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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