Checking your SOCCs and feet: the molecular mechanisms of Ca2+ entry in skeletal muscle

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 calci...

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Published inThe Journal of physiology Vol. 587; no. 13; pp. 3139 - 3147
Main Author Dirksen, Robert T.
Format Journal Article
LanguageEnglish
Published Oxford, UK The Physiological Society 01.07.2009
Blackwell Publishing Ltd
Blackwell Science Inc
Subjects
Animals
Calcium - metabolism
Calcium Channels - chemistry
Calcium Channels - metabolism
Humans
Membrane Proteins - chemistry
Membrane Proteins - metabolism
Models, Biological
Muscle, Skeletal - metabolism
Neoplasm Proteins - chemistry
Neoplasm Proteins - metabolism
ORAI1 Protein
Ryanodine Receptor Calcium Release Channel - metabolism
Stromal Interaction Molecule 1
Symposium Section Reviews and s: Calsequestrin, Triadin and More
T-Lymphocytes - metabolism
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Summary: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.
Bibliography:The Journal of Physiology
which took place at the 53rd Biophysical Society Annual Meeting at Boston, MA, USA on 27 February 2009. It was commissioned by the Editorial Board and reflects the views of the authors.
This review was presented at
Calsequestrin, triadin and more: the proteins that modulate calcium release in cardiac and skeletal muscle
Symposium on
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This review was presented at The Journal of Physiology Symposium on Calsequestrin, triadin and more: the proteins that modulate calcium release in cardiac and skeletal muscle, which took place at the 53rd Biophysical Society Annual Meeting at Boston, MA, USA on 27 February 2009. It was commissioned by the Editorial Board and reflects the views of the authors.
ISSN:0022-3751
1469-7793
DOI:10.1113/jphysiol.2009.172148