Abstract
Ethanol inhibits the function of the glutamate NMDA receptors in the central nervous system. This action contributes to some of the acute central effects of ethanol, for example: amnestic, anticonvulsant or neuroprotective activity. Chronic ethanol exposure results in up-regulation of the NMDA receptors. Overactivity of the glutamatergic neurotransmission after cessation of chronic alcohol treatment is implicated in the occurrence of seizures and neuronal damage during ethanol withdrawal. Moreover, NMDA receptors may be involved in reinforcing properties of ethanol.