论文部分内容阅读
直接和间接的证据已清楚地表明,通过多磷酸肌醇(PI)水解活化受体使Ca~(2+)内流反应增加是由两个时相组成:早期高峰,主要由于肌醇1、4、5三磷酸(IP_3)诱发特异性细胞贮存钙释放;继之平台期,是由细胞外钙内流维持。虽然细胞内钙释放已被详细地研究,并且IP_3的受体纯化,克隆以及它在细胞内的分布在小脑浦肯野神经元已被确定,但Ca~(2+)内流的调节和机制仍然不清。
Both direct and indirect evidence have clearly shown that the increase in Ca2 + influx through the activation of PIs by PI is composed of two phases: the early peak, mainly due to inositol 1, 4,5 triphosphate (IP_3) induced specific cell storage of calcium release; followed by plateau, is maintained by extracellular calcium influx. Although intracellular calcium release has been studied in detail, and IP3 receptor purification, cloning and its intracellular distribution have been identified in the cerebellar Purkinje neurons, the regulation and mechanism of Ca2 + influx Still unclear.