ArticleThe Journal of physiology2005
Calcium transients in developing mouse skeletal muscle fibres.
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. An erratum has been issued. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 60 citations in OpenAlex.
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- Excitation-contraction coupling in mammalian skeletal muscle: Blending old and last-decade research.Frontiers in physiology · 2022Review
- Matured Myofibers in Bioprinted Constructs with In Vivo Vascularization and Innervation.Gels (Basel, Switzerland) · 2021Article
- Pre-assembled Ca2+ entry units and constitutively active Ca2+ entry in skeletal muscle of calsequestrin-1 knockout mice.The Journal of general physiology · 2020Article
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- Mouse model of severe recessive RYR1-related myopathy.Human molecular genetics · 2019Article
- A Novel Microplate 3D Bioprinting Platform for the Engineering of Muscle and Tendon Tissues.SLAS technology · 2018Article
- Doublet stimulation increases CaThe Journal of general physiology · 2017Article
- Disruption of action potential and calcium signaling properties in malformed myofibers from dystrophin-deficient mice.Physiological reports · 2015Article
- Primary Murine Myotubes as a Model for Investigating Muscular Dystrophy.BioMed research international · 2015Article
- Cholesterol removal from adult skeletal muscle impairs excitation-contraction coupling and aging reduces caveolin-3 and alters the expression of other triadic proteins.Frontiers in physiology · 2015Article
- Tetanic Ca2+ transient differences between slow- and fast-twitch mouse skeletal muscle fibres: a comprehensive experimental approach.Journal of muscle research and cell motility · 2014Article
- Physiological and ultrastructural features of human induced pluripotent and embryonic stem cell-derived skeletal myocytes in vitro.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Analysis of embryonic and larval zebrafish skeletal myofibers from dissociated preparations.Journal of visualized experiments : JoVE · 2013Article
- Orai1-dependent calcium entry promotes skeletal muscle growth and limits fatigue.Nature communications · 2013Article
- Structural and functional evaluation of branched myofibers lacking intermediate filaments.American journal of physiology. Cell physiology · 2012Article
- Intracellular calcium movements during excitation-contraction coupling in mammalian slow-twitch and fast-twitch muscle fibers.The Journal of general physiology · 2012Review
- Muscle weakness in myotonic dystrophy associated with misregulated splicing and altered gating of Ca(V)1.1 calcium channel.Human molecular genetics · 2012Article
Corrections and comments
- Erratum issued
Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ca(2)(+) transients elicited by action potentials were measured using MagFluo-4, at 20-22 degrees C, in intact muscle fibres enzymatically dissociated from mice of different ages (7, 10, 15 and 42 days). The rise time of the transient (time from 10 to 90% of the peak) was 2.4 and 1.1 ms in fibres of 7- and 42-day-old mice, respectively. The decay of the transient was described by a double exponential function, with time constants of 1.8 and 16.4 ms in adult, and of 4.6 and 105 ms in 7-day-old animals. The fractional recovery of the transient peak amplitude after 10 ms, F(2(10))/F(1), determined using twin pulses, was 0.53 for adult fibres and ranged between 0.03 and 0.60 in fibres of 7-day-old animals This large variance may indicate differences in the extent of inactivation of Ca(2)(+) release, possibly related to the difference in ryanodine receptor composition between young and old fibres. At the 7 and 10 day stages, fibres responded to Ca(2)(+)-free solutions with a larger decrease in the transient peak amplitude (25% versus 11% in adult fibres), possibly indicating a contribution of Ca(2)(+) influx to the Ca(2)(+) transient in younger animals. Cyclopiazonic acid (1 mum), an inhibitor of the sarcoplasmic reticulum (SR) Ca(2)(+)-ATPase, abolished the Ca(2)(+) transient decay in fibres of 7- and 10-day-old animals and significantly reduced its rate in older animals. Analysis of the transients with a Ca(2)(+) removal model showed that the results are consistent with a larger relative contribution of the SR Ca(2)(+) pump and a lower expression of myoplasmic Ca(2)(+) buffers in fibres of young versus old animals.
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