ArticleThe Journal of physiology2006
Sarcoplasmic reticulum Ca2+ release and depletion fail to affect sarcolemmal ion channel activity in mouse skeletal muscle.
Article in The Journal of physiology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 32 citations in OpenAlex.
- A mechano- and heat-gated two-pore domain KProceedings of the National Academy of Sciences of the United States of America · 2023Article
- Excitation-contraction coupling in mammalian skeletal muscle: Blending old and last-decade research.Frontiers in physiology · 2022Review
- Review
- A quantitative description of tubular system Ca(2+) handling in fast- and slow-twitch muscle fibres.The Journal of physiology · 2016Article
- Phosphoinositides in Ca(2+) signaling and excitation-contraction coupling in skeletal muscle: an old player and newcomers.Journal of muscle research and cell motility · 2015Review
- Quantifying SOCE fluorescence measurements in mammalian muscle fibres. The effects of ryanodine and osmotic shocks.Journal of muscle research and cell motility · 2013Article
- Enhanced dihydropyridine receptor calcium channel activity restores muscle strength in JP45/CASQ1 double knockout mice.Nature communications · 2013Article
- Partial opening and subconductance gating of mechanosensitive ion channels in dystrophic skeletal muscle.The Journal of physiology · 2012Article
- Temperature and RyR1 regulate the activation rate of store-operated Ca²+ entry current in myotubes.Biophysical journal · 2012Article
- A study of store dependent Ca²⁺ influx in frog skeletal muscle.Journal of muscle research and cell motility · 2012Article
- The role of store-operated calcium influx in skeletal muscle signaling.Cell calcium · 2011Review
- Toward the roles of store-operated Ca2+ entry in skeletal muscle.Pflugers Archiv : European journal of physiology · 2010Review
- Store-operated Ca2+ entry in malignant hyperthermia-susceptible human skeletal muscle.The Journal of biological chemistry · 2010Article
- Sarcoplasmic reticulum Ca2+ depletion in adult skeletal muscle fibres measured with the biosensor D1ER.Pflugers Archiv : European journal of physiology · 2010Article
- New factors contributing to dynamic calcium regulation in the skeletal muscle triad-a crowded place.Biophysical reviews · 2010Review
- Transient receptor potential canonical type 1 (TRPC1) operates as a sarcoplasmic reticulum calcium leak channel in skeletal muscle.The Journal of biological chemistry · 2009Article
- Factors affecting SOCE activation in mammalian skeletal muscle fibers.The journal of physiological sciences : JPS · 2009Article
- Rapid Ca2+ flux through the transverse tubular membrane, activated by individual action potentials in mammalian skeletal muscle.The Journal of physiology · 2009Article
- Electrically silent divalent cation entries in resting and active voltage-controlled muscle fibers.Biophysical journal · 2009Article
- Differential dependence of store-operated and excitation-coupled Ca2+ entry in skeletal muscle on STIM1 and Orai1.The Journal of physiology · 2008Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In skeletal muscle, sarcoplasmic reticulum (SR) Ca2+ depletion is suspected to trigger a calcium entry across the plasma membrane and recent studies also suggest that the opening of channels spontaneously active at rest and possibly involved in Duchenne dystrophy may be regulated by SR Ca2+ depletion. Here we simultaneously used the cell-attached and whole-cell voltage-clamp techniques as well as intracellular Ca2+ measurements on single isolated mouse skeletal muscle fibres to unravel any possible change in membrane conductance that would depend upon SR Ca2+ release and/or SR Ca2+ depletion. Delayed rectifier K+ single channel activity was routinely detected during whole-cell depolarizing pulses. In addition the activity of channels carrying unitary inward currents of approximately 1.5 pA at -80 mV was detected in 17 out of 127 and in 21 out of 59 patches in control and mdx dystrophic fibres, respectively. In both populations of fibres, large whole-cell depolarizing pulses did not reproducibly increase this channel activity. This was also true when, repeated application of the whole-cell pulses led to exhaustion of the Ca2+ transient. SR Ca2+ depletion produced by the SR Ca2+ pump inhibitor cyclopiazonic acid (CPA) also failed to induce any increase in the resting whole-cell conductance and in the inward single channel activity. Overall results indicate that voltage-activated SR Ca2+ release and/or SR Ca2+ depletion are not sufficient to activate the opening of channels carrying inward currents at negative voltages and challenge the physiological relevance of a store-operated membrane conductance in adult skeletal muscle.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.