphetamine Derivatives-Induced Neurotoxicity

III. Model of Semipurified Synaptosomes

IV. Methamphetamine-Induced ROS Production in Semipurified Synaptosomes

V. Different Oxidative Profile and Nitric Oxide Dependence of Amphetamine and MDMA

VI. Nicotinic Antagonists Block METH and MDMA-Induced ROS Production

VII. MLA as a Neuroprotective Substance for METH- and MDMA-Induced Dopaminergic Neurotoxicity

VIII. Memantine: A New Tool to Prevent Amphetaminic Neurotoxicity

IX. Effects on Serotonin and Dopamine Uptake: Nicotinic Receptor Modulation

X. Nicotinic Receptors and the Cognitive Impairment Induced by Amphetamine Derivatives

XI. Amphetamine Derivative Interaction with Nicotinic Receptors

References

Chapter 7: Ethanol Alters the Physiology of Neuron-Glia Communication

I. Introduction

II. Cytoarchitecture in the CNS

III. Focus onto Macroglía: The ``Special´´ Role of Astrocytes in the CNS

IV. Receptors in Glial Cells Cellular Signalization

V. Release of Intercellular Messengers

VI. Effects of Ethanol on Developing CNS

VII. Ethanol and Glial Oxidative Stress

VIII. Ethanol, Inflammation, and Glial Cell Death

IX. Astroglia and Neuroprotection

X. Conclusion

Acknowledgment

References

Chapter 8: Therapeutic Targeting of "DARPP-32": A key signaling Molecule in the dopiminergic pathway for the Treatment of opiate addiction

I. Introduction

II. Study Design

III. Material and Methods

IV. Results

V. Discussion

Acknowledgments

References

Chapter 9: Pharmacological and Neurotoxicological Actions Mediated By Bupropion and Diethylpropion

I. Introduction

II. Neurotransmitter Release Modulation by Bupropion and Diethylpropion

III. Neurotoxicity of DEP and BP

IV. Molecular Interaction of BP with DAT and NET

V. Role of AChRs in Depression and in the Pharmacological Action of Antidepressants

VI. Conclusions

Acknowledgments

References

Chapter 10: Neural and Cardiac Toxicities Associated With 3,4-Methylenedioxymethamphetamine (MDMA)

I. Introduction

II. Effects of MDMA on Monoamine Neurons

III. Long-Term Effects of MDMA on 5-HT Systems

IV. Scaling Methods and MDMA Dosing

V. Functional Consequences of MDMA-Induced 5-HT Depletion

VI. Reversal of MDMA-Induced 5-HT Depletion by l-5-Hydroxytryptophan

VII. MDMA and Valvular Heart Disease

VIII. Summary

Acknowledgments

References

Chapter 11: Cocaine-Induced Breakdown of the Blood-Brain Barrier and Neurotoxicity

I. Introduction

II. Cocaine Facilitates Blood-Brain Barrier Transport to HIV-1 in the Brain

III. Cocaine and Cytotoxicity

IV. Cocaine Affects Astrocytic Functions

V. Cocaine Induces Stress Response and Upregulates Heat Shock Protein Expression

VI. Cocaine Influences Serotonin Metabolism

VII. Cocaine Affects Cerebral Circulation

VIII. Cocaine-Induced Hyperthermia

IX. Our Investigations on Cocaine-Induced Neurotoxicity

X. Novel Observations on Cocaine-Induced Brain Pathology

XI. Modulation of Serotonin 5-HT2 and 5-HT3 Receptors Influences Cocaine-Induced Neurotoxicity

XII. Cocaine-Induced BBB Dysfunction and Neurotoxicity Is Age Related

XIII. General Conclusion and Future Perspectives

Acknowledgments

References

Chapter 12: Cannabinoid Receptors in Brain: Pharmacogenetics, Neuropharmacology, Neurotoxicology, and Potential Therapeutic Applications

I. Introduction

II. Cannabinoid Genomics

III. Cannabinoid Neuropharmacology, Neurogenesis, Neurotoxicology, and Neuroprotective Properties

IV. Chromosomal Mapping of the CNR Genes

V. Polymorphic Structure of CNR Genes

VI. Genes Encoding Endocannabinoid Transporter(s) as Pharmacotherapeutic Targets

VII. Variations in Cannabinoid Receptor Genes: Functional and Pharmacotherapeutic Implications

VIII. Genetic Basis of Cannabis use and Dependence

IX. Functional Implication of Cannabinoid Pharmacotherapeutics

X. Conclusions and Future Directions

Acknowledgments

References

Chapter 13: Intermittent Dopaminergic Stimulation causes Behavioral Sensitization in the Addicted Brain and Parkinsonism

I. General Overview

II. DA Release Produced by METH in the Normal Striatum

III. Increase of Extracellular DA Produced by Supplementing Exogenous l-DOPA in a DA-Denervated Striatum

IV. The Postsynaptic Site: Occurrence of Sensitization Converge on Common Phosphorylation Processes

V. The Postsynaptic Site: Common Gene Expression

VI. The Common Trigger at the Postsynaptic Site: Inappropriate Activation of D1 Receptors

VII. Convergence on Common Pathways: From Activation of D1 Receptors to Gene-Dependent Plastic Changes

VIII. Convergence on Ultrastructural Changes and Site Specificity

IX. Behavioral Sensitization: METH-Induced Addiction and l-DOPA-Induced Dyskinesia: Two Faces of a Coin

Acknowledgment

References

Chapter 14: The Role of the Somatotrophic Axis in Neuroprotection and Neuroregeneration of the Addictive Brain

I. Introduction

II. The Somatotrophic Axis in Brain Function

III. Reversal of Drug-Induced Effects by GH

IV. Conclusion

Acknowledgments

References

Index

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