Mechanisms of Ca(2)+ handling in zebrafish ventricular myocytes Journal Article

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Authors: Bovo, E; Dvornikov, A. V.; Mazurek, S. R.; de Tombe, P. P.; Zima, A. V.
Article Title: Mechanisms of Ca(2)+ handling in zebrafish ventricular myocytes
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 approximately 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+)].
Journal Title: Pflugers Archiv : European journal of physiology
Volume: 465
Issue: 12
ISSN: 1432-2013; 0031-6768
Publisher: Unknown  
Journal Place: Germany
Date Published: 2013
Start Page: 1775
End Page: 1784
Language: eng
DOI/URL:

10.1007/s00424-013-1312-2
Notes: GR: HL62426/HL/NHLBI NIH HHS/United States; GR: HL75494/HL/NHLBI NIH HHS/United States; GR: P01 HL062426/HL/NHLBI NIH HHS/United States; GR: R01 HL075494/HL/NHLBI NIH HHS/United States; JID: 0154720; 0 (Ryanodine Receptor Calcium Release Channel); 1F7A44V6OU (Colforsin); 3G6A5W338E (Caffeine); EC 2.7.11.11 (Cyclic AMP-Dependent Protein Kinases); EC 3.6.3.8 (Sarcoplasmic Reticulum Calcium-Transporting ATPases); SY7Q814VUP (Calcium); 2013/05/06 [received]; 2013/06/12 [accepted]; 2013/06/10 [revised]; 2013/07/03 [aheadofprint]; ppublish