Calcium-Calmodulin Kinase Type II-Mediated Glutamatergic Plasticity Underlies Expression of Benzodiazepine-Withdrawal Anxiety

Elizabeth I. Tietz and Damien E. Earl
Departments of Physiology and Pharmacology and Neurosciences University of Toledo College of Medicine, Toledo OH, USA

Series: Neuroscience Research Progress, Protein Biochemistry, Synthesis, Structure and Cellular Functions
BISAC: SCI089000

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Special issue: Resilience in breaking the cycle of children’s environmental health disparities
Edited by I Leslie Rubin, Robert J Geller, Abby Mutic, Benjamin A Gitterman, Nathan Mutic, Wayne Garfinkel, Claire D Coles, Kurt Martinuzzi, and Joav Merrick

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Prolonged treatment with CNS depressant drugs, such as the benzodiazepine anti-anxiety drugs increases the possibility of physical dependence manifested as withdrawal anxiety. This review will present an overview of the physiological mechanisms underlying glutamatergic plasticity in the CA1 region of the hippocampus that regulate the expression of benzodiazepine withdrawal-anxiety. The methodological approaches, outcomes and interpretations from which these glutamatergic mechanisms were derived are further detailed in the publications cited. The mechanisms will be discussed in the context of the mechanisms underlying activity-dependent glutamatergic plasticity, as well as drug-induced plasticity to other drugs of abuse. (Imprint: Nova)

Preface

Abstract

Role of glutamate neurotransmission in benzodiazepine withdrawal-anxiety

Chronic benzodiazepine treatment and withdrawal

Bi-directional regulation of AMPAR and NMDAR currents

Modulation of benzodiazepine withdrawal-anxiety by systemic glutamate antagonists

Stepwise AMPAR potentiation during drug withdrawal

Convergent mechanisms of activity and drug-induced plasticity

Acknowledgments

References

Index

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