COLCHICINE ALTERS APAMIN RECEPTORS, ELECTRICAL-ACTIVITY, AND SKELETAL-MUSCLE RELAXATION

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 repo rted that axonal flow blockade of rat nerves, induced by colchicine, c aused a transient increase in muscle apamin receptors, determined by I -125-apamin binding to membrane fractions. The increase in apamin rece ptors was correlated with repetitive discharges resembling myotonic po tentials 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 pre sence of myotonic-like alterations in the electromyogram and a slowing of muscle relaxation when muscle apamin receptors are increased sugge sts that these channels may participate, among other factors, in the g eneration of some kinds of myotonia. (C) 1993 John Wiley & Sons, Inc.