ArticleThe Journal of physiology1998
Local calcium release in mammalian skeletal muscle.
Article in The Journal of physiology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
83 citing papers in PubMed.
- Allosteric interactions between RyR channels justify intracellular Ca2+ release of skeletal muscle in quantitative detail.The Journal of general physiology · 2026Article
- Decoding ultrasensitive self-assembly of the calcium-regulated Tetrahymena cytoskeletal protein Tcb2 using optical actuation.The Journal of biological chemistry · 2025Article
- Decoding ultrasensitive self-assembly of the calcium-regulatedbioRxiv : the preprint server for biology · 2025Article
- Technologies and Sensors for Artificial Muscles in Rehabilitation.Sensors (Basel, Switzerland) · 2024Review
- Quantal Properties of Voltage-Dependent CaThe Journal of membrane biology · 2024Article
- Evolutionary isolation of ryanodine receptor isoform 1 for muscle-based thermogenesis in mammals.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Elementary calcium release events in the skeletal muscle cells of the honey bee Apis mellifera.Scientific reports · 2021Article
- Detection of Ca2+ transients near ryanodine receptors by targeting fluorescent Ca2+ sensors to the triad.The Journal of general physiology · 2021Article
- From synaptic input to muscle contraction: arm muscle cells of Octopus vulgaris show unique neuromuscular junction and excitation-contraction coupling properties.Proceedings. Biological sciences · 2019Article
- Voltage sensing mechanism in skeletal muscle excitation-contraction coupling: coming of age or midlife crisis?Skeletal muscle · 2018Review
- Calcium-induced release of calcium in muscle: 50 years of work and the emerging consensus.The Journal of general physiology · 2018Review
- The relationship between form and function throughout the history of excitation-contraction coupling.The Journal of general physiology · 2018Review
- Impaired excitation-contraction coupling in muscle fibres from the dynamin2The Journal of physiology · 2017Article
- Coupling of excitation to CaThe Journal of physiology · 2017Article
- Calcium Dynamics Mediated by the Endoplasmic/Sarcoplasmic Reticulum and Related Diseases.International journal of molecular sciences · 2017Review
- Structural and functional properties of ryanodine receptor type 3 in zebrafish tail muscle.The Journal of general physiology · 2015Article
- Raptor ablation in skeletal muscle decreases Cav1.1 expression and affects the function of the excitation-contraction coupling supramolecular complex.The Biochemical journal · 2015Article
- Activation and propagation of Ca2+ release from inside the sarcoplasmic reticulum network of mammalian skeletal muscle.The Journal of physiology · 2014Article
- β1a490-508, a 19-residue peptide from C-terminal tail of Cav1.1 β1a subunit, potentiates voltage-dependent calcium release in adult skeletal muscle fibers.Biophysical journal · 2014Article
- Analysis of osmotic stress induced Ca2+ spark termination in mammalian skeletal muscle.Indian journal of biochemistry & biophysics · 2013Article
23 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
Abstract
1. Fluo-3 fluorescence associated with Ca2+ release was recorded with confocal microscopy in single muscle fibres mechanically dissected from fast twitch muscle of rats or frogs, voltage clamped in a two Vaseline-gap chamber. 2. Interventions that elicited Ca2+ sparks in frog skeletal muscle (low voltage depolarizations, application of caffeine) generated in rat fibres images consistent with substantial release from triadic regions, but devoid of resolvable discrete events. Ca2+ sparks were never observed in adult rat fibres. In contrast, sparks of standard morphology were abundant in myotubes from embryonic mice. 3. Depolarization-induced gradients of fluorescence between triadic and surrounding regions (which are proportional to Ca2+ release flux) peaked at about 20 ms and then decayed to a steady level. Gradients were greater in frog fibres than in rat fibres. The ratio of peak over steady gradient (R) was steeply voltage dependent in frogs, reaching a maximum of 4.8 at -50 mV (n = 7). In rats, R had an essentially voltage-independent value of 2.3 (n = 5). 4. Ca2+-induced Ca2+ release, resulting in concerted opening of several release channels, is thought to underlie Ca2+ sparks and the peak phase of release in frog skeletal muscle. A diffuse 'small event' release, similar to that observed in these rats, is also present in frogs and believed to be directly activated by voltage. The present results suggest that in these rat fibres there is little contribution by CICR to Ca2+ release triggered by depolarization, and a lack of concerted channel opening.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.