title: Bridging the myoplasmic gap II: more recent advances in skeletal muscle excitation-contraction coupling.
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.
authors.affiliation: Department of Medicine-Cardiology Division, University of Colorado Denver-Anschutz Medical Campus, 12700 East 19th Avenue, Room 8006, B-139, Aurora, CO 80045, USA roger.bannister@ucdenver.edu.
authors.forename: Roger A
authors.initials: RA
authors.lastname: Bannister
mesh_terms: D000818:Animals; D020746:Calcium Channels, L-Type / Q000378:metabolism; D056966:Excitation Contraction Coupling; D006801:Humans; D015640:Ion Channel Gating; D018482:Muscle, Skeletal / Q000378:metabolism* / Q000648:ultrastructure; D019837:Ryanodine Receptor Calcium Release Channel / Q000378:metabolism; D012519:Sarcoplasmic Reticulum / Q000378:metabolism
chemical_list: D020746:Calcium Channels, L-Type; D019837:Ryanodine Receptor Calcium Release Channel
keywords: 1,4-dihydropyridine receptor; CaV1.1; DHPR; Excitation–contraction coupling; L-type; Skeletal muscle; α1S