Ion channel modulation as the basis for general anesthesia

Toxicol Lett. 1998 Nov 23;100-101:185-91. doi: 10.1016/s0378-4274(98)00184-2.


(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.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.
  • Review

MeSH terms

  • Anesthesia, General*
  • Anesthetics, General / pharmacology*
  • Animals
  • Humans
  • Ion Channels / drug effects*
  • Receptors, GABA-A / chemistry
  • Receptors, GABA-A / drug effects


  • Anesthetics, General
  • Ion Channels
  • Receptors, GABA-A