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Ethanol Inhibition of N ‐Methyl‐D‐Aspartate‐Stimulated Endogenous Dopamine Release from Rat Striatal Slices: Reversal by Glycine
Author(s) -
Woodward John J.,
Gonzales Rueben A.
Publication year - 1990
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1990.tb01931.x
Subject(s) - dopamine , chemistry , ethanol , glycine , tetrodotoxin , inhibitory postsynaptic potential , nmda receptor , magnesium , calcium , endogeny , medicine , endocrinology , biochemistry , receptor , biology , amino acid , organic chemistry
N ‐Methyl‐D‐aspartate stimulated a concentration‐dependent release of endogeneous dopamine from rat striatal slices. The threshold for activation was between 10 and 25 μM and reached a maximum at 1 m M . Release was completely blocked by magnesium or tetrodotoxin. Ethanol (10–200 m M ) significantly inhibited the N ‐methyl‐D‐aspartate‐stimulated release of dopamine by 20–45%, with half‐maximal inhibition occurring at ∼21 m M . Addition of ethanol plus increasing concentrations of magnesium resulted in a greater inhibition of N ‐methyl‐D‐aspartate‐stimulated dopamine release than that observed with magnesium alone. However, this effect appeared to be due to a noninteractive additive effect of the two antagonists, as the IC 50 value for magnesium inhibition was not significantly altered by ethanol. Glycine, which had no effect on dopamine release by itself, completely reversed the inhibitory effects of ethanol (25 m M ) at low micromolar concentrations. These results suggest that ethanol may produce its effects in striatal slices by interfering with a glycine modulatory site of the N ‐methyl‐D‐aspartate receptor‐ionophore complex.