ArticleJournal of muscle research and cell motility2007
Ca2+ store determines gating of store operated calcium entry in mammalian skeletal muscle.
Article in Journal of muscle research and cell motility, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 19 citations in OpenAlex.
- Excitation-contraction coupling in mammalian skeletal muscle: Blending old and last-decade research.Frontiers in physiology · 2022Review
- Malignant hyperthermia: a review.Orphanet journal of rare diseases · 2015Review
- The Sick and the Weak: Neuropathies/Myopathies in the Critically Ill.Physiological reviews · 2015Review
- The excitation-contraction coupling mechanism in skeletal muscle.Biophysical reviews · 2014Review
- Quantifying SOCE fluorescence measurements in mammalian muscle fibres. The effects of ryanodine and osmotic shocks.Journal of muscle research and cell motility · 2013Article
- A study of store dependent Ca²⁺ influx in frog skeletal muscle.Journal of muscle research and cell motility · 2012Article
- Toward the roles of store-operated Ca2+ entry in skeletal muscle.Pflugers Archiv : European journal of physiology · 2010Review
- Two inhibitors of store operated Ca2+ entry suppress excitation contraction coupling in frog skeletal muscle.Journal of muscle research and cell motility · 2010Article
- New factors contributing to dynamic calcium regulation in the skeletal muscle triad-a crowded place.Biophysical reviews · 2010Review
- Factors affecting SOCE activation in mammalian skeletal muscle fibers.The journal of physiological sciences : JPS · 2009Article
- Role of Ca2+, membrane excitability, and Ca2+ stores in failing muscle contraction with aging.Experimental gerontology · 2009Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This work describes the gating of the store operated calcium entry (SOCE) in adult mammalian skeletal muscle. Flexor digitorum brevis fibers (FDB) were isolated from adult mice and exposed to conditions to deplete the sarcoplasmic reticulum (SR). A transient SR depletion caused either by repetitive depolarizations, chlorocresol (CMC) or, cyclopiazonic acid (CPA) induced a bell shaped calcium entry that raised the [Ca(2+)](i) to a maximum of 27.09 +/- 4.35 nM from the resting value. The activation time to reach 10-90% of the maximum amplitude was 112 +/- 10 s (n = 22). On the other hand, any mechanism that caused a permanent SR depletion (like thapsigargin, continuous CPA, or continuous CMC) triggered a calcium entry pathway that lasted 325 +/- 23 s and raised the [Ca(2+)](i )to 129.50 +/- 13.05 nM from the resting level (n = 28). Then, a prolonged depletion triggered an increase in [Ca(2+)](i) to higher values and for a longer time than when the SR is transiently depleted (p < 0.001). Our results, in skeletal muscle, showed that calcium store depletion was the signal for SOCE activation and how the SR got depleted was not relevant. Also, we found that SOCE deactivation was not caused by [Ca(2+)](i) but by the SR content. Our results suggest that the SR calcium content plays an important role in SOCE gating in mammalian skeletal muscle and a calcium sensor is located inside the SR.
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