Zong X, Hofmann F
Institut für Pharmakologie und Toxikologie, Technischen Universität München, Germany.
FEBS Lett. 1996 Jan 8;378(2):121-5. doi: 10.1016/0014-5793(95)01434-9.
The stably expressed Ca2+ channel alpha 1C-a and alpha 1C-b subunit were used to investigate the molecular basis for Ca(2+)-dependent inactivation of the L-type current. The Ba2+ current (IBa) of both channels had similar kinetics and inactivated with one time constant of about 400 ms at +20 mV, whereas the Ca2+ current (ICa) could be fitted only with a bi-exponential function. The fast (tau f) and the slow (tau s) time constant were about 20 ms and 400 ms, respectively. The inactivation of ICa strongly depended on the entry of Ca2+ as shown by prepulses and variation of the intracellular Ca2+ chelator. Coexpression of the alpha 1C subunits with the auxiliary alpha 2/delta and beta subunits accelerated the voltage-dependent but not the Ca(2+)-dependent inactivation of the channels. These results suggest that the alpha 1C subunit of L-type Ca2+ channels itself mediates the Ca(2+)-dependent inactivation of the current.
利用稳定表达的Ca2+通道α1C-a和α1C-b亚基来研究L型电流的Ca(2+)依赖性失活的分子基础。两种通道的Ba2+电流（IBa）具有相似的动力学，并且在+20 mV时以约400 ms的单一时间常数失活，而Ca2+电流（ICa）只能用双指数函数拟合。快速（τf）和慢速（τs）时间常数分别约为20 ms和400 ms。如预脉冲和细胞内Ca2+螯合剂的变化所示，ICa的失活强烈依赖于Ca2+的进入。α1C亚基与辅助α2/δ和β亚基的共表达加速了通道的电压依赖性失活，但未加速Ca(2+)依赖性失活。这些结果表明，L型Ca2+通道的α1C亚基本身介导了电流的Ca(2+)依赖性失活。
