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Neuronal NOS deficiency promotes apoptotic cell death of spinal cord neurons after peripheral nerve transection

Authors
Journal
Nitric Oxide
1089-8603
Publisher
Elsevier
Publication Date
Volume
10
Issue
2
Identifiers
DOI: 10.1016/j.niox.2004.03.008
Keywords
  • Apoptosis
  • Endothelial Nos
  • Inducible Nos
  • Neuronal Nos
  • Knock-Out Mice
  • Sciatic Nerve Transection
  • Spinal Cord
Disciplines
  • Chemistry

Abstract

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.

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