Abstract
The actions of glutamate, the major excitatory amino acid in the CNS, are mediated by three receptor subtypes: kainate, quisqualate and N-methyl-D-aspartate (NMDA) receptors. Ethanol, in vitro, is a potent and selective inhibitor of the actions of agonists at the NMDA receptor. Following chronic ethanol ingestion, the number of NMDA receptor-ion channel complexes in certain brain areas is increased. This increase may contribute to the generation of ethanol withdrawal seizures, since administration of an NMDA receptor antagonist can reduce these seizures. The results suggest that certain acute behavioral effects of ethanol, such as effects on memory, as well as certain aspects of ethanol withdrawal, may involve the NMDA receptor.
Original language | English (US) |
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Pages (from-to) | 229-231 |
Number of pages | 3 |
Journal | Alcohol |
Volume | 7 |
Issue number | 3 |
DOIs | |
State | Published - 1990 |
Externally published | Yes |
Keywords
- Calcium influx
- Cyclic GMP
- Ethanol
- Ethanol withdrawal seizures
- Glutamate
- MK-801 binding
- NMDA receptor
ASJC Scopus subject areas
- Health(social science)
- Biochemistry
- Toxicology
- Neurology
- Behavioral Neuroscience