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

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)


Table of Contents

Table of Contents



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





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