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Krystal, J.H. et al.

Krystal, Petrakis, Limoncelli, Webb, Gueorgueva, D'Souza, Boutros, Trevisan, Charney,

Altered NMDA glutamate receptor antagonist response in recovering ethanol-dependent patients.

Ethanol is an antagonist of the N-methyl-D-aspartate (NMDA) glutamate receptor. Ethanol dependence upregulates NMDA receptors and contributes to crosstolerance with selective NMDA receptor antagonists in animals. This study evaluated whether recovering ethanol-dependent patients show evidence of a reduced level of response to the effects of the NMDA receptor antagonist, ketamine. In this double-blind study, 34 recently detoxified alcohol-dependent patients and 26 healthy comparison subjects completed 3 test days involving a 40-min infusion of saline, ketamine 0.1 mg/kg, or ketamine 0.5 mg/kg in a randomized order. Recovering ethanol-dependent patients showed reduced perceptual alterations, dysphoric mood, and impairments in executive cognitive functions during ketamine infusion relative to the healthy comparison group. No attenuation of ketamine-induced amnestic effects, euphoria, or activation was observed. The alterations in NMDA receptor function observed in recovering ethanol-dependent patients may have important implications for ethanol tolerance, ethanol dependence, and the treatment of alcoholism.[1]

References

Altered NMDA glutamate receptor antagonist response in recovering ethanol-dependent patients. Krystal, J.H., Petrakis, I.L., Limoncelli, D., Webb, E., Gueorgueva, R., D'Souza, D.C., Boutros, N.N., Trevisan, L., Charney, D.S. Neuropsychopharmacology (2003) [Pubmed]

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