Effect of Ethanol on [3H]dopamine Release in Rat Nucleus Accumbens and Striatal Slices

Overview

Journal Neurochem Res

Specialties Chemistry
Neurology

Date 1988 May 1

PMID 3405375

Citations 8

Authors

V A Russell

M C Lamm

J J Taljaard

Affiliations

Soon will be listed here.

Abstract

Ethanol (10-200 mM) transiently increased tritium overflow from superfused rat nucleus accumbens slices previously incubated with [3H]dopamine (DA) and [14C]choline. The effect was greater in striatal tissue and did not appear to be a non-specific membrane effect since [14C]acetylcholine (ACh) release was not affected. Lack of antagonism by picrotoxin suggested that gamma-aminobutyric acid (GABA) receptors were not involved. Calcium was not a requirement and the DA uptake blocker, nomifensine, was without effect. Ethanol appeared to be causing [3H]DA release into the cytoplasm. K+ -stimulated release of [3H]DA and [14C]ACh from nucleus accumbens and striatal slices was not affected. Clonidine-mediated inhibition of the K+-evoked release of [3H]DA remained unaltered. Ethanol attenuated the isoproterenol-induced enhancement of [3H]DA release. Ethanol therefore appeared to interact with components of the DA terminal causing a transient increase in the release of neurotransmitter without impairing K+-evoked release but apparently interfering with the isoproterenol-induced effect.

Citing Articles

Enhanced Striatal Dopamine Release to Expectation of Alcohol: A Potential Risk Factor for Alcohol Use Disorder.

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A single, moderate ethanol exposure alters extracellular dopamine levels and dopamine d receptor function in the nucleus accumbens of wistar rats.

Franklin K, Engleman E, Ingraham C, McClaren J, Keith C, McBride W Alcohol Clin Exp Res. 2009; 33(10):1721-30.

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