During cardiac development, there is a reciprocal relationship between card
iac morphogenesis and force production (contractility). In the early embryo
nic myocardium, the sarcoplasmic reticulum is poorly developed, and plasma
membrane calcium (Ca2+) channels are critical for maintaining both contract
ility and excitability. In the present study, we identified the Ca(V)3.1d m
RNA expressed in embryonic day 14 (E14) mouse heart. Ca(V)3.1d is a splice
variant of the alpha 1G, T-type Ca2+ channel. Immunohistochemical localizat
ion showed expression of alpha 1G Ca2+ channels in E14 myocardium, and stai
ning of isolated ventricular myocytes revealed membrane localization of the
alpha 1G channels. Dihydropyridine-resistant inward Ba2+ or Ca2+ currents
were present in all fetal ventricular myocytes tested. Regardless of charge
carrier, inward current inactivated with sustained depolarization and mirr
ored steady-state inactivation voltage dependence of the alpha 1G channel e
xpressed in human embryonic kidney-293 cells. Ni2+ blockade discriminates a
mong T-type Ca2+ channel isoforms and is a relatively selective blocker of
T-type channels over other cardiac plasma membrane Ca2+ handling proteins.
We demonstrate that 100 mu mol/L Ni2+ partially blocked alpha 1G currents u
nder physiological external Ca2+. We conclude that alpha 1G T-type Ca2+ cha
nnels are functional in midgestational fetal myocardium.