ArticleBiophysical journal2004
Slow calcium signals after tetanic electrical stimulation in skeletal myotubes.
Article in Biophysical journal, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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
16 citing papers in PubMed.
- Article
- PPARδ and FOXO1 Mediate Palmitate-Induced Inhibition of Muscle Pyruvate Dehydrogenase Complex and CHO Oxidation, Events Reversed by Electrical Pulse Stimulation.International journal of molecular sciences · 2020Article
- Role of defective CaJournal of cell communication and signaling · 2018Review
- NO-sGC Pathway Modulates CaFrontiers in physiology · 2017Article
- Article
- Phosphoinositides in Ca(2+) signaling and excitation-contraction coupling in skeletal muscle: an old player and newcomers.Journal of muscle research and cell motility · 2015Review
- ROS Production via P2Y1-PKC-NOX2 Is Triggered by Extracellular ATP after Electrical Stimulation of Skeletal Muscle Cells.PloS one · 2015Article
- Electrical stimulation induces IL-6 in skeletal muscle through extracellular ATP by activating Ca(2+) signals and an IL-6 autocrine loop.American journal of physiology. Endocrinology and metabolism · 2014Article
- Electrical stimuli release ATP to increase GLUT4 translocation and glucose uptake via PI3Kγ-Akt-AS160 in skeletal muscle cells.Diabetes · 2013Article
- Analysis of spontaneous and nerve-evoked calcium transients in intact extraocular muscles in vitro.Experimental eye research · 2012Article
- Membrane depolarization increases membrane PtdIns(4,5)P2 levels through mechanisms involving PKC βII and PI4 kinase.The Journal of biological chemistry · 2011Article
- The muscle fiber type-fiber size paradox: hypertrophy or oxidative metabolism?European journal of applied physiology · 2010Review
- IP(3)-dependent, post-tetanic calcium transients induced by electrostimulation of adult skeletal muscle fibers.The Journal of general physiology · 2010Article
- Depolarization increases phosphatidylinositol (PI) 4,5-bisphosphate level and KCNQ currents through PI 4-kinase mechanisms.The Journal of biological chemistry · 2010Article
- ATP released by electrical stimuli elicits calcium transients and gene expression in skeletal muscle.The Journal of biological chemistry · 2009Article
- Conformational activation of Ca2+ entry by depolarization of skeletal myotubes.Proceedings of the National Academy of Sciences of the United States of America · 2004Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The fluorescent calcium signal from rat myotubes in culture was monitored after field-stimulation with tetanic protocols. After the calcium signal sensitive to ryanodine and associated to the excitation-contraction coupling, a second long-lasting calcium signal refractory to ryanodine was consistently found. The onset kinetics of this slow signal were slightly modified in nominally calcium-free medium, as were both the frequency and number of pulses during tetanus. No signal was detected in the presence of tetrodotoxin. The participation of the dihydropyridine receptor (DHPR) as the voltage sensor for this signal was assessed by treatment with agonist and antagonist dihydropyridines (Bay K 8644 and nifedipine), showing an enhanced and inhibitory response, respectively. In the dysgenic GLT cell line, which lacks the alpha1(S) subunit of the DHPR, the signal was absent. Transfection of these cells with the alpha1(S) subunit restored the slow signal. In myotubes, the inositol 1,4,5-trisphosphate (IP(3)) mass increase induced by a tetanus protocol preceded in time the slow calcium signal. Both an IP(3) receptor blocker and a phospholipase C inhibitor (xestospongin C and U73122, respectively) dramatically inhibit this signal. Long-lasting, IP(3)-generated slow calcium signals appear to be a physiological response to activity-related fluctuations in membrane potential sensed by the DHPR.
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.