Spinal microglia dependent BDNF as a key modulator in Thermal Hyperalgesia and spinal neuron apoptosis association

Background and Aim : Inflammatory pain is a major clinical problem in several disorder. Following peripheral inflammation, neuronal and microglia cells release inflammatory mediators and growth factors like BDNF. BDNF, is a neurotrophic factor with important biologic roles in neuronal survival and differentiation not only produced by neurons but also by microglia. On the other hand, functional and structural changes (apoptosis) of pain pathway due to release of various mediators, play a sophisticated role in development of chronic pain. In this study, we investigated the role of microglia dependent BDNF in the complex scenario of interaction between spinal neuron apoptosis and pain behavioral responses.Methods : Thermal hyperalgesia assessed by means of Radiant heat apparatus on 0, 7, 21 days of study after Persistent inflammation induction by CFA. Minocycline, as microglia inhibitor, was administered during the 21 days of study. Microglial activity, microglia dependent BDNF expression and apoptosis assessed by western blotting.Results : Our findings revealed that CFA-induced inflammation significantly increased hyperalgesia and spinal neuron apoptosis increased at first week after injection and decreased at the third week of study. Moreover, in parallel with these variations, Microglial activity and microglia dependent BDNF significantly increased during acute phase of CFA-induced inflammation.Conclusion : These results suggested that during CFA induced inflammatory pain model, thermal hyperalgesia increased due to increment of spinal neuron apoptosis. In our study, we showed that peripheral inflammatory pain can be effectively controlled by microglia dependent mediators specially, BDNF which required further investigations.

کلیدواژه ها:

Inflammatory pain ، Microglia ، Apoptosis ، Thermal hyperalgesia ، BDNF