Role of mitochondrial Ca 2+ regulation in neuronal and glial cell signalling 1 Published on the World Wide Web on December 3rd 1997. 1

Role of mitochondrial Ca 2+ regulation in neuronal and glial cell signalling 1 Published on the... It is becoming increasingly clear that mitochondrial Ca 2+ uptake from and release into the cytosol has important consequences for neuronal and glial activity. Ca 2+ regulates mitochondrial metabolism, and mitochondrial Ca 2+ uptake and release modulate physiological and pathophysiological cytosolic responses. In glial cells, inositol 1,4,5-trisphosphate-dependent Ca 2+ responses are faithfully translated into elevations in mitochondrial Ca 2+ levels, which modifies cytosolic Ca 2+ wave propagation and may activate mitochondrial enzymes. The location of mitochondria within neurones may partially determine their role in Ca 2+ signalling. Neuronal death due to NMDA-evoked Ca 2+ 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 Ca 2+ regulation as a modulator of cellular energetics, endoplasmic reticulum Ca 2+ release and neurotoxicity. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Brain Research Reviews Elsevier

Role of mitochondrial Ca 2+ regulation in neuronal and glial cell signalling 1 Published on the World Wide Web on December 3rd 1997. 1

Brain Research Reviews, Volume 26 (1) – Mar 1, 1998

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Publisher
Elsevier
Copyright
Copyright © 1998 Elsevier Science B.V.
ISSN
0165-0173
D.O.I.
10.1016/S0165-0173(97)00056-8
Publisher site
See Article on Publisher Site

Abstract

It is becoming increasingly clear that mitochondrial Ca 2+ uptake from and release into the cytosol has important consequences for neuronal and glial activity. Ca 2+ regulates mitochondrial metabolism, and mitochondrial Ca 2+ uptake and release modulate physiological and pathophysiological cytosolic responses. In glial cells, inositol 1,4,5-trisphosphate-dependent Ca 2+ responses are faithfully translated into elevations in mitochondrial Ca 2+ levels, which modifies cytosolic Ca 2+ wave propagation and may activate mitochondrial enzymes. The location of mitochondria within neurones may partially determine their role in Ca 2+ signalling. Neuronal death due to NMDA-evoked Ca 2+ 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 Ca 2+ regulation as a modulator of cellular energetics, endoplasmic reticulum Ca 2+ release and neurotoxicity.

Journal

Brain Research ReviewsElsevier

Published: Mar 1, 1998

References

  • The permeability transition pore. Control points of a cyclosporin A-sensitive mitochondrial channel involved in cell death
    Bernardi, P
  • Apoptosis: mitochondria resurrected?
    Henkar, P.A; Grinstein, S
  • Distribution of glutathione and glutathione-related enzyme systems in mitochondria and cytosol of cultured cerebellar astrocytes and granule cells
    Huang, J; Philbert, M.A
  • Nitric oxide (nitrogen monoxide) stimulates insulin secretion by inducing calcium release from mitochondria
    Laffranchi, R; Gogvadze, V; Richter, C; Spinas, G.A
  • Alcohol inhibits the activation of NAD-linked dehydrogenases by calcium in brain and heart mitochondria
    Li, H.L; Moreno-Sanchez, R; Rottenberg, H
  • Role of mitochondria in the etiology and pathogenesis of Parkinson's disease
    Mizuno, Y; Ikebe, S.-I; Hattori, N; Nakagawa-Hattori, Y; Mochizuki, H; Tanka, M; Ozawa, T
  • Mitochondrial calcium transport
    Nicholls, D; Akerman, K
  • Bcl-2 inhibits the mitochondrial release of an apoptogenic protease
    Susin, S.A; Zamzami, N; Castedo, M; Hirsch, T; Marchetti, P; Macho, A; Daugas, E; Geuskens, M; Kroemer, G

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