ArticlePflugers Archiv : European journal of physiology2013
Mechanisms of Ca²+ handling in zebrafish ventricular myocytes.
Article in Pflugers Archiv : European journal of physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 66 citations in OpenAlex.
- Mathematical model of the zebrafish ventricular cardiomyocyte action potential and calcium transient.The Journal of physiology · 2026Article
- The RyR-like-FKBP12-PKA Complex Regulates Intracellular CaInternational journal of molecular sciences · 2026Article
- Effect of the gut microbiota metabolite phenylacetylglycine on cardiac CaBiophysical reports · 2026Article
- Thermal plasticity of adrenaline-mediated, frequency-dependent calcium homeostasis in rainbow trout ventricular cardiomyocytes.The Journal of experimental biology · 2026Article
- Mitochondrial Dysfunction Contributes to Decompensation in a Zebrafish Model of Isoproterenol-Induced Heart Failure.Acta physiologica (Oxford, England) · 2025Article
- Protein carbonylation causes sarcoplasmic reticulum CaPflugers Archiv : European journal of physiology · 2024Article
- Zebrafish Congenital Heart Disease Models: Opportunities and Challenges.International journal of molecular sciences · 2024Review
- Forward genetic screen using a gene-breaking trap approach identifies a novel role ofFrontiers in cell and developmental biology · 2024Article
- Regulation of cardiac calcium signaling by newly identified calcium pump modulators.Biochemical and biophysical research communications · 2023Article
- Arrhythmic Effects Evaluated onACS nano · 2023Article
- Zebrafish as a Model of Cardiac Pathology and Toxicity: Spotlight on Uremic Toxins.International journal of molecular sciences · 2023Review
- New N-aryl-N-alkyl-thiophene-2-carboxamide compound enhances intracellular CaBiophysical journal · 2023Article
- TheFrontiers in physiology · 2023Article
- Stx4 is required to regulate cardiomyocyte CaHGG advances · 2022Article
- Modeling Human Cardiac Arrhythmias: Insights from Zebrafish.Journal of cardiovascular development and disease · 2022Review
- Drivers of Sinoatrial Node Automaticity in Zebrafish: Comparison With Mechanisms of Mammalian Pacemaker Function.Frontiers in physiology · 2022Article
- Simultaneous imaging of calcium and contraction in the beating heart of zebrafish larvae.Theranostics · 2022Article
- Seeing the Light: The Use of Zebrafish for Optogenetic Studies of the Heart.Frontiers in physiology · 2021Review
- Zebrafish Heart Failure Models.Frontiers in cell and developmental biology · 2021Review
- Mapping Calcium Dynamics in the Heart of Zebrafish Embryos with Ratiometric Genetically Encoded Calcium Indicators.International journal of molecular sciences · 2020Article
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5 authors at 1 institution in 1 country.
Funding
Abstract
The zebrafish serves as a promising transgenic animal model that can be used to study cardiac Ca(2+) regulation. However, mechanisms of sarcoplasmic reticulum (SR) Ca(2+) handling in the zebrafish heart have not been systematically explored. We found that in zebrafish ventricular myocytes, the action potential-induced Ca(2+) transient is mainly (80 %) mediated by Ca(2+) influx via L-type Ca(2+) channels (LTCC) and only 20 % by Ca(2+) released from the SR. This small contribution of the SR to the Ca(2+) transient was not the result of depleted SR Ca(2+) load. We found that the ryanodine receptor (RyR) expression level in zebrafish myocytes was ∼72 % lower compared to rabbit myocytes. In permeabilized myocytes, increasing cytosolic [Ca(2+)] from 100 to 350 nM did not trigger SR Ca(2+) release. However, an application of a low dose of caffeine activated Ca(2+) sparks. These results show that the zebrafish cardiac RyR has low sensitivity to the mechanism of Ca(2+)-induced Ca(2+) release. Activation of protein kinase A by forskolin increased phosphorylation of the RyR in zebrafish myocardium. In half of the studied cells, an increased Ca(2+) transient by forskolin was entirely mediated by augmentation of LTCC current. In the remaining myocytes, the forskolin action was associated with an increase of both LTCC and SR Ca(2+) release. These results indicate that the mechanism of excitation-contraction coupling in zebrafish myocytes differs from the mammalian one mainly because of the small contribution of SR Ca(2+) release to the Ca(2+) transient. This difference is due to a low sensitivity of RyRs to cytosolic [Ca(2+)].
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