Alterations in neurotransmitter activity after acute and chronic ethanol treatment: studies of transmitter interactions.
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 trasmitters in the caudate nucleus may occur after acute and chronic ethanol treatment.
D000109:Acetylcholine / Q000378:metabolism; D000437:Alcoholism / Q000378:metabolism*; D000818:Animals; D004298:Dopamine / Q000378:metabolism; D000431:Ethanol / Q000494:pharmacology*; D006801:Humans; D018377:Neurotransmitter Agents / Q000378:metabolism*; D051381:Rats; D011950:Receptors, Cholinergic / Q000378:metabolism; D011954:Receptors, Dopamine / Q000378:metabolism; D013373:Substance P / Q000378:metabolism; D013997:Time Factors; D005680:gamma-Aminobutyric Acid / Q000378:metabolism
D018377:Neurotransmitter Agents; D011950:Receptors, Cholinergic; D011954:Receptors, Dopamine; D013373:Substance P; D000431:Ethanol; D005680:gamma-Aminobutyric Acid; D000109:Acetylcholine; D004298:Dopamine