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• W2015805931 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." @default.
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• W2015805931 date "1990-02-01" @default.
• W2015805931 modified "2023-09-26" @default.
• W2015805931 title "Ethanol withdrawal seizures and the NMDA receptor complex" @default.
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• W2015805931 doi "https://doi.org/10.1016/0014-2999(90)90022-x" @default.
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