Dose-Related Ethanol-like Effects of the NMDA Antagonist, Ketamine, in Recently Detoxified Alcoholics

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Abstract
A GROWING body of research indicates that the capacity of ethanol to block glutamate effects at the N-methyl-D-aspartate (NMDA) receptor contributes to its acute behavioral effects and to the natural history and neuropathology of alcoholism.1 Ethanol reduces NMDA-stimulated ion currents in a noncompetitive and concentration-dependent fashion across the range of ethanol concentrations (5-100 mmol/L) associated with human ethanol intoxication.2-7 Long-term ethanol administration increases the levels of NMDA receptor subunits, up-regulates NMDA receptor-related binding, and produces cross-tolerance with other noncompetitive NMDA antagonists.8-12 Increased NMDA receptor function produced by long-term ethanol administration contributes to withdrawal-related seizures10 and neurotoxic effects.13