| Literature DB >> 10049141 |
T Narahashi1, G L Aistrup, J M Lindstrom, W Marszalec, K Nagata, F Wang, J Z Yeh.
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 microM was very potent in accelerating the desensitization of currents induced by acetylcholine. (5) The ethanol modulation was subunit- and state-dependent, occurring in the alpha3beta4 combination but only weakly in the alpha3beta2 combination. (6) In contrast, halothane at 430 microM (approximately 1 MAC) potently suppressed ACh-induced currents in the alpha3beta2 subunit combination.Entities:
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Year: 1998 PMID: 10049141 DOI: 10.1016/s0378-4274(98)00184-2
Source DB: PubMed Journal: Toxicol Lett ISSN: 0378-4274 Impact factor: 4.372