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Journal of Neuroscience, Vol 16, 2325-2334, Copyright © 1996 by Society for Neuroscience
Nitric oxide delays the death of trophic factor-deprived PC12 cells and sympathetic neurons by a cGMP-mediated mechanism
SE Farinelli, DS Park and LA Greene
Department of Pathology, Columbia University College of Physicians and Surgeons, New York, 10032, USA.
We have used cultured PC12 cells and rat sympathetic neurons as model
systems to examine the regulation of neuronal cell death and survival.
Because nitric oxide (NO) may be involved in nerve growth factor (NGF)
signaling in PC12 cells, we tested NO-generating compounds for their
ability to protect PC12 cells and sympathetic neurons from death after
withdrawal of trophic support. Three such agents, S-nitroso-N-
acetylpenicillamine (SNAP), diethylenetriamine NO adduct (DETA-NO), and
sodium nitroprusside provide (SNP), were found to promote complete
short-term survival after removal of serum from naive PC12 cells and of NGF
from neuronally differentiated PC12 cells and sympathetic neurons. One
major target of NO action is guanylate cyclase, which is activated by
nitrosylation of its heme prosthetic group. We observed that inhibition of
guanylate cyclase blocks the protective effects of the NO generators on
trophic factor-deprived PC12 cells and sympathetic neurons without
preventing NGF-induced survival. We also found that permeant cGMP analogs
and an inhibitor of cGMP-specific phosphodiesterase enhance cell survival,
suggesting that the protective effects of NO are mediated by activation of
guanylate cyclase and increased intracellular cGMP. N-Nitro-L-arginine
methyl ester, a NO synthase inhibitor, did not block NGF-promoted PC12 cell
or sympathetic neuron survival. These findings indicate that like NGF, NO
has survival- promoting actions on neurons but that the two agents work by
initially independent mechanisms.
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