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Journal Article

Ethanol inhibits glutamate-induced currents in heteromeric NMDA receptor subtypes

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Kuner,  Thomas
Department of Molecular Neurobiology, Max Planck Institute for Medical Research, Max Planck Society;
Department of Cell Physiology, Max Planck Institute for Medical Research, Max Planck Society;

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Schöpfer,  Ralf
Department of Molecular Neurobiology, Max Planck Institute for Medical Research, Max Planck Society;

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Citation

Kuner, T., Schöpfer, R., & Korpi, E. R. (1993). Ethanol inhibits glutamate-induced currents in heteromeric NMDA receptor subtypes. NeuroReport, 5(3), 297-300. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/7905294.


Cite as: http://hdl.handle.net/11858/00-001M-0000-0019-AAC2-C
Abstract
Maximal L-glutamate/glycine-evoked currents were inhibited by ethanol in Xenopus laevis oocytes expressing recombinant heteromeric NMDA receptors consisting of NR1-NR2A, NR1-NR2B, and NR1-NR2C subunit combinations. Concentration-dependent inhibition was observed at ethanol concentrations of > or = 50 mM both in Ca(2+)-containing and Ca(2+)-deficient, Ba(2+)-containing Mg(2+)-free media. The NR1-NR2C channels were slightly less sensitive to ethanol inhibition than the other heteromeric channels in Ca(2+)-deficient, Ba(2+)-containing medium. The inhibition was unaffected by the clamping-voltage and by a mutation [NR1-NR2A(N595Q)] that prevents the Mg(2+)-blockade of the channels, indicating that the mechanism of action of ethanol differs from that of Mg2+. The results are consistent with the hypothesis that the NMDA receptor subtypes can mediate many behavioural actions of ethanol.