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J. Cell Biol.,
Volume 144, Number 5, March 8, 1999 883-889
* Serono Pharmaceutical Research Institute, Ares Serono International S.A., CH-1228 Plan-les-Ouates, Geneva, Switzerland;
and During apoptosis induced by various stimuli,
cytochrome c is released from mitochondria into the cytosol where it participates in caspase activation. This
process has been proposed to be an irreversible consequence of mitochondrial permeability transition pore
opening, which leads to mitochondrial swelling and
rupture of the outer mitochondrial membrane. Here we
present data demonstrating that NGF-deprived sympathetic neurons protected from apoptosis by caspase inhibitors possess mitochondria which, though depleted of cytochrome c and reduced in size, remained structurally intact as viewed by electron microscopy. After re-exposure of neurons to NGF, mitochondria recovered
their normal size and their cytochrome c content, by a
process requiring de novo protein synthesis. Altogether, these data suggest that depletion of cytochrome
c from mitochondria is a controlled process compatible
with function recovery. The ability of sympathetic neurons to recover fully from trophic factor deprivation
provided irreversible caspase inhibitors have been present during the insult period, has therapeutical implications for a number of acute neuropathologies.
Center of Electron Microscopy, University of Lausanne, CH-1005 Lausanne, Switzerland
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