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• W2074604251 abstract "To study the role of endogenous NO in survival and recovery of spinal cord neurons after nerve lesions, wild type mice were compared to knock-out mice lacking neuronal, endothelial or inducible NO synthase (NOS) after sciatic nerve transection. The NO-generating capacities were assessed by NOS immunohistochemistry and NADPH-diaphorase staining. The feature of affected neurons was evaluated following Nissl- and TUNEL-staining, by immunocytochemical demonstration of cytochrome c-translocation, and by ultrastructural examination. Time point of cell loss was found to be independent of the mice type and occurred only at later post-axotomy states. The extent of neuronal degeneration, however, depended on the NO supply. Whereas a lack of endothelial or inducible NOS was well tolerated, deficiency of neuronal NOS enhanced the competence-to-die and led to a substantial apoptotic cell death of spinal cord neurons. Thus, NO supply turned out to be essential for cell survival and recovery with reference to the neuronal NOS isoform." @default.
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• W2074604251 date "2004-03-01" @default.
• W2074604251 modified "2023-10-17" @default.
• W2074604251 title "Neuronal NOS deficiency promotes apoptotic cell death of spinal cord neurons after peripheral nerve transection" @default.
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• W2074604251 doi "https://doi.org/10.1016/j.niox.2004.03.008" @default.
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