Role of mitochondrial Ca2+ regulation in neuronal and glial cell signalling

被引:101
作者
Simpson, PB
Russell, JT [1 ]
机构
[1] NICHHD, Lab Cellular & Mol Neurophysiol, NIH, Bethesda, MD 20892 USA
[2] Uniformed Serv Univ Hlth Sci, Dept Anat & Cell Biol, Bethesda, MD 20814 USA
关键词
intracellular calcium mobilization; inositol 1,4,5-trisphosphate receptor; transporter; Ca2+ wave; mitochondrion; mitochondrial impairment;
D O I
10.1016/S0165-0173(97)00056-8
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
It is becoming increasingly clear that mitochondrial Ca2+ uptake from and release into the cytosol has important consequences for neuronal and glial activity. Ca2+ regulates mitochondrial metabolism, and mitochondrial Ca2+ uptake and release modulate physiological and pathophysiological cytosolic responses. In glial cells, inositol 1,4,5-trisphosphate-dependent Ca2+ responses are faithfully translated into elevations in mitochondrial Ca2+ levels, which modifies cytosolic Ca2+ wave propagation and may activate mitochondrial enzymes. The location of mitochondria within neurones may partially determine their role in Ca2+ signalling, Neuronal death due to NMDA-evoked Ca2+ entry can be delayed by an inhibitor of the mitochondrial permeability transition pore, and mitochondrial dysfunction is being increasingly implicated in a number of neurodegenerative conditions. These findings are illustrative of an emerging realization by neuroscientists of the importance of mitochondrial Ca2+ regulation as a modulator of cellular energetics, endoplasmic reticulum Ca2+ release and neurotoxicity. (C) 1998 Elsevier Science B.V.
引用
收藏
页码:72 / 81
页数:10
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