Bridging the myoplasmic gap II: more recent advances in skeletal muscle excitation-contraction coupling

J Exp Biol. 2016 Jan;219(Pt 2):175-82. doi: 10.1242/jeb.124123.

Abstract

In skeletal muscle, excitation-contraction (EC) coupling relies on the transmission of an intermolecular signal from the voltage-sensing regions of the L-type Ca(2+) channel (Ca(V)1.1) in the plasma membrane to the channel pore of the type 1 ryanodine receptor (RyR1) nearly 10 nm away in the membrane of the sarcoplasmic reticulum (SR). Even though the roles of Ca(V)1.1 and RyR1 as voltage sensor and SR Ca(2+) release channel, respectively, have been established for nearly 25 years, the mechanism underlying communication between these two channels remains undefined. In the course of this article, I will review current viewpoints on this topic with particular emphasis on recent studies.

Keywords: 1,4-dihydropyridine receptor; CaV1.1; DHPR; Excitation–contraction coupling; L-type; Skeletal muscle; α1S.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Calcium Channels, L-Type / metabolism
  • Excitation Contraction Coupling*
  • Humans
  • Ion Channel Gating
  • Muscle, Skeletal / metabolism*
  • Muscle, Skeletal / ultrastructure
  • Ryanodine Receptor Calcium Release Channel / metabolism
  • Sarcoplasmic Reticulum / metabolism

Substances

  • Calcium Channels, L-Type
  • Ryanodine Receptor Calcium Release Channel