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J Neurophysiol 87: 740-749, 2002;
0022-3077/02 $5.00
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The Journal of Neurophysiology Vol. 87 No. 2 February 2002, pp. 740-749
Copyright ©2002 by the American Physiological Society

NMDA-Induced Calcium Loads Recycle Across the Mitochondrial Inner Membrane of Hippocampal Neurons in Culture

Guang Jian Wang and Stanley A. Thayer

Department of Pharmacology, University of Minnesota Medical School, Minneapolis, Minnesota 55455-0217

Wang, Guang Jian and Stanley A. Thayer. NMDA-Induced Calcium Loads Recycle Across the Mitochondrial Inner Membrane of Hippocampal Neurons in Culture. J. Neurophysiol. 87: 740-749, 2002. Mitochondria sequester N-methyl-D-aspartate (NMDA)-induced Ca2+ loads and regulate the shape of intracellular Ca2+ concentration ([Ca2+]i) responses in neurons. When isolated mitochondria are exposed to high [Ca2+], Ca2+ enters the matrix via the uniporter and returns to the cytosol by Na+/Ca2+ exchange. Released Ca2+ may re-enter the mitochondrion recycling across the inner membrane dissipating respiratory energy. Ca2+ recycling, the continuous uptake and release of Ca2+ by mitochondria, has not been described in intact neurons. Here we used single-cell microfluorimetry to measure [Ca2+]i and mitochondrially targeted aequorin to measure matrix Ca2+ concentration ([Ca2+]mt) to determine whether Ca2+ recycles across the mitochondrial inner membrane in intact neurons following treatment with NMDA. We used ruthenium red and CGP 37157 to block uptake via the uniporter and release via Na+/Ca2+ exchange, respectively. As predicted by the Ca2+ recycling hypothesis, blocking the uniporter immediately following challenge with 200 µM NMDA produced a rapid and transient increase in cytosolic Ca2+ without a corresponding increase in matrix Ca2+. Blocking mitochondrial Ca2+ release produced the opposite effect, depressing cytosolic Ca2+ levels and prolonging the time for matrix Ca2+ levels to recover. The Ca2+ recycling hypothesis uniquely predicts these reciprocal changes in the Ca2+ levels between the two compartments. Ca2+ recycling was not detected following treatment with 20 µM NMDA. Thus Ca2+ recycling across the inner membrane was more pronounced following treatment with a high relative to a low concentration of NMDA, consistent with a role in Ca2+-dependent neurotoxicity.




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