ArticleThe Journal of physiology1999
Intracellular calcium signals measured with indo-1 in isolated skeletal muscle fibres from control and mdx mice.
Article in The Journal of physiology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 73 citations in OpenAlex.
- Reduced voltage-activated Ca2+ release flux in muscle fibers from a rat model of Duchenne dystrophy.The Journal of general physiology · 2025Article
- Superfast excitation-contraction coupling in adult zebrafish skeletal muscle fibers.The Journal of general physiology · 2022Article
- Abnormal Calcium Handling in Duchenne Muscular Dystrophy: Mechanisms and Potential Therapies.Frontiers in physiology · 2021Review
- Genetic evidence in the mouse solidifies the calcium hypothesis of myofiber death in muscular dystrophy.Cell death and differentiation · 2015Review
- Disruption of action potential and calcium signaling properties in malformed myofibers from dystrophin-deficient mice.Physiological reports · 2015Article
- Critical Role of Intracellular RyR1 Calcium Release Channels in Skeletal Muscle Function and Disease.Frontiers in physiology · 2015Review
- The role of proteases in excitation-contraction coupling failure in muscular dystrophy.American journal of physiology. Cell physiology · 2015Article
- Increased sarcolipin expression and decreased sarco(endo)plasmic reticulum Ca2+ uptake in skeletal muscles of mouse models of Duchenne muscular dystrophy.Journal of muscle research and cell motility · 2013Article
- Structural and functional evaluation of branched myofibers lacking intermediate filaments.American journal of physiology. Cell physiology · 2012Article
- Sarcoplasmic reticulum Ca2+ permeation explored from the lumen side in mdx muscle fibers under voltage control.The Journal of general physiology · 2012Article
- Calcium indicators and calcium signalling in skeletal muscle fibres during excitation-contraction coupling.Progress in biophysics and molecular biology · 2011Review
- In vivo expression of G-protein beta1gamma2 dimer in adult mouse skeletal muscle alters L-type calcium current and excitation-contraction coupling.The Journal of physiology · 2010Article
- Transient receptor potential canonical type 1 (TRPC1) operates as a sarcoplasmic reticulum calcium leak channel in skeletal muscle.The Journal of biological chemistry · 2009Article
- Calcium influx is sufficient to induce muscular dystrophy through a TRPC-dependent mechanism.Proceedings of the National Academy of Sciences of the United States of America · 2009Article
- T-tubule disorganization and defective excitation-contraction coupling in muscle fibers lacking myotubularin lipid phosphatase.Proceedings of the National Academy of Sciences of the United States of America · 2009Article
- Malformed mdx myofibers have normal cytoskeletal architecture yet altered EC coupling and stress-induced Ca2+ signaling.American journal of physiology. Cell physiology · 2009Article
- Expression of the muscular dystrophy-associated caveolin-3(P104L) mutant in adult mouse skeletal muscle specifically alters the Ca(2+) channel function of the dihydropyridine receptor.Pflugers Archiv : European journal of physiology · 2008Article
- Comparison of the myoplasmic calcium transient elicited by an action potential in intact fibres of mdx and normal mice.The Journal of physiology · 2008Article
- Design of a disulfide-less, pharmacologically inert, and chemically competent analog of maurocalcine for the efficient transport of impermeant compounds into cells.The Journal of biological chemistry · 2008Article
- Transient loss of voltage control of Ca2+ release in the presence of maurocalcine in skeletal muscle.Biophysical journal · 2006Article
Corrections and comments
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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
1. Intracellular free calcium concentration ([Ca2+]i) was measured with the fluorescent indicator indo-1 in single skeletal fibres enzymatically isolated from the flexor digitorum brevis and interosseus muscles of control and dystrophic mdx C57BL/10 mice. Measurements were taken from a portion of fibre that was voltage clamped to allow detection of depolarization-induced changes in [Ca2+]i. 2. The mean (+/- s.e.m.) initial resting [Ca2+]i from all control and mdx fibres tested was 56 +/- 5 nM (n = 72) and 48 +/- 7 nM (n = 57), respectively, indicating no significant overall difference between the two groups. However, when comparing a batch of control and mdx fibres obtained from mice older than approximately 35 weeks, resting [Ca2+]i was significantly lower in mdx (16 +/- 4 nM, n = 11) than in control fibres (71 +/- 10 nM, n = 14). 3. Changes in [Ca2+]i elicited by short (5-35 ms) depolarizing pulses from -80 to 0 mV showed similar properties in control and mdx fibres. After a 5 ms duration pulse the mean time constant of [Ca2+]i decay was, however, significantly elevated in mdx as compared to control fibres, by a factor of 1.5-2. For longer pulses, no significant difference could be detected. 4. In response to 50 ms duration depolarizing pulses of various amplitudes the threshold for detection of an [Ca2+]i change and the peak [Ca2+]i reached for a given potential were similar in control and mdx fibres. 5. Overall results show that mdx skeletal muscle fibres are quite capable of handling [Ca2+]i at rest and in response to membrane depolarizations.
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Registered trials
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.