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Vol. 53, Issue 6, 974-980, June 1998
Departments of
Neurology (T.-I.P., J.T.G.) and
Pharmacology (J.T.G.) and the
Wesley Woods Laboratory for
Brain Sciences (T.-I.P., J.T.G.), Emory University School of Medicine,
Atlanta, Georgia 30322
Mitochondrial Ca2+ uptake responds dynamically and
sensitively to changes in cytosolic Ca2+ levels and plays a
crucial role in sequestering the large Ca2+ load induced by
N-methyl-D-aspartate (NMDA) receptor
activation. However, the precise interrelationships between NMDA
receptor activation, cytosolic Ca2+ increase, and
mitochondrial Ca2+ uptake remain obscure. To reliably,
independently, and simultaneously detect cytosolic and mitochondrial
Ca2+ concentration changes in the same cell, we loaded
primary striatal neurons with two Ca2+ indicators, calcium
green 1N and rhod-2, and visualized the fluorescence signals from
single neurons with laser scanning confocal fluorescence microscopy. In
kinetic data analysis, only calcium green signals from predefined
cytosolic areas and rhod-2 signals from predefined mitochondrial
regions were used, and attention was focused on the initial rapid
rising phase of the responses. When neurons were treated with 100 µM NMDA, increases of cytosolic and mitochondrial Ca2+ showed similar time courses and rates of change, and
seemed to be time-locked. In contrast, when neurons were treated with
100 µM kainate, 50 mM KCl, or 0.3 µM ionomycin, mitochondrial Ca2+ increases
lagged behind cytosolic Ca2+ increases. These data suggest
that mitochondrial Ca2+ uptake in response to an increase
of cytosolic Ca2+ is faster and more tightly coupled during
NMDA receptor activation than during non-NMDA receptor or
voltage-dependent Ca2+ channel activation. This proficient
mitochondrial Ca2+ uptake may avert a large rise in
cytosolic Ca2+ concentration in response to NMDA receptor
activation. Yet, it may lead to excessive Ca2+ accumulation
inside mitochondria and render mitochondria susceptible to
Ca2+ mediated injury.
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