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A hypothesis for the mechanism of sodium channel opening by batrachotoxin and related toxins

Authors
Journal
FEBS Letters
0014-5793
Publisher
Wiley Blackwell (John Wiley & Sons)
Publication Date
Volume
163
Issue
2
Identifiers
DOI: 10.1016/0014-5793(83)80810-2

Abstract

Abstract The mechanism of action of one class of sodium channel opening agents (batrachotoxinin, veratridine, aconitine and grayanotoxin) is proposed to involve complexation of a triad of agent oxygen atoms with the ε-ammonium ion of a channel lysing side chain, holding open the mouth or exit of the ion channel. This idea complements the oxygen triad model derived by structural considerations (Masutani, T., Seyama, I., Narahashi, T. and Iwasa, J. (1981) J. Pharm. Exp. Therap. 217,812) and extended by crystal structure comparisons (Codding, P.W. (1983) J. Am. Chem. Soc. 105, 3172). The mechanism is based on results for acetylcholine receptor ion channel gating, structure and function, using single group rotation (SGR) theory (cf. Kosower, E.M. (1983) Biochem. Biophys. Res. Commun. 111, 1022 and in press (1983); FEBS Lett. (1983) 155, 245; ibid. 157, 144; Biophys. J. (1983) 45, in press).

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