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J. Cell Biol.,
Volume 145, Number 4, May 17, 1999 795-808
Department of Physiology, University College London, London, WC1E 6BT, United Kingdom
We have used digital fluorescence imaging
techniques to explore the interplay between mitochondrial Ca2+ uptake and physiological Ca2+ signaling
in rat cortical astrocytes. A rise in cytosolic Ca2+
([Ca2+]cyt), resulting from mobilization of ER
Ca2+ stores was followed by a rise in mitochondrial Ca2+
([Ca2+]m, monitored using rhod-2). Whereas [Ca2+]cyt
recovered within ~1 min, the time to recovery for
[Ca2+]m was ~30 min. Dissipating the mitochondrial
membrane potential (
m, using the mitochondrial uncoupler carbonyl cyanide p-trifluoromethoxy-phenyl-hydrazone [FCCP] with oligomycin) prevented mitochondrial Ca2+ uptake and slowed the rate of decay of
[Ca2+]cyt transients, suggesting that mitochondrial Ca2+
uptake plays a significant role in the clearance of physiological [Ca2+]cyt loads in astrocytes. Ca2+ signals in
these cells initiated either by receptor-mediated ER
Ca2+ release or mechanical stimulation often consisted
of propagating waves (measured using fluo-3). In response to either stimulus, the wave traveled at a mean
speed of 22.9 ± 11.2 µm/s (n = 262). This was followed
by a wave of mitochondrial depolarization (measured using tetramethylrhodamine ethyl ester [TMRE]), consistent with Ca2+ uptake into mitochondria as the Ca2+
wave traveled across the cell. Collapse of m to prevent mitochondrial Ca2+ uptake significantly increased
the rate of propagation of the Ca2+ waves by 50%.
Taken together, these data suggest that cytosolic Ca2+
buffering by mitochondria provides a potent mechanism to regulate the localized spread of astrocytic Ca2+ signals.
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