ArticleThe Journal of physiology2015
Voltage-gated Ca(2+) influx through L-type channels contributes to sarcoplasmic reticulum Ca(2+) loading in skeletal muscle.
Article in The Journal of physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 30 citations in OpenAlex.
- Direct Effects of Capsaicin on Voltage-Dependent Calcium Channels of Mammalian Skeletal Muscle.Biomolecules · 2026Article
- Reduced voltage-activated Ca2+ release flux in muscle fibers from a rat model of Duchenne dystrophy.The Journal of general physiology · 2025Article
- Advances in CaChannels (Austin, Tex.) · 2023Review
- A mechano- and heat-gated two-pore domain KProceedings of the National Academy of Sciences of the United States of America · 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
- Equivalent L-type channel (CaBiochemical and biophysical research communications · 2020Article
- Porcine deltacoronavirus (PDCoV) modulates calcium influx to favor viral replication.Virology · 2020Article
- CaCells · 2019Review
- When muscle CaThe Journal of physiology · 2018Review
- A skeletal muscle L-type CaThe Journal of biological chemistry · 2018Article
- Molecular Basis for Exercise-Induced Fatigue: The Importance of Strictly Controlled Cellular CaCold Spring Harbor perspectives in medicine · 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
- Elevated resting HThe Journal of physiology · 2017Article
- Functional impact of an oculopharyngeal muscular dystrophy mutation in PABPN1.The Journal of physiology · 2017Article
- How and why are calcium currents curtailed in the skeletal muscle voltage-gated calcium channels?The Journal of physiology · 2017Review
- NO-sGC Pathway Modulates CaFrontiers in physiology · 2017Article
- A quantitative description of tubular system Ca(2+) handling in fast- and slow-twitch muscle fibres.The Journal of physiology · 2016Article
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
Muscle contraction is triggered by Ca(2+) ions released from the sarcoplasmic reticulum (SR) in response to depolarization of skeletal muscle fibres. Muscle activation is also associated with a voltage-activated trans-sarcolemmal Ca(2+) influx early identified as a current flowing through L-type Ca(2+) channels. Because removal of external Ca(2+) does not impede fibres from contracting, a negligible role was given to this voltage-activated Ca(2+) entry, although the decline of Ca(2+) release is more pronounced in the absence of Ca(2+) during long-lasting activation. Furthermore, it is not clearly established whether Ca(2+) exclusively flows through L-type channels or in addition through a parallel voltage-activated pathway distinct from L-type channels. Here, by monitoring the quenching of fura-2 fluorescence resulting from Mn(2+) influx in voltage-controlled mouse and zebrafish isolated muscle fibres, we show that the L-type current is the only contributor to Ca(2+) influx during long-lasting depolarizations in skeletal muscle. Calibration of the Mn(2+) quenching signal allowed us to estimate a mean Mn(2+) current of 0.31 ± 0.06 A F(-1) flowing through L-type channels during a train of action potentials. Measurements of SR Ca(2+) changes with fluo-5N in response to depolarization revealed that an elevated voltage-activated Ca(2+) current potentiated SR Ca(2+) loading and addition of external Mn(2+) produced quenching of fluo-5N in the SR, indicating that voltage-activated Ca(2+) /Mn(2+) influx contributes to SR Ca(2+) /Mn(2+) loading.
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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.