title: Molecular and functional changes in voltage-gated Na⁺ channels in cardiomyocytes during mouse embryogenesis.
abstract: BACKGROUND
  Embryonic cardiomyocytes undergo profound changes in their electrophysiological properties during development. However, the molecular and functional changes in Na⁺ channel during cardiogenesis are not yet fully explained.
  
  
  RESULTS
  To study the functional changes in the Na⁺ channel during cardiogenesis, Na⁺ currents were recorded in the early (EDS) and late (LDS) developmental stages of cardiomyocytes in embryonic mice. Compared with EDS myocytes, LDS myocytes exhibited a larger peak current density, a more negative shift in the voltage of half inactivation, a larger fast inactivation component and a smaller slow inactivation component, and smaller time constants for recovery from inactivation. Additionally, multiple Na⁺ channel α-subunits (Nav 1.1-1.6) and β-subunits (Nav β1-β3) of mouse embryos were investigated. Transcripts of Nav 1.1-1.3 were absent or present at very low levels in embryonic hearts. Transcripts encoding Nav 1.4-1.6 and Nav β1-β3 increased during embryogenesis. Data on the sensitivity of total Na⁺ currents to tetrodotoxin (TTX) showed that TTX-resistant Nav 1.5 is the predominant isoform expressed in the heart of the mouse embryo.
  
  
  CONCLUSIONS
  The results indicate that significant changes in the functional properties of Na⁺ channels develop in the cardiomyocytes of the mouse embryo, and that different Na⁺ channel subunit genes are strongly regulated during embryogenesis, which further support a physiological role for voltage-gated Na⁺ channels during heart development.
authors.affiliation: Chinese-German Stem Cell Center, Department of Physiology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.
authors.forename: Liangzhu
authors.initials: L
authors.lastname: Yu
authors.forename: Shijun
authors.initials: S
authors.lastname: Gao
authors.forename: Li
authors.initials: L
authors.lastname: Nie
authors.forename: Ming
authors.initials: M
authors.lastname: Tang
authors.forename: Weifeng
authors.initials: W
authors.lastname: Huang
authors.forename: Hongyan
authors.initials: H
authors.lastname: Luo
authors.forename: Xinwu
authors.initials: X
authors.lastname: Hu
authors.forename: Jiaoya
authors.initials: J
authors.lastname: Xi
authors.forename: Minjie
authors.initials: M
authors.lastname: Zhu
authors.forename: Yunjie
authors.initials: Y
authors.lastname: Zheng
authors.forename: Linlin
authors.initials: L
authors.lastname: Gao
authors.forename: Lanqiu
authors.initials: L
authors.lastname: Zhang
authors.forename: Yuanlong
authors.initials: Y
authors.lastname: Song
authors.forename: Jürgen
authors.initials: J
authors.lastname: Hescheler
authors.forename: Huamin
authors.initials: H
authors.lastname: Liang
mesh_terms: D000818:Animals; D002478:Cells, Cultured; D004622:Embryo, Mammalian / Q000166:cytology / Q000196:embryology*; D047108:Embryonic Development / Q000502:physiology*; D005260:Female; D018507:Gene Expression Regulation, Developmental / Q000502:physiology; D006321:Heart / Q000196:embryology*; D015640:Ion Channel Gating / Q000502:physiology*; D051379:Mice; D009124:Muscle Proteins / Q000096:biosynthesis*; D009206:Myocardium / Q000166:cytology / Q000378:metabolism*; D032383:Myocytes, Cardiac / Q000166:cytology / Q000378:metabolism*; D020033:Protein Isoforms / Q000378:metabolism; D015222:Sodium Channels / Q000096:biosynthesis*; D014158:Transcription, Genetic / Q000502:physiology
chemical_list: D009124:Muscle Proteins; D020033:Protein Isoforms; D015222:Sodium Channels