Journal of Neurocytology

, Volume 23, Issue 8, pp 453–459

Co-induction of neuronal interferon-gamma and nitric oxide synthase in rat motor neurons after axotomy: a role in nerve repair or death?


  • K. Kristensson
    • Department of NeuroscienceKarolinska Institute
  • M. Aldskogius
    • Department of NeuroscienceKarolinska Institute
  • Z. -C. Peng
    • Institute of Anatomy and HistologiUniversity of Verona
  • T. Olsson
    • Department of Clinical NeuroscienceHuddinge University Hospital
  • H. Aldskogius
    • Department of NeuroscienceKarolinska Institute
  • M. Bentivoglio
    • Institute of Anatomy and HistologiUniversity of Verona

DOI: 10.1007/BF01184069

Cite this article as:
Kristensson, K., Aldskogius, M., Peng, Z.-. et al. J Neurocytol (1994) 23: 453. doi:10.1007/BF01184069


Induction of an interferon-gamma-like molecule, previously isolated from neurons (N-IFN-γ), and of the neuronal isoform I of the synthetic enzyme of the free radical nitric oxide, nitric oxide synthase I, as well as of NADPH-diaphorase, were examined in axotomized dorsal motor vagal and hypoglossal neurons. Unilateral transection of the vagal and hypoglossal nerves was performed in the same rat and an induction of N-IFN-γ and nitric oxide synthase I immunostaining as well as NADPH-diaphorase histochemical positivity was observed in the ipsilateral motoneurons after 2–4 days. The immuno- and enzyme- histochemical positivities were much stronger in the dorsal motor vagal neurons than in hypoglossal neurons. Two and 4 weeks after axotomy N-IFN-γ immunoreactivity and NADPH-diaphorase positivity persisted in the former, but started to decrease in the latter neurons. Previous data have shown that 23 weeks after nerve transection the majority of the dorsal motor vagal neurons are lost, while the majority of the hypoglossal neurons survive. The high and persistent expression of N-IFN-γ and nitric oxide synthase I after axotomy in the dorsal motor vagal neurons, that are largely destined to die, indicates that the co-induction of these two molecules may be implicated in the pathogenesis of neuronal degeneration.

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© Chapman and Hall 1994