Finkbeiner S M
Department of Medicine, University of California, San Francisco 94143-0114.
Glia. 1993 Oct;9(2):83-104. doi: 10.1002/glia.440090202.
This review summarizes current knowledge relating intracellular calcium and glial function. During steady state, glia maintain a low cytosolic calcium level by pumping calcium into intracellular stores and by extruding calcium across the plasma membrane. Glial Ca2+ increases in response to a variety of physiological stimuli. Some stimuli open membrane calcium channels, others release calcium from intracellular stores, and some do both. The temporal and spatial complexity of glial cytosolic calcium changes suggest that these responses may form the basis of an intracellular or intercellular signaling system. Cytosolic calcium rises effect changes in glial structure and function through protein kinases, phospholipases, and direct interaction with lipid and protein constituents. Ultimately, calcium signaling influence glial gene expression, development, metabolism, and regulation of the extracellular milieu. Disturbances in glial calcium homeostasis may have a role in certain pathological conditions. The discovery of complex calcium-based glial signaling systems, capable of sensing and influencing neural activity, suggest a more integrated neuro-glial model of information processing in the central nervous system.
本综述总结了目前有关细胞内钙与神经胶质细胞功能的知识。在稳态期间，神经胶质细胞通过将钙泵入细胞内储存库以及通过将钙挤出质膜来维持低细胞质钙水平。神经胶质细胞的Ca2+会因各种生理刺激而增加。一些刺激会打开膜钙通道，另一些会从细胞内储存库释放钙，还有一些则两者兼具。神经胶质细胞质钙变化的时间和空间复杂性表明，这些反应可能构成细胞内或细胞间信号系统的基础。细胞质钙升高通过蛋白激酶、磷脂酶以及与脂质和蛋白质成分的直接相互作用来影响神经胶质细胞的结构和功能。最终，钙信号传导会影响神经胶质细胞的基因表达、发育、代谢以及细胞外环境的调节。神经胶质细胞钙稳态的紊乱可能在某些病理状况中起作用。能够感知并影响神经活动的基于钙的复杂神经胶质细胞信号系统的发现，提示了中枢神经系统中一种更加整合的神经-胶质细胞信息处理模型。
