Immunostaining and mrna levels for Bcl 2 were noticed in the lumbar enlargement of intact controls and were not modified by sciatic axotomy. The constitutive expression of ALK inhibitor in virtually all cell types of unlesioned animals might be related to its recognized function of encouraging cellular survival. As to axotomized rats, it is possible that the small upsurge in Bcl 2 expression occurred without having to be detected by immunohistochemistry. In cases like this, Bcl 2 might have desired the maintenance of transected motoneurons and/or little Bax positive cells. Especially, the latter could have been prevented from completing the cell death process. Another possibility is that several cells did overexpress Bcl 2. Nevertheless, such fact would not have been verified by RT PCR since this system establishes total mRNA levels of the whole lumbar enlargement. Regardless of these possible functions, our results showing no changes in mRNA levels and immunostaining pattern for Bcl 2 in motoneurons suggest that a significant increase in Bcl 2 term isn’t necessary for saving axotomized premature lumbar motoneurons, as seen in other neuronal types. Dietz et al. reported the amount of ganglion cells present in the retina of bcl 2?/? or wild type adult rats was similar after optic nerve axotomy. Allsopp et al. When cultured in the absence of these neurotrophic factors, examined neuronal cells from chicken embryo in-vitro and noticed that NGF, BDNF or NT 3 dependent sensory Cellular differentiation neurons were protected from apoptosis by microinjection of a Bcl 2 indicating vector. On the other hand, CNTF dependent ciliary neurons were not recovered by this vector after being deprived of CNTF. The authors concluded that there could be different neuronal cell death pathways that could be connected or never to Bcl 2 action and the trophic factors on which the cells depend. Since axotomized sciatic motoneurons of neonatal rats are guarded by CNTF, other anti apoptotic elements could have been upregulated as an answer to the injury in the present experimental design. Melatonin management considerably protected the motoneurons. This effect was specially buy axitinib noted on the first time after sciatic transection inasmuch as MSR of treated animals was much like that of the intact controls. Conversely, at the same time point, MSR of vehicle treated puppies was reduced by 25-60. Regardless of the progressive neuronal damage, MSR of melatonin treated animals was higher-than that of mice that received just the dilution vehicle. Consequently, such protective action of melatonin appears to bemore successful throughout the first day after lesion. Melatonin administration prevented the increase in how many TUNEL positive cells in the ipsilateral dorsal horn 1 day after patch, compared with vehicle treated group. But, the neurohormone did not alter the amount of Bax positive cells at the same time point.