Neuroprotective effect of deprenyl on motoneurons of spinal cord after axotomy of peripheral nerves such as sciatic has been well established. Deprenyl is an inhibitor of monoamine oxidase type-B (MAO-B). The main function of this agent is the release of neurotransmitters from pre-synaptic terminals. Acetylcholine is a neurotransmitter that is synthesized by choline acetyltransferase (ChAT) and is widely used as a marker to assess the function of neurons. Synaptophysin is one of the synaptic vesicle neuronal terminal residual proteins which is also used as a marker for some neurotransmitters.The aim of this research was to study the effect of deprenyl (2.5 mg/kg) injection on synaptophysin and ChAT immunoreactivity. The intraperitoneal injection of deprenyl was done following axotomy and continued for 21 days. Then, the animals were perfused with paraformaldehyde (4%) and spinal cord segment L4-L6 proccessed for immunohistochemistry. The results obtained in this study showed that deprenyl-treated axotomized mice had higher ChAT and synaptophysin expression as compared to untreated axotomized animals.

Background and Objective: Because of the critical role of cell death in the pathology of neurodegenerative diseases, its prevention is regarded as one of the most salient ends in neuroprotective strategies. Concerning the bulk of reports about the putative neuroprotective effects of erythropoietin (Epo), in the present study following axotomy, the effects of different doses of Epo on spinal moto neurons in neonates was investigated.Materials and Methods: Following transection of the right sciatic nerve of 20 two-day-old neonate rats and induction of apoptotic cell death in related moto neurons, the animals were subdivided into three experimental and one control groups. The experimental groups received different doses of 2500, 5000, 10000U/kg recombinant human Erythropoietin (rhEpo), and the control group was treated with equal volume of normal saline, intraperitoneally for 5 successive days. 24 hours following the last injection, histologic sections from the neonate spinal cords were prepared for counting of spinal moto neurons. In all samples, the intact side was regarded as the internal control.Results: The difference between moto neuron means of intact and axotomy sides was significant in all groups, which advocates the efficacy of axotomy in cell death induction. Comparison of axotomized side of different groups indicated significant differences between both 5000 and 10000U/kg groups with control, and also between 10000 and 2500 groups, but no significant differences could be seen between other groups. Thus, 5000U/kg of rhEpo can be considered as the neuroprotective dose which can prevent cell death of axotomized moto neurons.Conclusion: rhEpo has dose-dependent neuroprotective effects on axotomized spinal moto neurons.

In this research the effects of axotomy on the spinal cord histology of neonatal rats were studied. 40 rat pups of both sexes were operated under ice-induced anesthesia within 5 days of birth. Via hypothermia and under sterile conditions, the right sciatic nerve was transected at mid-thigh level. The left side was used as a control. operated rats were sacrificed at 3,5,7,10 and 14 days of axotomy. All animals were perfused and killed with an overdose of ether. After routine processing and embedding in paraffin, transverse serial sections were taken at 8 µm from the lumbar spinal cord and stained with cresyl violet and Hematoxylin and Eosin. Moreover, the spinal cord was processed for semithin sections by perfusing the animals with 2.2% glutaradehyde in phosphate buffer, postfixed 1% osmium tetroxide and dehydrated in graded acetone followed by epoxy and resin. Slices 500-800 µm thick were cut and stained with Tolidine blue. Slides were studied by superimposing an ocular grid and counting vital and nonvital motoneurons. Comparisons between counts on the right and left sides of operated animals were made. ANOVA was used to evaluate the significance of the differences between the results obtained in different periods and the neuronal loss on the operated side was determined by student t-test. Quantitative studies confirm the death of motoneurons on operated side. Mean survival rates of motoneurons in all groups was lower on the operated side and this difference was significant (P<0.01). Furthermore the mean number of live motoneurons 10 days after surgery was lower than other groups (P < 0.01). There was a relation between loss of motoneurons and increase of dead cells. Microscopic observation showed nuclear changes and cytoplasmic vesicles in the spinal motoneurons. Scattered cells with a dense cytoplasm with piknotic nuclei were seen. These cells represented characteristic apoptotic features. Some motoneurons showed changes such as nuclear condensation and peripheral displacement. In conclusion, axotomy resulted in apoptotic cell death of motoneurons as well as progressive definitive time-course reduction of cell number after axotomy with a peak cell loss at day 10.

The neuro protective effects of deprenylin motoneuron of spinal cord after axotomy peripheral nerve such as sciatic is reported, it is a mono amino axidase type-B (MAO-B) inhibitor. The neuron function is the release of neurotransmitters from pre-synaptic vesicle to synaptic cleft. One of the neurotransmitter is acetylcholine which is synthesized by chorine acetyltransferase (ChAT) and is used as a marker for function.Synaptophysin is one of synaptic vesicle protein and is used as a marker for neurotransmitter.The aim of this research is to study the effect of deprenyl (2.5mg/kg) injection on synaptophysin and ChAT immunoreactivity. Intra peritoneal injection was done following axotomy and continued for 21 days, they perfuse with paraformaldehhyde (4%) and spinal cord segment L4-L6 processed for immuno-histochemistry.The results showed that deprenyl (treated) axotomized had higher ChAT and synaptophysin expression as compared with those untreated axotomized.