ArticleBiophysical journal2002
Ca(2+) influx and opening of Ca(2+)-activated K(+) channels in muscle fibers from control and mdx mice.
Article in Biophysical journal, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
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Who cites it
12 citing papers in PubMed.
- Reduced voltage-activated Ca2+ release flux in muscle fibers from a rat model of Duchenne dystrophy.The Journal of general physiology · 2025Article
- Modeling Duchenne Muscular Dystrophy Cardiomyopathy with Patients' Induced Pluripotent Stem-Cell-Derived Cardiomyocytes.International journal of molecular sciences · 2023Review
- Review
- Genetic evidence in the mouse solidifies the calcium hypothesis of myofiber death in muscular dystrophy.Cell death and differentiation · 2015Review
- Partial opening and subconductance gating of mechanosensitive ion channels in dystrophic skeletal muscle.The Journal of physiology · 2012Article
- Article
- Increased store-operated Ca2+ entry in skeletal muscle with reduced calsequestrin-1 expression.Biophysical journal · 2010Article
- Electrically silent divalent cation entries in resting and active voltage-controlled muscle fibers.Biophysical journal · 2009Article
- Article
- Article
- Sarcoplasmic reticulum Ca2+ release and depletion fail to affect sarcolemmal ion channel activity in mouse skeletal muscle.The Journal of physiology · 2006Article
- Sarcolemmal ion channels in dystrophin-deficient skeletal muscle fibres.Journal of muscle research and cell motility · 2006Review
Corrections and comments
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Using the patch-clamp technique, we demonstrate that, in depolarized cell-attached patches from mouse skeletal muscle fibers, a short hyperpolarization to resting value is followed by a transient activation of Ca(2+)-activated K(+) channels (K(Ca)) upon return to depolarized levels. These results indicate that sparse sites of passive Ca(2+) influx at resting potentials are responsible for a subsarcolemmal Ca(2+) load high enough to induce K(Ca) channel activation upon muscle activation. We then investigate this phenomenon in mdx dystrophin-deficient muscle fibers, in which an elevated Ca(2+) influx and a subsequent subsarcolemmal Ca(2+) overload are suspected. The number of Ca(2+) entry sites detected with K(Ca) was found to be greater in mdx muscle. K(Ca) activity reflecting subsarcolemmal Ca(2+) load was also found to be independent of the activity of leak channels carrying inward currents at negative potentials in mdx muscle. These results indicate that the sites of passive Ca(2+) influx newly described in this study could represent the Ca(2+) influx pathways responsible for the subsarcolemmal Ca(2+) overload in mdx muscle fibers.
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