Morteza Behnam-Rasouli, Mohammad Reza Nikravesh, Naser Mhadavi-Shahri, Maryam Tehranipour,
Volume 4, Issue 1 (1-2000)
Abstract
There are extensive evidences that show axonal processes of the nervous system (peripheral and/or central) may be degenerated after nerve injuries. Wallerian degeneration and chromatolysis are the most conspicuous phenomena that occur in response to injuries. In this research, the effects of post-operative time following sciatic nerve crush on the number of spinal motoneurons were investigated. Twelve adult male Wistar rats, whose left sciatic nerves were highly compressed for 30 s, assigned to experimental groups 1 and 2 (n = 6). After 3 and 8 weeks post-operative (in groups 1 and 2 respectively) the lumbar segments of spinal cord were sampled, processed, sectioned serially and stained with toluidine blue (pH 4.65). By using stereological quantitative technique (physical disector), the number of alpha motoneurons in the right and the left ventral horns of spinal cord were counted and compared with each other. Statistical analyses showed a remarkable reduction in the number of alpha motoneurons in the left side (experimental or operated) when compared with the right side (control or unoperated) both in 3 and 8 weeks post-operative groups. This reduction may be due to the blockade of retrograde axonal transport.
Zahra Fallah,
Volume 9, Issue 3 (7-2005)
Abstract
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.
.png)
