(1) Modulation of the function of the GABA(A) and neuronal nicotinic acetyl
choline receptor channels caused by general anesthetics and modulation of t
he GABA(A) receptor-channel by halothane, enflurane, isoflurane, and n-octa
nol was channel state-dependent. (3) Halothane modulation of the GABA(A) re
ceptor was independent of subunits, but n-octanol modulation was subunit-de
pendent. (4) Ethanol at 30-100 mu M was very potent in accelerating the des
ensitization of currents induced by acetylcholine. (5) The ethanol modulati
on was subunit: and state-dependent, occurring in the alpha 3 beta 4 combin
ation but only weakly in the alpha 3 beta 2 combination. (6) In contrast, h
alothane at 430 mu M (similar to 1 MAC) potently suppressed ACh-induced cur
rents in the alpha 3 beta 2 subunit combination. (C) 1998 Elsevier Science
Ireland Ltd. All rights reserved.