Abstract
(1) Modulation of the function of the GABA A and neuronal nicotinic acetylcholine receptor channels caused by general anesthetics and modulation of the GABA A receptor-channel by halothane, enflurane, isoflurane, and n-octanol was channel state-dependent. (3) Halothane modulation of the GABA A receptor was independent of subunits, but n-octanol modulation was subunit-dependent. (4) Ethanol at 30–100 μM was very potent in accelerating the desensitization of currents induced by acetylcholine. (5) The ethanol modulation was subunit- and state-dependent, occurring in the α3 β4 combination but only weakly in the α3 β2 combination. (6) In contrast, halothane at 430 μM (∼1 MAC) potently suppressed ACh-induced currents in the α3 β2 subunit combination.
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