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

doi:10.1016/S0378-4274(98)00184-2

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 journal › Article › peer-review

24 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 language	English (US)
Pages (from-to)	185-191
Number of pages	7
Journal	Toxicology Letters
Volume	100-101
DOIs	https://doi.org/10.1016/S0378-4274(98)00184-2
State	Published - Nov 23 1998

Keywords

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

ASJC Scopus subject areas

Toxicology

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10.1016/S0378-4274(98)00184-2

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@article{f34671371a284ce390032e1611e82d71,

title = "Ion channel modulation as the basis for general anesthesia",

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.",

keywords = "GABA(A), General anesthesia, Ion channel modulation, Nicotinic acetylcholine receptor channels",

author = "Toshio Narahashi and Aistrup, {Gary L.} and Lindstrom, {Jon M.} and William Marszalec and Keiichi Nagata and Fan Wang and Yeh, {Jay Z.}",

note = "Funding Information: The work described in this paper were supported by grants from the NIH R01 NS 14144 (TN), R01 AA07836 (TN), F32 AA05447 (GA), R01 NS11323 (JML), the Muscular Dystrophy Association (JML) and the Smokeless Tobacco Research Council (JML). We thank Nayla Hasan for technical assistance and Julia Irizarry for secretarial assistance.",

year = "1998",

month = nov,

day = "23",

doi = "10.1016/S0378-4274(98)00184-2",

language = "English (US)",

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pages = "185--191",

journal = "Toxicology Letters",

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T1 - Ion channel modulation as the basis for general anesthesia

AU - Narahashi, Toshio

AU - Aistrup, Gary L.

AU - Lindstrom, Jon M.

AU - Marszalec, William

AU - Nagata, Keiichi

AU - Wang, Fan

AU - Yeh, Jay Z.

N1 - Funding Information: The work described in this paper were supported by grants from the NIH R01 NS 14144 (TN), R01 AA07836 (TN), F32 AA05447 (GA), R01 NS11323 (JML), the Muscular Dystrophy Association (JML) and the Smokeless Tobacco Research Council (JML). We thank Nayla Hasan for technical assistance and Julia Irizarry for secretarial assistance.

PY - 1998/11/23

Y1 - 1998/11/23

N2 - (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.

AB - (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.

KW - GABA(A)

KW - General anesthesia

KW - Ion channel modulation

KW - Nicotinic acetylcholine receptor channels

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JO - Toxicology Letters

JF - Toxicology Letters

ER -

Ion channel modulation as the basis for general anesthesia

Abstract

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