ArticlePflugers Archiv : European journal of physiology1993
A possible role of sarcoplasmic Ca2+ release in modulating the slow Ca2+ current of skeletal muscle.
Article in Pflugers Archiv : European journal of physiology, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 24 citations in OpenAlex.
- Direct Effects of Capsaicin on Voltage-Dependent Calcium Channels of Mammalian Skeletal Muscle.Biomolecules · 2026Article
- Gold nanoparticle-mediated laser stimulation induces a complex stress response in neuronal cells.Scientific reports · 2018Article
- Voltage modulates halothane-triggered CaThe Journal of general physiology · 2018Article
- Ca2+/CaM-dependent inactivation of the skeletal muscle L-type Ca2+ channel (Cav1.1).Pflugers Archiv : European journal of physiology · 2008Article
- Intramembrane charge movement and L-type calcium current in skeletal muscle fibers isolated from control and mdx mice.Biophysical journal · 2003Article
- Absence of Ca2+ current facilitation in skeletal muscle of transgenic mice lacking the type 1 ryanodine receptor.The Journal of physiology · 1996Article
- Caffeine enhances intramembranous charge movement in frog skeletal muscle by increasing cytoplasmic Ca2+ concentration.The Journal of physiology · 1996Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
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Abstract
Ca2+ channels are regulated in a variety of different ways, one of which is modulation by the Ca2+ ion itself. In skeletal muscle, Ca2+ release sites are presumably located in the vicinity of the dihydropyridine-sensitive Ca2+ channel. In this study, we have tried to investigate the effects of Ca2+ release from the sarcoplasmic reticulum on the L-type Ca2+ channel in frog skeletal muscle, using the double Vaseline gap technique. We found an increase in Ca2+ current amplitude on application of caffeine, a well-known potentiator of Ca2+ release. Addition of the fast Ca2+ buffer BAPTA to the intracellular solution led to a gradual decline in Ca2+ current amplitude and eventually caused complete inhibition. Similar observations were made when the muscle fibre was perfused internally with the Ca2+ release channel blocker ruthenium red. The time course of Ca2+ current decline followed closely the increase in ruthenium red concentration. This suggests that Ca2+ release from the sarcoplasmic reticulum is involved in the regulation of L-type Ca2+ channels in frog skeletal muscle.
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