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Vol. 289, Issue 2, 774-780, May 1999
Department of Neurosciences, University of New Mexico Health
Sciences Center, Albuquerque, New Mexico (R.A.C., C.F.V.);
Department
of Pharmacology, University of Colorado Health Sciences Center, Denver,
Colorado (S.J.B.);
SIBIA Neurosciences, Inc., La Jolla, California
(L.E.C.-N.);
National Center for Genome Resources, Santa Fe, New Mexico
(M.H.); and
Institute for Cellular and Molecular Biology, University of
Texas, Austin, Texas (R.A.H.)
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 in
Xenopus oocytes. Ethanol (75 mM) potentiated ACh-induced currents in 
2
4,
44, 22, and
42 receptors. This effect was due to an
increase in Emax, without a change in the
EC50 or Hill coefficient. hnAChR
24 did not develop tolerance to repeated applications of ethanol or continuous exposure (10 min). The
32 and 34
combinations were insensitive to ethanol. Low concentrations of ethanol
(25 and 50 mM) significantly inhibited homomeric 7 receptor 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.
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