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Previous Article | Next Article
The Journal of Neuroscience, September 1, 1999, 19(17):7476-7485
BAX Translocation Is a Critical Event in Neuronal Apoptosis: Regulation by Neuroprotectants, BCL-2, and Caspases
Girish V. Putcha, Mohanish Deshmukh, and Eugene M. Johnson Jr Departments of Neurology and Molecular Biology and Pharmacology, Washington University School of Medicine, St. Louis, Missouri 63110
Members of the BCL-2 family of proteins either promote or repress programmed cell death. Here we report that neonatal sympathetic neurons undergoing apoptosis after nerve growth factor (NGF) deprivation exhibited a protein synthesis-dependent, caspase-independent subcellular redistribution of BAX from cytosol to mitochondria, followed by a loss of mitochondrial cytochrome c and cell death. Treatment with elevated concentrations of the neuroprotectants KCl or cAMP at the time of deprivation prevented BAX translocation and cytochrome c release. However, administration of KCl or cAMP 12 hr after NGF withdrawal acutely prevented loss of mitochondrial cytochrome c, but not redistribution of BAX; rescue with NGF acutely prevented both events. Overexpression of Bcl-2 neither altered the normal subcellular localization of BAX nor prevented its redistribution with deprivation but did inhibit the subsequent release of cytochrome c, caspase activation, and cell death. Bcl-2 overexpression did not prevent cell death induced by cytoplasmic microinjection of cytochrome c into NGF-deprived competent-to-die neurons. These observations suggest that the subcellular redistribution of BAX is a critical event in neuronal apoptosis induced by trophic factor deprivation. BCL-2 acts primarily, if not exclusively, at the level of mitochondria to prevent BAX-mediated cytochrome c release, whereas NGF, KCl, or cAMP may abort the apoptotic program at multiple checkpoints.
Key words: apoptosis; cAMP; cell death; depolarization; neuron; neuroprotective agents
Copyright © 1999 Society for Neuroscience 0270-6474/99/19177476-10$05.00/0
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