Dissociation of microglial activation and neuropathic pain behaviors following peripheral nerve injury in the rat.

摘要: Peripheral nerve injury commonly leads to neuropathic pain states fostered, in part, by neuroimmunologic events. We used two models of (L5 spinal cryoneurolysis (SPCN) and chronic constriction (CCI)) assess the role glial activation responses producing behaviors. Scoring subjectively encompassed changes cell morphology, density intensity immunoreactivity with specific markers (OX-42 anti-glial fibrillary acidic protein (GFAP) for microglia astrocytes, respectively). Glial were compared tactile sensitivity (mechanical allodynia) at 1, 3 or 10 days following SPCN thermal hyperalgesia CCI group. Neuropathic behaviors preceded did not closely correlate microglial either model. Perineural application bupivacaine prior prevented but Spinal astrocytic early, robust altered bupivacaine. The current findings support use as a tool suppress challenge putative initiating potentiating which result from injury.