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Alterations in Neurotransmitter Activity After Acute and Chronic Ethanol Treatment: Studies of Transmitter Interactions
Author(s) -
Hunt Walter A.,
Majchrowicz Edward,
Dalton Thomas K.,
Swartzwelder H. S.,
Wixon Henry
Publication year - 1979
Publication title -
alcoholism: clinical and experimental research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.267
H-Index - 153
eISSN - 1530-0277
pISSN - 0145-6008
DOI - 10.1111/j.1530-0277.1979.tb05336.x
Subject(s) - neurotransmitter , dopamine , dopaminergic , cholinergic , ethanol , medicine , chemistry , endocrinology , caudate nucleus , neurotransmitter receptor , acetylcholine , pharmacology , receptor , biochemistry
Acute and chronic ethanol treatment has multiple effects on the neurotransmitter systems in the nigrostriatal complex. A single dose of ethanol increases striatal dopamine release at low doses, but depresses it at high doses. In ethanol‐dependent rats, dopamine release is accelerated during intoxication, but is reduced during a withdrawal syndrome. Concomitantly, high‐affinity choline uptake, an index of cholinergic activity, is elevated at times when dopamine release is depressed. Changes in dopaminergic or cholinergic receptor activity do not induce or result from these effects. Neither has a role for GABA or substance P yet been implicated. The data suggest that interactions between at least two transmitters in the caudate nucleus may occur after acute and chronic ethanol treatment.