(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 α3β4 combination but only weakly in the α3β2 combination. (6) In contrast, halothane at 430 μM (~1 MAC) potently suppressed ACh-induced currents in the α3β2 subunit combination. Copyright (C) 1998 Elsevier Science Ireland Ltd.
- General anesthesia
- Ion channel modulation
- Nicotinic acetylcholine receptor channels
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