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Neuropsychopharmacology. 2003 Nov;28(11):2020-8.

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

Author information

1
Department of Veterans Affairs Alcohol Research Center, VA Connecticut Healthcare System (116-A), West Haven, CT, USA. john.krystal@yale.edu

Abstract

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.

PMID:
12888778
DOI:
10.1038/sj.npp.1300252
[Indexed for MEDLINE]
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