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Ethanol withdrawal seizures and the NMDA receptor complex
K A Grant1, P Valverius, M Hudspith
1Unit for Special Projects, National Institute on Alcohol Abuse and Alcoholism, Rockville, MD 20852.
European Journal of Pharmacology
|February 13, 1990
Summary
Chronic ethanol exposure increases NMDA receptors in the hippocampus, leading to withdrawal seizures. Blocking these receptors with MK-801 reduces seizure severity, suggesting NMDA receptor up-regulation mediates ethanol withdrawal seizures.
Area of Science:
- Neuroscience
- Pharmacology
- Biochemistry
Background:
- Low doses of ethanol inhibit calcium influx via N-methyl-D-aspartate (NMDA) receptors.
- Chronic ethanol consumption can alter neurotransmitter systems in the brain.
Purpose of the Study:
- To investigate the role of NMDA receptor systems in ethanol withdrawal seizures.
- To determine if NMDA receptor up-regulation contributes to seizure activity during ethanol withdrawal.
Main Methods:
- Assessed the number of NMDA receptor/ionophore complexes in the hippocampus of ethanol-treated mice.
- Induced withdrawal seizures using NMDA-exacerbated handling in ethanol-dependent mice.
- Administered the NMDA receptor antagonist MK-801 to assess its effect on seizure occurrence and severity.
Main Results:
- Chronic ethanol treatment increased NMDA receptor/ionophore complexes in the hippocampus.
- NMDA-exacerbated handling induced withdrawal seizures in ethanol-dependent mice.
- MK-801 dose-dependently decreased the occurrence and severity of ethanol withdrawal seizures.
Conclusions:
- The up-regulation of NMDA receptor systems following chronic ethanol exposure may mediate ethanol withdrawal seizures.
- NMDA receptor systems play a critical role in the pathophysiology of ethanol withdrawal.
- Targeting NMDA receptors could be a potential therapeutic strategy for managing ethanol withdrawal symptoms.