ArticleBiophysical journal2003
Voltage-activated calcium signals in myotubes loaded with high concentrations of EGTA.
Article in Biophysical journal, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 26 citations in OpenAlex.
- The distal C terminus of the dihydropyridine receptor βProceedings of the National Academy of Sciences of the United States of America · 2022Article
- Detection of Ca2+ transients near ryanodine receptors by targeting fluorescent Ca2+ sensors to the triad.The Journal of general physiology · 2021Article
- Optogenetic approach for targeted activation of global calcium transients in differentiated C2C12 myotubes.Scientific reports · 2017Article
- 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
- Hypermuscular mice with mutation in the myostatin gene display altered calcium signalling.The Journal of physiology · 2014Article
- Modulation of sarcoplasmic reticulum Ca2+ release in skeletal muscle expressing ryanodine receptor impaired in regulation by calmodulin and S100A1.American journal of physiology. Cell physiology · 2011Article
- S100A1 promotes action potential-initiated calcium release flux and force production in skeletal muscle.American journal of physiology. Cell physiology · 2010Article
- Dissecting cooperative calmodulin binding to CaM kinase II: a detailed stochastic model.Journal of computational neuroscience · 2009Article
- Local calcium signals induced by hyper-osmotic stress in mammalian skeletal muscle cells.Journal of muscle research and cell motility · 2009Article
- IQ-motif proteins influence intracellular free Ca2+ in hippocampal neurons through their interactions with calmodulin.Journal of neurophysiology · 2008Article
- Neurogranin controls the spatiotemporal pattern of postsynaptic Ca2+/CaM signaling.Biophysical journal · 2007Article
- Effect of TPEN on the calcium release of cultured C2C12 mouse myotubes.Journal of muscle research and cell motility · 2007Article
- Contribution from P2X and P2Y purinoreceptors to ATP-evoked changes in intracellular calcium concentration on cultured myotubes.Pflugers Archiv : European journal of physiology · 2007Article
- Differentiation-dependent alterations in the extracellular ATP-evoked calcium fluxes of cultured skeletal muscle cells from mice.Pflugers Archiv : European journal of physiology · 2007Article
- A possible role of the junctional face protein JP-45 in modulating Ca2+ release in skeletal muscle.The Journal of physiology · 2006Article
- Calcium transients in developing mouse skeletal muscle fibres.The Journal of physiology · 2005Article
- Functional interaction of CaV channel isoforms with ryanodine receptors studied in dysgenic myotubes.Biophysical journal · 2005Article
- Voltage-controlled Ca2+ release and entry flux in isolated adult muscle fibres of the mouse.The Journal of physiology · 2005Article
- Altered inactivation of Ca2+ current and Ca2+ release in mouse muscle fibers deficient in the DHP receptor gamma1 subunit.The Journal of general physiology · 2004Article
- How source content determines intracellular Ca2+ release kinetics. Simultaneous measurement of [Ca2+] transients and [H+] displacement in skeletal muscle.The Journal of general physiology · 2004Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In the present study we describe the analysis of optically recorded whole cell Ca(2+) transients elicited by depolarization in cultured skeletal myotubes. Myotubes were obtained from the mouse muscle-derived cell line C2C12 and from mouse satellite cells. The cells were voltage-clamped and perfused with an artificial intracellular solution containing 15 mM EGTA to ensure that the bulk of the Ca(2+) mobilized by depolarization is bound to this extrinsic buffer. The apparent on- and off-rate constants of EGTA and the dissociation rate constant of fura-2 in the cell were estimated by investigating the Ca(2+)-dependence of kinetic components of the fluorescence decay after repolarization. These parameters were used to calculate the time course of the total voltage-controlled flux of Ca(2+) to the myoplasmic space (Ca(2+) input flux). The validity of the procedure was confirmed by model simulations using artificial Ca(2+) input fluxes. Both C2C12 and primary-cultured myotubes showed a very similar phasic-tonic time course of the Ca(2+) input flux. In most measurements, the input flux was considerably larger and showed a different time course than the estimated Ca(2+) flux carried by the L-type Ca(2+) channels, indicating that it consists mainly of voltage-controlled Ca(2+) release from the sarcoplasmic reticulum. In cells with extremely small fluorescence transients, the calculated input fluxes matched the kinetic characteristics of the Ca(2+) inward current, indicating that Ca(2+) release was absent. These measurements served as a control for the fidelity of the fluorimetric flux analysis. The procedures promise a deeper insight into alterations of Ca(2+) release gating in studies employing myotube expression systems for mutant or chimeric protein components of excitation-contraction coupling.
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