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Colchicine alters apamin receptors, electrical activity, and skeletal muscle relaxation
Author(s) -
Vergara Cecilia,
Ramirez Beatriz,
Behrens María Isabel
Publication year - 1993
Publication title -
muscle and nerve
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.025
H-Index - 145
eISSN - 1097-4598
pISSN - 0148-639X
DOI - 10.1002/mus.880160908
Subject(s) - apamin , endocrinology , medicine , skeletal muscle , sk channel , chemistry , receptor , colchicine , potassium channel , biophysics , biology , ion channel
A low conductance calcium‐activated K + channel is thought to regulate the rate of firing of several excitable cells. In skeletal muscle the expression of this channel is under nerve control. Previously, we reported that axonal flow blockade of rat nerves, induced by colchicine, caused atransient increase in muscle apamin receptors, determined by 125 I‐apamin binding to membrane fractions. The increase in apamin receptors was correlated with repetitive discharges resembling myotonic potentials in the electromyogram, that were blockable by apamin. Here we show that the increase in muscle apamin receptors and the alteration of the electromyogram are followed closely by a slowing of the twitch relaxation, that in turn, is decreased by apamin. Furthermore, the presence of myotonic‐like alterations in the electromyogram and a slowing of muscle relaxation when muscle apaminreceptors are increased suggests that these channels may participate, amongother factors, in the generation of some kinds of myotonia. © 1993 John Wiley & Sons, Inc.