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Molecular Pharmacology

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Research ArticleArticle

A Novel Mode of Neurotoxin Action

A Polypeptide Toxin Isolated from Anemonia sulcata Shifts the Voltage Dependence of the Maximal Rate of Rise of Na+ Action Potentials in a Mouse Neuronal Clone

MICHIHISA MIYAKE and SHOJI SHIBATA
Molecular Pharmacology November 1981, 20 (3) 453-456;
MICHIHISA MIYAKE
Mitsubishi-Kasei Institute of Life Sciences, Machida, Tokyo 194, Japan, and Department of Pharmacology, University of Hawaii School of Medicine, Honolulu, Hawaii 96822
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SHOJI SHIBATA
Mitsubishi-Kasei Institute of Life Sciences, Machida, Tokyo 194, Japan, and Department of Pharmacology, University of Hawaii School of Medicine, Honolulu, Hawaii 96822
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Abstract

Mouse neuroblastoma N-18 cells, which evoked a mixed Na+ and Ca2+ action potential under appropriate tissue culture conditions, were used to study the electrophysiological pharmacology of a polypeptide neurotoxin (ATX-II) from a sea anemone. When applied extracellularly, ATX-II in concentrations as low as 10-7 M increased reversibly the electrical excitability of N-18 cells, e.g., the toxin caused spontaneous firing in which the duration and the maximal rate of rise of each action potential were increased. A set of results obtained in this work strongly suggests that this effect of the toxin was mainly due to its interaction with the inactivation gate of the Na+ channel of N-18 cells, i.e., ATX-II inhibited both the time-dependent and the steady-state processes of Na+ channel inactivation. Accordingly, this toxin is a useful tool for elucidating the molecular structure of the voltage-sensitive inactivation gate of the Na+ channel.

  • Copyright © 1981 by The American Society for Pharmacology and Experimental Therapeutics

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Molecular Pharmacology
Vol. 20, Issue 3
1 Nov 1981
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Research ArticleArticle

A Novel Mode of Neurotoxin Action

MICHIHISA MIYAKE and SHOJI SHIBATA
Molecular Pharmacology November 1, 1981, 20 (3) 453-456;

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Research ArticleArticle

A Novel Mode of Neurotoxin Action

MICHIHISA MIYAKE and SHOJI SHIBATA
Molecular Pharmacology November 1, 1981, 20 (3) 453-456;
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