Axotomy along with hypoxia enhances the neuronal NADPH-d/NOS expression inlower brain stem motor neurons of adult rats

This study was aimed to determine whether axotomy coupled with hypoxia woul d exert a more profound effect on injury-induced neuronal nitric oxide synt hase (NOS) expression. In this connection, the vagus and the hypoglossal ne rves of adult rats were transected unilaterally in the same animal, and hal f of the operated animals were subjected to hypoxia treatment.. Both the ne uronal NOS immunohistochemistry and the nicotinamide adenine dinucleotide p hosphate-diaphorase (NADPH-d) histochemistry were used to assess the neuron al NOS expression. The present results have shown that the number of NADPH- d/NOS-positive [NADPH-d/NOS(1)] neurons in the hypoglossal nucleus (EN) pea ked at 14 days after axotomy, while that in dorsal motor nucleus of vagus ( DMN) and nucleus ambiguus (NA) was progressively increased up to 60 days. T he up-regulation of NADPH-d/NOS in HN and DMN was more pronounced in hypoxi c than in normoxic animals, a feature that was not evident in the NA. Quant itative analysis showed that the number of surviving motoneurons in normoxi c animals was significantly higher than those subjected to hypoxia at 14 da ys postaxotomy in HN and at all postaxotomy time points in DMN. The differe nce may be attributed to their different functional components. Since O-2 d eprivation leads to poor cellular function, the stronger expression of NADP H-d/NOS and the more drastic neuronal loss following nerve transection in t he hypoxic animals compared with the controls suggest that hypoxia plays an important role in peripheral neuropathies in which NO is implicated. (C) 2 001 Academic Press.