PT  - JOURNAL ARTICLE
AU  - Rita A. Cardoso
AU  - Susan J. Brozowski
AU  - Laura E. Chavez-Noriega
AU  - Michael Harpold
AU  - C. Fernando Valenzuela
AU  - R. Adron Harris
TI  - Effects of Ethanol on Recombinant Human Neuronal Nicotinic Acetylcholine Receptors Expressed in <em>Xenopus</em>Oocytes
DP  - 1999 May 01
TA  - Journal of Pharmacology and Experimental Therapeutics
PG  - 774--780
VI  - 289
IP  - 2
4099  - http://jpet.aspetjournals.org/content/289/2/774.short
4100  - http://jpet.aspetjournals.org/content/289/2/774.full
SO  - J Pharmacol Exp Ther1999 May 01; 289
AB  - Alcohol and tobacco use is highly correlated in humans, and studies with animal models suggest an interaction of alcohol with neuronal nicotinic acetylcholine receptors (nAChRs). The aim of the present study was to characterize the effect of acute ethanol treatment on different combinations of human nAChR (hnAChR) subunits expressed inXenopus oocytes. Ethanol (75 mM) potentiated ACh-induced currents in α2β4, α4β4, α2β2, and α4β2 receptors. This effect was due to an increase in E max, without a change in the EC50 or Hill coefficient. hnAChR α2β4 did not develop tolerance to repeated applications of ethanol or continuous exposure (10 min). The α3β2 and α3β4combinations were insensitive to ethanol. Low concentrations of ethanol (25 and 50 mM) significantly inhibited homomeric α7receptor function, but these receptors showed highly variable responses to ethanol. These results indicate that ethanol effects on hnAChRs depend on the receptor subunit composition. In light of recent evidence indicating that nAChRs mediate and modulate synaptic transmission in the central nervous system, we postulate that acute intoxication might involve ethanol-induced alterations in the function of these receptors. U.S. Government