PUBLICATION
Calcium handling in zebrafish ventricular myocytes
- Authors
- Zhang, P.C., Llach, A., Sheng, X.Y., Hove-Madsen, L., and Tibbits, G.F.
- ID
- ZDB-PUB-101018-1
- Date
- 2011
- Source
- American journal of physiology. Regulatory, integrative and comparative physiology 300(1): R56-R66 (Journal)
- Registered Authors
- Keywords
- zebrafish, myocyte, L-type calcium channels, contraction
- MeSH Terms
-
- Amino Acid Sequence
- Animals
- Calcium/metabolism*
- Calcium Channels, L-Type/metabolism
- Cell Size
- Molecular Sequence Data
- Myocytes, Cardiac/cytology
- Myocytes, Cardiac/metabolism*
- Patch-Clamp Techniques
- Sodium-Calcium Exchanger/metabolism
- Zebrafish/metabolism*
- PubMed
- 20926764 Full text @ Am. J. Physiol. Regul. Integr. Comp. Physiol.
Citation
Zhang, P.C., Llach, A., Sheng, X.Y., Hove-Madsen, L., and Tibbits, G.F. (2011) Calcium handling in zebrafish ventricular myocytes. American journal of physiology. Regulatory, integrative and comparative physiology. 300(1):R56-R66.
Abstract
The zebrafish (Danio rerio) is an important model for the study of vertebrate cardiac development with a rich array of genetic mutations and biological reagents for functional interrogation. The similarity of the zebrafish cardiac action potential with that of humans further enhances the relevance of this model. In spite of this, little is known about excitation-contraction coupling in the zebrafish heart. To address this issue, adult zebrafish cardiomyocytes were isolated by enzymatic perfusion of the cannulated ventricle, and subjected to amphotericin-perforated patch clamp technique, confocal calcium imaging, and/or measurements of cell shortening. Simultaneous recordings of the voltage dependence of the L-type calcium current (I(Ca,L)) amplitude and cell shortening showed a typical bell-shaped I-V relationship for I(Ca,L) with a maximum at +10 mV whereas calcium transients and cell shortening showed a monophasic increase with membrane depolarization, that reached a plateau at membrane potentials above +20 mV. I(Ca,L) values were 53, 100, and 17% of maximum at -20, +10 and +40 mV while the corresponding calcium transient amplitudes were 64, 92, 98% and cell shortening values were 62, 95, and 96% of maximum respectively, suggesting that I(Ca,L) is the major contributor to the activation of contraction at voltages below +10 mV whereas the contribution of reverse-mode NCX becomes increasingly more important at membrane potentials above +10 mV. Comparison of the recovery of I(Ca,L) from acute and steady-state inactivation showed that reduction of I(Ca,L) upon elevation of the stimulation frequency is primarily due to calcium dependent I(Ca,L) inactivation. In conclusion, zebrafish ventricular myocytes differed from that of large mammals by having larger I(Ca,L) density and a monophasically increasing contraction-voltage relationship, suggesting that some caution should be taken upon extrapolation of the functional impact of mutations on calcium handling and contraction in zebrafish cardiomyocytes.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping