Expression and roles of Cav1.3 (α1D) L-type Ca²+ channel in atrioventricular node automaticity

Title
Expression and roles of Cav1.3 (α1D) L-type Ca²+ channel in atrioventricular node automaticity
Authors
Qian ZhangaValeriy TimofeyevaHong QiuaLing LuaNing LiaAnil SingapuriaCyril L. Toradoa신희섭Nipavan Chiamvimonva
Keywords
Cav1.3 channel; Atrioventricular nodes
Issue Date
2011-01
Publisher
Journal of molecular and cellular cardiology
Citation
VOL 50, NO 1, 194-202
Abstract
Atrioventricular node (AV node) is the hub where electrical input from the atria is propagated and conveyed to the ventricles. Despite its strategic position and role in governing impulse conduction between atria and ventricles, there is paucity of data regarding the contribution of specific ion channels to the function of the AV node. Here, we examined the roles of Cav1.3 L-type Ca2+ channel in AV node by taking advantage of a mouse model with null mutation of Cav1.3 (Cav1.3−/−). Cav1.3 null mutant mice show evidence of AV node dysfunction with AV block, suggesting the tissue-specific function of the Cav1.3 channel. In keeping with this assertion, we demonstrate that Cav1.3 isoform is highly expressed in the isolated AV node cells. Furthermore, AV node isolated from Cav1.3 null mutant mice show a significant decrease in the firing frequency of spontaneous action potentials suggesting that Cav1.3 L-type Ca2+ channel plays significant roles in the automaticity of the AV node. Because of the distinct voltage-dependence of Cav1.2 and Cav1.3 Ca2+ channels, Cav1.2 alone does not suffice to maintain normal AV node function. Cav1.3 currents activate at more hyperpolarizing voltage compared to Cav1.2 currents. Consequently, Cav1.2 Ca2+ channel cannot functionally substitute for Cav1.3 isoform in the AV node of Cav1.3 null mutant mice. Thus, our study demonstrates that the distinct biophysical properties of Cav1.3 Ca2+ channel play critical roles in the firing frequency of AV node tissues.
URI
http://pubs.kist.re.kr/handle/201004/41072
ISSN
0022-2828
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KIST Publication > Article
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