ArticleThe Journal of physiology2012
Synthetic localized calcium transients directly probe signalling mechanisms in skeletal muscle.
Article in The Journal of physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 33 citations in OpenAlex.
- Cryo-EM Brings the Mechanisms of Activation, Inactivation, and Inhibition of Ryanodine Receptors into Focus.Advances in experimental medicine and biology · 2026Review
- RyR1-mediated CaProceedings of the National Academy of Sciences of the United States of America · 2025Article
- Age-Dependent Effects of Muscle Resting Calcium on Fasting Blood Glucose: Implications for Prediabetes Risk.Endocrinology, diabetes & metabolism · 2025Article
- Quantal Properties of Voltage-Dependent CaThe Journal of membrane biology · 2024Article
- Distinct pathophysiological characteristics in developing muscle from patients susceptible to malignant hyperthermia.British journal of anaesthesia · 2023Article
- Article
- 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
- Disrupted T-tubular network accounts for asynchronous calcium release in MTM1-deficient skeletal muscle.The Journal of physiology · 2023Article
- Finite element analysis predicts CaScientific reports · 2021Article
- The Orai1 inhibitor BTP2 has multiple effects on Ca2+ handling in skeletal muscle.The Journal of general physiology · 2021Article
- The binding interactions that maintain excitation-contraction coupling junctions in skeletal muscle.The Journal of general physiology · 2019Article
- Abnormal calcium signalling and the caffeine-halothane contracture test.British journal of anaesthesia · 2019Article
- Calcium-induced release of calcium in muscle: 50 years of work and the emerging consensus.The Journal of general physiology · 2018Review
- The structural basis of ryanodine receptor ion channel function.The Journal of general physiology · 2017Review
- In vivo CaPhysiological reports · 2017Article
- Phosphatidylinositol 3-kinase inhibition restores Ca2+ release defects and prolongs survival in myotubularin-deficient mice.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Differential effects of contractile potentiators on action potential-induced CaJournal of muscle research and cell motility · 2016Article
- Raptor ablation in skeletal muscle decreases Cav1.1 expression and affects the function of the excitation-contraction coupling supramolecular complex.The Biochemical journal · 2015Article
- Critical Role of Intracellular RyR1 Calcium Release Channels in Skeletal Muscle Function and Disease.Frontiers in physiology · 2015Review
- Activation and propagation of Ca2+ release from inside the sarcoplasmic reticulum network of mammalian skeletal muscle.The Journal of physiology · 2014Article
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9 authors at 4 institutions in 3 countries.
Funding
Abstract
The contribution of Ca2+-induced Ca2+ release (CICR) to trigger muscle contraction is controversial. It was studied on isolated muscle fibres using synthetic localized increases in Ca2+ concentration, SLICs, generated by two-photon photorelease from nitrodibenzofuran (NDBF)-EGTA just outside the permeabilized plasma membrane. SLICs provided a way to increase cytosolic [Ca2+] rapidly and reversibly, up to 8 μM, levels similar to those reached during physiological activity. They improve over previous paradigms in rate of rise, locality and reproducibility. Use of NDBF-EGTA allowed for the separate modification of resting [Ca2+], trigger [Ca2+] and resting [Mg2+]. In frog muscle, SLICs elicited propagated responses that had the characteristics of CICR. The threshold [Ca2+] for triggering a response was 0.5 μM or less. As this value is much lower than concentrations prevailing near channels during normal activity, the result supports participation of CICR in the physiological control of contraction in amphibian muscle. As SLICs were applied outside cells, the primary stimulus was Ca2+, rather than the radiation or subproducts of photorelease. Therefore the responses qualify as ‘classic' CICR. By contrast, mouse muscle fibres did not respond unless channel-opening drugs were present at substantial concentrations, an observation contrary to the physiological involvement of CICR in mammalian excitation–contraction coupling. In mouse muscle, the propagating wave had a substantially lower release flux, which together with a much higher threshold justified the absence of response when drugs were not present. The differences in flux and threshold may be ascribed to the absence of ryanodine receptor 3 (RyR3) isoforms in adult mammalian muscle.
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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.