Ethanol withdrawal seizures and the NMDA receptor complex

Kathleen A. Grant, Peter Valverius, Michael Hudspith, Boris Tabakoff

    Research output: Contribution to journalArticle

    378 Scopus citations

    Abstract

    Prior biochemical and electrophysiological studies have shown that low doses of ethanol inhibited calcium influx through the N-methyl-D-aspartate (NMDA) receptor/ionophore. The present data show that chronic ethanol treatment results in an increase in the number of NMDA receptor/ionophore complexes in the hippocampus, a brain area known to be associated with ethanol withdrawal seizure activity. Treatment during withdrawal with NMDA-exacerbated handling induced withdrawal seizures in the ethanol-dependent mice, while administration of the NMDA receptor-associated calcium channel antagonist MK-801 decreased the occurrence and severity of the withdrawal seizures in a dose-dependent manner. The results are consistent with the hypothesis that the up-regulation of the NMDA receptor systems following chronic ethanol treatment may mediate the seizures associated with ethanol withdrawal in dependent animals.

    Original languageEnglish (US)
    Pages (from-to)289-296
    Number of pages8
    JournalEuropean Journal of Pharmacology
    Volume176
    Issue number3
    DOIs
    StatePublished - Feb 13 1990

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    Keywords

    • (Mouse)
    • Ca channels
    • Ethanol dependence
    • MK-801
    • NMDA (N-methyl-D-aspartate)
    • Withdrawal seizures

    ASJC Scopus subject areas

    • Pharmacology

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