Chapter

GABA<sub>A</sub> Receptor Plasticity in Alcohol Withdrawal

Richard W. Olsen and Igor Spigelman

in Jasper's Basic Mechanisms of the Epilepsies

Fourth edition

Published on behalf of ©Jeffrey L. Noebels, Massimo Avoli, Michael A. Rogawski, Richard W. Olsen, and Antonio V. Delgado-Escueta

Published in print July 2012 | ISBN: 9780199746545
Published online April 2013 | e-ISBN: 9780199322817 | DOI: http://dx.doi.org/10.1093/med/9780199746545.003.0043

Series: Contemporary Neurology Series

GABAA Receptor Plasticity in Alcohol Withdrawal

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Alcohol, the fruit of the vine and the braumeister's ware, has been one of the most popular drugs in the world throughout history and one of the most abused. The development of dependence after chronic use of ethanol (EtOH) depends on two parallel effects of the drug on the brain each time it is used: stimulation of the reward pathway and subsequent triggering of a small but significant withdrawal. There is rebound hyperexcitability following the initial action of EtOH as a central nervous system (CNS) depressant and triggering of some adaptive process, that is, molecular changes associated with tolerance.1,2 Each of these “mini-withdrawals” reflects transient plasticity in the brain affecting the balance of excitation and inhibition. The simplest description of the changes could be, for example, the ratio of glutamate and gamma-aminobutyric acid (GABA) neurotransmitter activities.

Chapter.  7920 words.  Illustrated.

Subjects: Neurology

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