Constitutive and inducible nitric oxide synthases after dynorphin-induced spinal cord injury

Wen Hui Hu*, Wen An Qiang, Fang Li, Na Liu, Guo Qiang Wang, Hai Yan Wang, Xuancai S T Wan, Wei Hong Liao, Jing Sheng Liu, Min Feng Jen

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

17 Scopus citations

Abstract

It has recently been demonstrated that selective inhibition of both neuronal constitutive and inducible nitric oxide synthases (ncNOS and iNOS) is neuroprotective in a model of dynorphin (Dyn) A(1-17)-induced spinal cord injury. In the present study, various methods including the conversion of 3H-L-arginine to 3H-citrulline, immunohistochemistry and in situ hybridization are employed to determine the temporal profiles of the enzymatic activities, immunoreactivities, and mRNA expression for both ncNOS and iNOS after intrathecal injection of a neurotoxic dose (20 nmol) of Dyn A(1-17). The expression of ncNOS immunoreactivity and mRNA increased as early as 30 min after injection and persisted for 1-4 h. At 24-48 h, the number of ncNOS positive cells remained elevated while most neurons died. The cNOS enzymatic activity in the ventral spinal cord also significantly increased at 30 min-48 h, but no significant changes in the dorsal spinal cord were observed. However, iNOS mRNA expression increased later at 2 h, iNOS immunoreactivity and enzymatic activity increased later at 4 h and persisted for 24-48 h after injection of 20 nmol Dyn A(1-17). These results indicate that both ncNOS and iNOS are associated with Dyn-induced spinal cord injury, with ncNOS predominantly involved at an early stage and iNOS at a later stage. Copyright (C) 2000 Elsevier Science B.V.

Original languageEnglish (US)
Pages (from-to)183-197
Number of pages15
JournalJournal of chemical neuroanatomy
Volume17
Issue number4
DOIs
StatePublished - Jan 1 2000

Keywords

  • Dynorphin
  • Neurotoxicity
  • Nitric oxide
  • Nitric oxide synthase
  • Spinal cord injury

ASJC Scopus subject areas

  • Cellular and Molecular Neuroscience

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