Ethanol withdrawal seizures and the NMDA receptor complex

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

doi:10.1016/0014-2999(90)90022-X

Ethanol withdrawal seizures and the NMDA receptor complex

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

Research output: Contribution to journal › Article › peer-review

393 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 language	English (US)
Pages (from-to)	289-296
Number of pages	8
Journal	European Journal of Pharmacology
Volume	176
Issue number	3
DOIs	https://doi.org/10.1016/0014-2999(90)90022-X
State	Published - Feb 13 1990
Externally published	Yes

Keywords

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

ASJC Scopus subject areas

Pharmacology

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10.1016/0014-2999(90)90022-X

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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.",

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T1 - Ethanol withdrawal seizures and the NMDA receptor complex

AU - Grant, Kathleen A.

AU - Valverius, Peter

AU - Hudspith, Michael

AU - Tabakoff, Boris

PY - 1990/2/13

Y1 - 1990/2/13

N2 - 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.

AB - 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.

KW - (Mouse)

KW - Ca channels

KW - Ethanol dependence

KW - MK-801

KW - NMDA (N-methyl-D-aspartate)

KW - Withdrawal seizures

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Ethanol withdrawal seizures and the NMDA receptor complex

Abstract

Keywords

ASJC Scopus subject areas

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