Peripheral inflammatory pain increases microglia activity and apoptotic cell death in the hippocampus

Background and Aim : Cognitive impairment is commonly associated with the pain experience. This impairment represents a major obstacle to daily activities and rehabilitation, especially in the chronic pain population. It has been suggested that inflammatory persistent pain led to microglia activation, but there is no evidence to learning and memory impairment. Therefore, the aim of the study is the Investigation of the relationship between microglial activity variation with apoptotic cell death, spatial memory during persistent peripheral inflammationMethods : Animals were randomly distributed to 3 groups, the groups were as including, first group as control group second group as CFA group (received 100 μL CFA) third group as CFA+Minocyclin group (received 100 μL CFA+40mg/kg/day minocycline). These groups also divided to 3 subgroups day 0(CFA0), 7(CFA7) and 21(CFA21) to assess different time points of study and each subgroup including 6 rats. Thermal hyperalgesia and the spatial memory was assessed using the radiant heat and Morris water maze respectively. To determine the potential mechanisms, hippocampal microglia activity was assessed by immunohistochemistry and apoptotic cell death of hippocampal neurons were measured using Western blot.Results : our results that CFA-induced inflammatory pain impaired spatial learning and memory associated with increase hippocampal microglia activity and apoptotic cell death in the hippocampus during first week of study. Also administration of Minocycline can effectively reduce pain-induced hippocampal microglia activity after CFA injection associated with the slower cell death rateConclusion : Therefore, we can suggest that peripheral inflammation lead to hippocampal microglia activation, which in turn impaired cognitive performance through neuron death in hippocampus.

کلیدواژه ها:

Microglia ، apoptosis ، pain ، inflammation