Effects of Ethanol on Monoamine and Amino Acid Release from Cerebral Cortical Slices of the Alcohol-Preferring P Line of Rats

Authors

  • W. J. McBride PhD,

    Corresponding author
    1. Departments of Physchiatry, Medicine, and Biochemistry, the Institute of Psychiatric Research, Indiana University School of Medicine and R. L. Roudebush Veterans Administration Center, Indianapolis, Indiana.
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  • J. M. Murphy PhD,

    1. Departments of Physchiatry, Medicine, and Biochemistry, the Institute of Psychiatric Research, Indiana University School of Medicine and R. L. Roudebush Veterans Administration Center, Indianapolis, Indiana.
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  • L. Lumeng MD,

    1. Departments of Physchiatry, Medicine, and Biochemistry, the Institute of Psychiatric Research, Indiana University School of Medicine and R. L. Roudebush Veterans Administration Center, Indianapolis, Indiana.
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  • T.-K. Li MD

    1. Departments of Physchiatry, Medicine, and Biochemistry, the Institute of Psychiatric Research, Indiana University School of Medicine and R. L. Roudebush Veterans Administration Center, Indianapolis, Indiana.
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*Dr. W. J. McBride, Indiana University School of Medicine, Institute of Psychiatric Research, 791 Union Dr., Indianapolis, IN 46223.

Abstract

The effects of 250 mg/100 ml ethanol on the efflux of 3,4-dihydrox-yphenylacetic acid (DOPAC) and the 35 nw K+-stimulated, Ca2+-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, Ca2+-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, Ca2+-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.

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