Over the past 30 years, the role of nitric oxide (NO) in biology has evolved from being recognized as an environmental pollutant to an endogenously produced substance involved in cell communication and signal transduction. NO can play a double role after injury of the PNS and CNS in accordance with its concentration, time of synthesis and type of NO-synthase participating in its production. Three isoforms of NOS have been reported – nNOS, eNOS and iNOS. They are reaching greatest expressions during the 2nd week, and the dynamic expression of individual isoforms is different. Since the protective or toxic effects of NO depend on its concentration, the cell type it is expressed, it is useful to apply donors or inhibitors of NOS in restrict time points after injury. It was established previously that increasing expression of iNOS results in death of neurons but nNOS plays neuroprotective role after PNS lesion. It is plausible that producing of NO with participation of nNOS provide the amount of NO which serves as a neuroprotective signal for neurons after injury. In this study, we studied the expression of caspase-3 in different population of DRG neurons using sciatic nerve transection with the purpose to explore the potential functional link between locally applied donor of NO and the ability of sensory neurons to survive. We observed better functional recovery in animals treated with L-arginine 7 days after nerve injury and decreasing of caspase-3 expression in DRGs L4-L5.
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