Ethanol withdrawal seizures and the NMDA receptor complex

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

Research output: Contribution to journalArticlepeer-review

380 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
Externally publishedYes

Keywords

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

ASJC Scopus subject areas

  • Pharmacology

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