ArticleThe Journal of physiology2005
Voltage-controlled Ca2+ release and entry flux in isolated adult muscle fibres of the mouse.
Article in The Journal of physiology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 38 citations in OpenAlex.
- Allosteric interactions between RyR channels justify intracellular Ca2+ release of skeletal muscle in quantitative detail.The Journal of general physiology · 2026Article
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- ECC meets CEU-New focus on the backdoor for calcium ions in skeletal muscle cells.The Journal of general physiology · 2020Article
- Improved Calcium Homeostasis and Force by Selenium Treatment and Training in Aged Mouse Skeletal Muscle.Scientific reports · 2020Article
- Measurement of intracellular ion activity in skeletal muscle fibers: Four microelectrodes or no deal.The Journal of general physiology · 2019Article
- No voltage change at skeletal muscle SR membrane during CaThe Journal of general physiology · 2018Article
- Voltage modulates halothane-triggered CaThe Journal of general physiology · 2018Article
- The CaNature communications · 2017Article
- Alternating bipolar field stimulation identifies muscle fibers with defective excitability but maintained local Ca(2+) signals and contraction.Skeletal muscle · 2016Article
- Altered Ca(2+) signaling in skeletal muscle fibers of the R6/2 mouse, a model of Huntington's disease.The Journal of general physiology · 2014Article
- Skeletal muscle fibers: Inactivated or depleted after long depolarizations?The Journal of general physiology · 2013Article
- Major contribution of sarcoplasmic reticulum Ca(2+) depletion during long-lasting activation of skeletal muscle.The Journal of general physiology · 2013Article
- The delayed rectifier potassium conductance in the sarcolemma and the transverse tubular system membranes of mammalian skeletal muscle fibers.The Journal of general physiology · 2012Article
- Residual sarcoplasmic reticulum Ca2+ concentration after Ca2+ release in skeletal myofibers from young adult and old mice.Pflugers Archiv : European journal of physiology · 2012Article
- Voltage clamp methods for the study of membrane currents and SR Ca(2+) release in adult skeletal muscle fibres.Progress in biophysics and molecular biology · 2012Review
- Synthetic localized calcium transients directly probe signalling mechanisms in skeletal muscle.The Journal of physiology · 2012Article
- Measurement of RyR permeability reveals a role of calsequestrin in termination of SR Ca(2+) release in skeletal muscle.The Journal of general physiology · 2011Article
- Calcium indicators and calcium signalling in skeletal muscle fibres during excitation-contraction coupling.Progress in biophysics and molecular biology · 2011Review
- Functional expression of transgenic 1sDHPR channels in adult mammalian skeletal muscle fibres.The Journal of physiology · 2011Article
- Muscle weakness in Ryr1I4895T/WT knock-in mice as a result of reduced ryanodine receptor Ca2+ ion permeation and release from the sarcoplasmic reticulum.The Journal of general physiology · 2011Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The voltage-activated fluxes of Ca(2+) from the sarcoplasmic reticulum (SR) and from the extracellular space were studied in skeletal muscle fibres of adult mice. Single fibres of the interosseus muscle were enzymatically isolated and voltage clamped using a two-electrode technique. The fibres were perfused from the current-passing micropipette with a solution containing 15 mm EGTA and 0.2 mm of either fura-2 or the faster, lower affinity indicator fura-FF. Electrical recordings in parallel with the fluorescence measurements allowed the estimation of intramembrane gating charge movements and transmembrane Ca(2+) inward current exhibiting half-maximal activation at -7.60 +/- 1.29 and 3.0 +/- 1.44 mV, respectively. The rate of Ca(2+) release from the SR was calculated after fitting the relaxation phases of fluorescence ratio signals with a kinetic model to quantify overall Ca(2+) removal. Results obtained with the two indicators were similar. Ca(2+) release was 2-3 orders of magnitude larger than the flux carried by the L-type Ca(2+) current. At maximal depolarization (+50 mV), release flux peaked at about 3 ms after the onset of the voltage pulse and then decayed in two distinct phases. The slower phase, most likely resulting from SR depletion, indicated a decrease in lumenal Ca(2+) content by about 80% within 100 ms. Unlike in frog fibres, the kinetics of the rapid phase of decay showed no dependence on the filling state of the SR and the results provide little evidence for a substantial increase of SR permeability on depletion. The approach described here promises insight into excitation-contraction coupling in future studies of genetically altered mice.
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