Putney James W
National Institute of Environmental Health Sciences, National Institutes of Health, Department of Health and Human Services, Research Triangle Park, NC 27709, USA.
Cell Calcium. 2003 Oct-Nov;34(4-5):339-44. doi: 10.1016/s0143-4160(03)00143-x.
Capacitative calcium entry is a process whereby the depletion of Ca(2+) from intracellular stores (likely endoplasmic or sarcoplasmic reticulum) activates plasma membrane Ca(2+) channels. Current research has focused on identification of capacitative calcium entry channels and the mechanism by which Ca(2+) store depletion activates the channels. Leading candidates for the channels are members of the transient receptor potential (TRP) superfamily, although no single gene or gene product has been definitively proven to mediate capacitative calcium entry. The mechanism for activation of the channels is not known; proposals fall into two general categories, either a diffusible signal released from the Ca(2+) stores when their Ca(2+) levels become depleted, or a more direct protein-protein interaction between constituents of the endoplasmic reticulum and the plasma membrane channels. Capacitative calcium entry is a major mechanism for regulated Ca(2+) influx in non-excitable cells, but recent research has indicated that this pathway plays an important role in the function of neuronal cells, and may be important in a number of neuropathological conditions. This review will summarize some of these more recent findings regarding the role of capacitative calcium entry in normal and pathological processes in the nervous system.
容量性钙内流是一种细胞内钙库(可能是内质网或肌浆网)中Ca(2+)耗竭激活质膜Ca(2+)通道的过程。目前的研究集中在容量性钙内流通道的鉴定以及Ca(2+)储存耗竭激活这些通道的机制上。尽管尚未有单个基因或基因产物被明确证明介导容量性钙内流,但该通道的主要候选者是瞬时受体电位(TRP)超家族的成员。通道激活的机制尚不清楚;相关假说主要分为两大类,一种是当Ca(2+)储存的Ca(2+)水平降低时从Ca(2+)储存中释放的可扩散信号,另一种是内质网成分与质膜通道之间更直接的蛋白质-蛋白质相互作用。容量性钙内流是调节非兴奋性细胞中Ca(2+)内流的主要机制,但最近的研究表明,该途径在神经元细胞的功能中起重要作用,并且可能在许多神经病理状况中具有重要意义。本综述将总结一些关于容量性钙内流在神经系统正常和病理过程中的作用的最新研究发现。