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Induction of NADPH diaphorase/nitric oxide synthase in the spinal cord motor neurons of rats following a single and multiple non-penetrative blasts

  • Kaur, C. [1] ; Singh, J. [2] ; Moochhala, S. [3] ; Lim, M.K. [3] ; Lu, J. [3] ; Ling, E. A. [1]
    1. [1] National University of Singapore

      National University of Singapore

      Singapur

    2. [2] Civil Aviation Medical Board, Tan Tock Seng Hospital Pte Ltd, Singapore
    3. [3] Defence Medical Research Institute, Defence Technology Tower B, Singapore
  • Localización: Histology and histopathology: cellular and molecular biology, ISSN-e 1699-5848, ISSN 0213-3911, Vol. 14, Nº. 2, 1999, págs. 417-425
  • Idioma: inglés
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  • Resumen
    • The prese nt study has demonstrated th e ind ucti on of ni co tin amid e ade nin e d inucl eo tid e phosph ate-diaphorase (NADPH-d) reactivity and nitric ox ide synthase-like immunoreactivity (NOS-LI) in the ve ntral horn motoneurons of the spinal co rd in ra ts subjected to a single or multiple underground, or a single surface blast. Both enzyme activities were first detected in some motoneurons in laminae VIII and IX of Rexed, 3 hours afte r the bl ast. Some NADPH-d and NOS-LJ posit ive neurons were also distributed in laminae VI and VII. The number and intensity of th e labe ll ed ce lls appeared to increase progressively, peaking at 2-3 days aft er the bl ast but we re drastically reduced thereafter, so that at 7 days after the bl ast only a few positive neurons we re observed. In rats killed at 2 wee ks and in longer surviving intervals, i.e . up to 1 month, NADPH-d/NOS reac ti v it y in th e ve ntra l horn moto r ne urons had diminished. The functional significa nce of the transient expression of neuronal NADPH-d/NOS after the blasts remains uncertain, although from a speculative point of view, the induction of these enzymes probabl y would retlect an increased production of nitric oxide (NO). In view of the lack of atrophic changes in most, if not all, of motor neurons, it is suggested that the increased levels of NO production after the blast injury may be involved in a neuroprotective function.


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