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.
Brain Research Reviews – Elsevier
Published: Mar 1, 1998
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