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Ca_v3.2 subunit underlies the functional T-type Ca²⁺ channel in murine hearts during the embryonic period

¹Departments of Circulation and Humoral Regulation, Division of Regulation of Organ Function, Research Institute of Environmental Medicine, Nagoya University, Nagoya 464-8601, Japan; and ²Department of Medical Physiology, University Medical Center Utrecht, 3508 TA Utrecht, The Netherlands

Submitted 10 November 2003 ; accepted in final form 13 February 2004

T-type Ca²⁺ channels are implicated in cardiac automaticity, cell growth, and cardiovascular remodeling. Two voltage-gated Ca²⁺ subtypes (Ca_v3.1 and Ca_v3.2) 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 was 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 (E9.5) and late embryonic days (E18) and from adult 10-wk-old mice. Large T-type Ca²⁺ current (I_Ca,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). I_Ca,T was undetectable in adult myocytes. Quantitative PCR analysis revealed that Ca_v3.2 mRNA is the predominant subtype encoding T-type Ca²⁺ channels at both E9.5 and E18. Ca_v3.1 mRNA increased from E9.5 to E18, but remained low compared with Ca_v3.2 mRNA during the whole embryonic period. In the adulthood, in contrast, Ca_v3.1 mRNA is greater than Ca_v3.2 mRNA. These results indicate that Ca_v3.2 underlies the functional T-type Ca²⁺ channels in the embryonic murine heart, and there is a subtype switching of transcripts from Ca_v3.2 to Ca_v3.1 in the perinatal period.

ion channel; gene expression; fetal development; ₁-subunit; cardiac myocyte

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