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PMID: 2027515 Published · ppublish English Journal Article Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, P.H.S.

Ethanol potentiation of GABA-induced electrophysiological responses in cerebellum: requirement for catecholamine modulation.

Neuroscience letters ·Vol. 122 ·No. 2 ·1991-01-28 ·Pages 154-8

Lin AM, Freund RK, Palmer MR

Abstract

In this study, we confirmed that microiontophoretically applied norepinephrine (NE) and isoproterenol potentiate the depressant effects of locally-applied gamma-aminobutyric acid (GABA) on cerebellar Purkinje neurons of anesthetized rats. Although ethanol (EtOH) does not reliably or efficaciously potentiate GABA-induced depressions of neuronal activity, we found that systemic or locally-applied EtOH does markedly potentiate GABA-induced inhibitions of Purkinje neuron firing rate if that response is concomitantly modulated by NE or isoproterenol. This study suggests that the EtOH sensitivity of the GABA mechanism of electrophysiological responses in the cerebellar cortex is regulated by the neuromodulatory effect of beta-adrenergic receptor activation.

MeSH Terms
Action Potentials/drug effects Animals Cerebellum/drug effects,physiology Drug Synergism Electrophysiology/methods Ethanol/pharmacology Iontophoresis Isoproterenol/pharmacology Kinetics Purkinje Cells/drug effects,physiology Rats gamma-Aminobutyric Acid/administration & dosage,pharmacology
Chemicals
Ethanol gamma-Aminobutyric Acid Isoproterenol
Authors & Affiliations
3 authors, click to expand affiliations / ORCID
Lin A M
Department of Pharmacology, University of Colorado Health Sciences Center, Denver 80262.
Freund R K
Palmer M R
Article Info
Journal
Neuroscience letters
Abbr.
Neurosci Lett
ISSN
0304-3940
Published
1991-01-28
Pages
154-8
Language
English
Region
Ireland
NLM ID
7600130
Subset
IM
Grants
NIAAA NIH HHS · AA00102 · United States
NIAAA NIH HHS · AA05915 · United States
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