Résumé
The rat brain class C calcium channel α 1 subunit cDNA, rbC-II, was subcloned into a vertebrate expression vector and transient expression was assayed following nuclear injection into
Xenopus oocytes. Whole cell recordings showed that rbC-II currents (recorded with 40 mM Ba
2+ as the charge carrier) had variable activation rates and minimal inactivation over an ∼ 700 msec depolarizing step pulse. The pharmacological properties of the rbC-II current were consistent with those of an L-type calcium channel, being sensitive to dihydropyridines (10 μM nifedipine blocked ∼ 85% of the current, 10 μM Bay K 8644 enhanced the current between 2- and 10-fold) and not affected by the N- and P-type calcium channel antagonists, ω-conotoxin GVIA and ω-agatoxin IVA, respectively. Coexpression of rbC-II with cloned rat neuronal calcium channel
α
2 and β subunits resulted in several changes to the electrophysiological properties of the rbC-II current including, an increased whole cell peak current, an increased rate of activation and a hyperpolarizing shift in the voltage dependence of activation. Taken together with results showing that the neuronal class D
α
1 subunit also encodes an L-type calcium channel [Williams M. E., Feldman D. H., McCue A. F., Brenner R., Velicelebi G., Ellis S. B. and Harpold M. M. (1992a)
Neuron
8: 71–84], these results indicate that the mammalian nervous system expresses two distinct genes encoding L-type calcium channels.