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Checking your SOCCs and feet: the molecular mechanisms of Ca 2+ entry in skeletal muscle
Author(s) -
Dirksen Robert T.
Publication year - 2009
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.2009.172148
Subject(s) - orai1 , ryanodine receptor , skeletal muscle , transient receptor potential channel , receptor , voltage dependent calcium channel , inositol trisphosphate , calcium signaling , depolarization , extracellular , microbiology and biotechnology , muscle contraction , chemistry , calcium , stim1 , inositol , biology , endocrinology , biochemistry , endoplasmic reticulum , organic chemistry
It has long been known that skeletal muscle contraction persists in the absence of extracellular Ca 2+ . Nevertheless, recent evidence indicates that multiple distinct Ca 2+ entry pathways exist in skeletal muscle: one active at negative potentials that requires store depletion (store‐operated calcium entry or SOCE) and a second that is independent of store depletion and is activated by depolarization (excitation‐coupled calcium entry or ECCE). This review highlights recent findings regarding the molecular identity, subcellular localization, and inter‐relationship between SOCE and ECCE in skeletal muscle. The respective roles of ryanodine receptors (RyRs), dihydropyridine receptors (DHPRs), inositol‐1,4,5‐trisphosphate receptors (IP 3 Rs), canonical transient receptor potential channels (TRPCs), STIM1 Ca 2+ sensor proteins, and Orai1 Ca 2+ permeable channels in mediating SOCE and ECCE in skeletal muscle are discussed. Differences between SOCE and ECCE in skeletal muscle with Ca 2+ entry mechanisms in non‐excitable cells are also reviewed. Finally, potential physiological roles for SOCE and ECCE in skeletal muscle development and function, as well as other currently unanswered questions and controversies in the field are also considered.