ArticleBiophysical journal2003
Intramembrane charge movement and L-type calcium current in skeletal muscle fibers isolated from control and mdx mice.
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 42 papers.
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42 citing papers in PubMed, 52 citations in OpenAlex.
- Disrupted T-tubular network accounts for asynchronous calcium release in MTM1-deficient skeletal muscle.The Journal of physiology · 2023Article
- Superfast excitation-contraction coupling in adult zebrafish skeletal muscle fibers.The Journal of general physiology · 2022Article
- Pannexin-1 and CaV1.1 show reciprocal interaction during excitation-contraction and excitation-transcription coupling in skeletal muscle.The Journal of general physiology · 2021Article
- Preserved CaDiabetologia · 2020Article
- Evaluation of mutant muscle CaThe Journal of general physiology · 2018Article
- When muscle CaThe Journal of physiology · 2018Review
- Na leak with gating pore properties in hypokalemic periodic paralysis V876E mutant muscle Ca channel.The Journal of general physiology · 2017Article
- The voltage sensor of excitation-contraction coupling in mammals: Inactivation and interaction with CaThe Journal of general physiology · 2017Article
- How and why are calcium currents curtailed in the skeletal muscle voltage-gated calcium channels?The Journal of physiology · 2017Review
- Characterization of a multiprotein complex involved in excitation-transcription coupling of skeletal muscle.Skeletal muscle · 2016Article
- Voltage-gated Ca(2+) influx through L-type channels contributes to sarcoplasmic reticulum Ca(2+) loading in skeletal muscle.The Journal of physiology · 2015Article
- Depression of voltage-activated Ca2+ release in skeletal muscle by activation of a voltage-sensing phosphatase.The Journal of general physiology · 2015Article
- Phosphoinositide substrates of myotubularin affect voltage-activated Ca²⁺ release in skeletal muscle.Pflugers Archiv : European journal of physiology · 2014Article
- Type 1 inositol (1,4,5)-trisphosphate receptor activates ryanodine receptor 1 to mediate calcium spark signaling in adult mammalian skeletal muscle.The Journal of biological chemistry · 2013Article
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- Microtubules underlie dysfunction in duchenne muscular dystrophy.Science signaling · 2012Article
- Junctophilin 1 and 2 proteins interact with the L-type Ca2+ channel dihydropyridine receptors (DHPRs) in skeletal muscle.The Journal of biological chemistry · 2011Article
- Functional expression of transgenic 1sDHPR channels in adult mammalian skeletal muscle fibres.The Journal of physiology · 2011Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dystrophin-deficient muscle fibers from mdx mice are believed to suffer from increased calcium entry and elevated submembranous calcium level, the actual source and functional consequences of which remain obscure. Here we compare the properties of the dihydropyridine receptor as voltage sensor and calcium channel in control and mdx muscle fibers, using the silicone-voltage clamp technique. In control fibers charge movement followed a two-state Boltzmann distribution with values for maximal charge, midpoint voltage, and steepness of 23 +/- 2 nC/ micro F, -37 +/- 3 mV, and 13 +/- 1 mV (n = 7). Essentially identical values were obtained in mdx fibers and the time course of charge recovery from inactivation was also similar in the two populations (tau approximately 6 s). In control fibers the voltage dependence of the slow calcium current elicited by 100-ms-long pulses gave values for maximal conductance, apparent reversal potential, half-activation potential, and steepness factor of 156 +/- 15 S/F, 65.5 +/- 2.9 mV, -0.76 +/- 1.2 mV, and 6.2 +/- 0.5 mV (n = 17). In mdx fibers, the half-activation potential of the calcium current was slightly more negative (-6.2 +/- 1.2 mV, n = 16). Also, when using longer pulses, the time constant of calcium current decay was found to be significantly larger (by a factor of 1.5-2) in mdx than in control fibers. These changes in calcium current properties are unlikely to be primarily responsible for a dramatic alteration of intracellular calcium homeostasis. They may be speculated to result, at least in part, from remodeling of the submembranous cytoskeleton network due to the absence of dystrophin.
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