ArticleBiophysical journal2009
Electrically silent divalent cation entries in resting and active voltage-controlled muscle fibers.
Article in Biophysical journal, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 27 citations in OpenAlex.
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- Voltage-gated Ca(2+) influx through L-type channels contributes to sarcoplasmic reticulum Ca(2+) loading in skeletal muscle.The Journal of physiology · 2015Article
- OSCA1 mediates osmotic-stress-evoked Ca2+ increases vital for osmosensing in Arabidopsis.Nature · 2014Article
- Major contribution of sarcoplasmic reticulum Ca(2+) depletion during long-lasting activation of skeletal muscle.The Journal of general physiology · 2013Article
- Dihydropyridine receptors actively control gating of ryanodine receptors in resting mouse skeletal muscle fibres.The Journal of physiology · 2012Article
- A study of store dependent Ca²⁺ influx in frog skeletal muscle.Journal of muscle research and cell motility · 2012Article
- Sarcoplasmic reticulum Ca2+ permeation explored from the lumen side in mdx muscle fibers under voltage control.The Journal of general physiology · 2012Article
- Toward the roles of store-operated Ca2+ entry in skeletal muscle.Pflugers Archiv : European journal of physiology · 2010Review
- New factors contributing to dynamic calcium regulation in the skeletal muscle triad-a crowded place.Biophysical reviews · 2010Review
- Role of TRPC1 channel in skeletal muscle function.American journal of physiology. Cell physiology · 2010Article
- Sildenafil inhibits chronically hypoxic upregulation of canonical transient receptor potential expression in rat pulmonary arterial smooth muscle.American journal of physiology. Cell 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
- The cardiac alpha(1C) subunit can support excitation-triggered Ca2+ entry in dysgenic and dyspedic myotubes.Channels (Austin, Tex.)Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ca2+ is known to enter skeletal muscle at rest and during activity. Except for the well-characterized Ca2+ entry through L-type channels, pathways involved in these Ca2+ entries remain elusive in adult muscle. This study investigates Ca2+ influx at rest and during activity using the method of Mn2+ quenching of fura-2 fluorescence on voltage-controlled adult skeletal muscle cells. Resting rate of Mn2+ influx depended on external [Mn2+] and membrane potential. At -80 mV, replacement of Mg2+ by Mn2+ gave rise to an outward current associated with an increase in cell input resistance. Calibration of fura-2 response indicated that Mn2+ influx was too small to be resolved as a macroscopic current. Partial depletion of the sarcoplasmic reticulum induced by a train of action potentials in the presence of cyclopiazonic acid led to a slight increase in resting Mn2+ influx but no change in cell input resistance and membrane potential. Trains of action potentials considerably increased Mn2+ entry through an electrically silent pathway independent of L-type channels, which provided 24% of the global Mn2+ influx at +30 mV under voltage-clamp conditions. Within this context, the nature and the physiological role of the Ca2+ pathways involved during muscle excitation still remain open questions.
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