EXCITATION CONTRACTION COUPLING IN NORMAL AND MDX MICE

The protein dystrophin is absent from patients with Duchenne muscular dystrophy and from the muscles of mdx mice. Recent studies have shown that dystrophin is located at the surface membrance and at the triadic junction, where it is associated with the transverse tubular membrane. Since the triadic junction is the site of excitation‐contraction (EC) coupling, we have investigated whether intramembrane charge movement, a step in EC coupling, is modified by the absence of dystrophin. Charge movements are thought to arise from the transverse tubular membrane and to underlie the dependence of sarcoplasmic reticulum Ca2+ release on transverse tubular membrane potential. We find no differences between intramembrane charge movements or passive membrane electrical properties measured in muscles from mdx mice compared with normal mice. If dystrophin does play a role in EC coupling, that role is likely to be subsequent to the charge movement step. Copyright © 1990 John Wiley & Sons, Inc.