We investigated differences in electrophysiological characteristics between peripheral and central N-type Ca2+ channels, containing α1B-a and a1B-c, respectively. In addition, we examined the inhibitory effects of cilnidipine, a dihydropyridine (DHP) derivative, on both channels. Both α1B subunits were transiently expressed in BHK cells, and then analyzed using the whole-cell patch-clamp technique. The current-voltage relationship showed that α1B-c currents were activated at more negative potentials than α1B-a currents. The voltage-dependent steady-state inactivation and activation showed that the V1/2 values for inactivation and activation of α1B-c (-88.5±1.3 and -33.2±1.3 mV) were both significantly more negative than those for α1B-a (-83.3±1.3 and -27.9±2.3 mV). Despite the different electrophysiological characteristics of these two N-type channels, cilnidipine blocked both with similar potency within the range 0.1 to 10 μM. Furthermore, cilnidipine had no effect on the I-V relationships or the steady-state inactivation curves. Our data indicate that the spliced positions of α1B-a and a1B-c may affect not only their voltage-sensing abilities but also the kinetics of channel activation and inactivation. The data also suggest that cilnidipine binds to sites independent of those controlling voltage-sensing and channel kinetics in these α1B subunits.
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