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

被引:102
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
相关论文
共 80 条
  • [1] Calcineurin and mitochondrial function in glutamate-induced neuronal cell death
    Ankarcrona, M
    Dypbukt, JM
    Orrenius, S
    Nicotera, P
    [J]. FEBS LETTERS, 1996, 394 (03): : 321 - 324
  • [2] GLUTAMATE-INDUCED NEURONAL DEATH - A SUCCESSION OF NECROSIS OR APOPTOSIS DEPENDING ON MITOCHONDRIAL-FUNCTION
    ANKARCRONA, M
    DYPBUKT, JM
    BONFOCO, E
    ZHIVOTOVSKY, B
    ORRENIUS, S
    LIPTON, SA
    NICOTERA, P
    [J]. NEURON, 1995, 15 (04) : 961 - 973
  • [3] Mitochondrial participation in the intracellular Ca2+ network
    Babcock, DF
    Herrington, J
    Goodwin, PC
    Park, YB
    Hille, B
    [J]. JOURNAL OF CELL BIOLOGY, 1997, 136 (04) : 833 - 844
  • [4] Morphological organization of oligodendrocyte processes during development in culture and in vivo
    Barry, C
    Pearson, C
    Barbarese, E
    [J]. DEVELOPMENTAL NEUROSCIENCE, 1996, 18 (04) : 233 - 242
  • [5] REGULATION OF THE MITOCHONDRIAL NA+/CA2+ ANTIPORT BY MATRIX PH
    BAYSAL, K
    BRIERLEY, GP
    NOVGORODOV, S
    JUNG, DW
    [J]. ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS, 1991, 291 (02) : 383 - 389
  • [6] NA+-DEPENDENT CA2+ EFFLUX MECHANISM OF HEART-MITOCHONDRIA IS NOT A PASSIVE CA2+/2NA+ EXCHANGER
    BAYSAL, K
    JUNG, DW
    GUNTER, KK
    GUNTER, TE
    BRIERLEY, GP
    [J]. AMERICAN JOURNAL OF PHYSIOLOGY, 1994, 266 (03): : C800 - C808
  • [7] DYNAMICS OF MITOCHONDRIA IN LIVING CELLS - SHAPE CHANGES, DISLOCATIONS, FUSION, AND FISSION OF MITOCHONDRIA
    BEREITERHAHN, J
    VOTH, M
    [J]. MICROSCOPY RESEARCH AND TECHNIQUE, 1994, 27 (03) : 198 - 219
  • [8] The permeability transition pore. Control points of a cyclosporin A-sensitive mitochondrial channel involved in cell death
    Bernardi, P
    [J]. BIOCHIMICA ET BIOPHYSICA ACTA-BIOENERGETICS, 1996, 1275 (1-2): : 5 - 9
  • [9] The permeability transition pore as a mitochondrial calcium release channel: A critical appraisal
    Bernardi, P
    Petronilli, V
    [J]. JOURNAL OF BIOENERGETICS AND BIOMEMBRANES, 1996, 28 (02) : 131 - 138
  • [10] INOSITOL TRISPHOSPHATE AND CALCIUM SIGNALING
    BERRIDGE, MJ
    [J]. NATURE, 1993, 361 (6410) : 315 - 325