Our previous studies have shown that median and ulnar nerve lesion induced calbindin (CB) immunoreactivity in some injured motoneurons in developing rats. Motoneuron death induced by sciatic nerve transection in neonatal rats has been related to induction of neuronal isoform of nitric oxide synthase (nNOS). The present study investigated whether expression of CB and nicotinomid adenin dinucleotide phosphate-diaphorase (NADPH-d) activity, a marker for nNOS, is related to the death or survival of forelimb motoneurons in response to axotomy. After median and ulnar nerve transection at either P2 or P7, NADPH-d histochemistry was performed on cervical spinal cord sections to analyze the induction of nNOS in motoneurons retrogradely labeled with FB and immunostained for CB. NADPH-d reactivity was not detectable in FB labeled motoneurones up to 2 weeks after nerve lesion at P2. However, following nerve lesion at P7, some FB labeled motoneurons showed NADPH-d activity 2 weeks after nerve lesion. These NADPH-d positive motoneurons were not CB immunoreactive. The results indicate the possible role of nitric oxide (NO) in nerve regeneration and the role of CB in neuroprotection from cell death or in mechanisms of neurodegeneration.

Keywords: Axotomy, Motoneuron, Nicotinomid adenin dinucleotide phosphate-diaphorase (NADPH-d), Calbindin (CB)

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