Identification of the t-type calcium channel (Ca(v)3.1d) in developing mouse heart

Circ Res. 2001 Mar 2;88(4):403-7. doi: 10.1161/01.res.88.4.403.


During cardiac development, there is a reciprocal relationship between cardiac morphogenesis and force production (contractility). In the early embryonic myocardium, the sarcoplasmic reticulum is poorly developed, and plasma membrane calcium (Ca(2+)) channels are critical for maintaining both contractility and excitability. In the present study, we identified the Ca(V)3.1d mRNA expressed in embryonic day 14 (E14) mouse heart. Ca(V)3.1d is a splice variant of the alpha1G, T-type Ca(2+) channel. Immunohistochemical localization showed expression of alpha1G Ca(2+) channels in E14 myocardium, and staining of isolated ventricular myocytes revealed membrane localization of the alpha1G channels. Dihydropyridine-resistant inward Ba(2+) or Ca(2+) currents were present in all fetal ventricular myocytes tested. Regardless of charge carrier, inward current inactivated with sustained depolarization and mirrored steady-state inactivation voltage dependence of the alpha1G channel expressed in human embryonic kidney-293 cells. Ni(2+) blockade discriminates among T-type Ca(2+) channel isoforms and is a relatively selective blocker of T-type channels over other cardiac plasma membrane Ca(2+) handling proteins. We demonstrate that 100 micromol/L Ni(2+) partially blocked alpha1G currents under physiological external Ca(2+). We conclude that alpha1G T-type Ca(2+) channels are functional in midgestational fetal myocardium.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Calcium Channels, T-Type / genetics
  • Calcium Channels, T-Type / isolation & purification*
  • Calcium Channels, T-Type / physiology
  • Fetal Heart / chemistry
  • Genetic Variation
  • Heart / embryology*
  • Heart Ventricles / chemistry
  • Ion Channel Gating / drug effects
  • Mice
  • Myocardium / chemistry
  • Myocardium / cytology
  • Nickel / pharmacology
  • RNA Splicing / genetics
  • RNA, Messenger / metabolism
  • Time Factors


  • Calcium Channels, T-Type
  • RNA, Messenger
  • Nickel