Ion channel modulation as the basis for general anesthesia

Toshio Narahashi*, Gary L. Aistrup, Jon M. Lindstrom, William Marszalec, Keiichi Nagata, Fan Wang, Jay Z. Yeh

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

21 Scopus citations

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 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.

Original languageEnglish (US)
Pages (from-to)185-191
Number of pages7
JournalToxicology Letters
Volume100-101
DOIs
StatePublished - Nov 23 1998

Keywords

  • GABA(A)
  • General anesthesia
  • Ion channel modulation
  • Nicotinic acetylcholine receptor channels

ASJC Scopus subject areas

  • Toxicology

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