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1 Departments of Circulation and Humoral Regulation, Division of Regulation of Organ Function, Research Institute of Environmental Medicine, Nagoya University, Nagoya, Japan
2 Department of Medical Physiology, University Medical Center Utrecht, Utrecht, The Netherlands
* To whom correspondence should be addressed. E-mail: kenji{at}riem.nagoya-u.ac.jp.
T-type Ca2+ channels are implicated in cardiac automaticity, cell growth and cardiovascular remodeling. Two subtypes (Cav3.1 and Cav3.2) have been cloned for the pore-forming 
1 subunit of the T-type Ca2+ channel in cardiac muscle, but their differential roles remain to be clarified. The aim of this study is to elucidate the relative contribution of the two subtypes in the normal development of mouse hearts. A whole-cell patch clamp was used to record ionic currents from ventricular myocytes isolated from mice of early and late embryonic days (E9.5 and E18) and from adult 10-week old mice. Large T-type Ca2+ current (ICa,T) was observed at both E9.5 and E18, displaying similar voltage-dependence and kinetics of activation and inactivation. The current was inhibited by Ni2+ at relatively low concentrations (IC50 26-31 µM). ICa,T was undetectable in adult myocytes. Quantitative PCR analysis revealed that Cav3.2 (1H) mRNA is the predominant subtype encoding T-type Ca2+ channels at both E9.5 and E18. Cav3.1 (1G) mRNA increased from E9.5 to E18, but remained low compared with Cav3.2 mRNA during the whole embryonic period. In the adulthood, in contrast, Cav3.1 mRNA is greater than Cav3.2 mRNA. These results indicate that Cav3.2 underlies the functional T-type Ca2+ channels in the embryonic murine heart, and there is a subtype switching of transcripts from Cav3.2 to Cav3.1 in the perinatal period.
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