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Effects of Ethanol on Monoamine and Amino Acid Release from Cerebral Cortical Slices of the Alcohol‐Preferring P Line of Rats
Author(s) -
McBride W. J.,
Murphy J. M.,
Lumeng L.,
Li T.K.
Publication year - 1986
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.1530-0277.1986.tb05072.x
Subject(s) - chemistry , glutamate receptor , monoamine neurotransmitter , cerebral cortex , ethanol , dopamine , medicine , endocrinology , serotonin , nmda receptor , neurotransmitter , biochemistry , biology , receptor
The effects of 250 mg/100 ml ethanol on the efflux of 3,4‐dihydrox‐yphenylacetic acid (DOPAC) and the 35 nw K+‐stimulated, Ca 2+ ‐dependent release of norepinephrine (NE), dopamine (DA), serotonin (5‐HT), γ‐aminobutyric acid (GABA), glutamate, and aspartate from cerebral cortical slices of the alcohol‐preferring P line of rats and stock Wistar rats were studied. The K+‐stimuiated, Ca 2+ ‐dependent release of GABA for the P rats was 35% lower, while the release of glutamate was almost twice that of the stock animals. The release of the other compounds was similar for the two groups. Addition of 250 mg/100 ml ethanol to the superfusion media did not after the release of NE, DA, and 5‐HT nor the efflux of DOPAC from cortical slices of either group of rats. However, the K+‐stimulated, Ca 2+ ‐dependent release of GABA, glutamate, and aspartate was significantly enhanced by ethanol for both the P and stock group of rats. These in vitro data do not support a direct action of ethanol on DA, NE, and 5‐HT release or on DOPAC efflux, but suggest a direct action on the transmitter release process for GABA, glutamate, and aspartate in the cerebral cortex.