DISSOCIATION OF MICROGLIAL ACTIVATION AND NEUROPATHIC PAIN BEHAVIORS FOLLOWING PERIPHERAL-NERVE INJURY IN THE RAT

Peripheral nerve injury commonly leads to neuropathic pain states fost ered, in part, by neuroimmunologic events. We used two models of neuro pathic pain (L5 spinal nerve cryoneurolysis (SPCN) and chronic constri ction injury (CCI)) to assess the role of spinal glial activation resp onses in producing pain behaviors. Scoring of glial responses subjecti vely encompassed changes in cell morphology, cell density and intensit y of immunoreactivity with specific activation markers (OX-42 and anti -glial fibrillary acidic protein (GFAP) for microglia and astrocytes, respectively). Glial responses were compared with tactile sensitivity (mechanical allodynia) at 1, 3 or 10 days following SPCN and with ther mal hyperalgesia at 10 days in the CCI group. Neuropathic pain behavio rs preceded and did not closely correlate with microglial responses in either model. Perineural application of bupivacaine prior to SPCN pre vented spinal microglial responses but not pain behaviors. Spinal astr ocytic responses to SPCN were early, robust and not altered by bupivac aine. The current findings support the use of bupivacaine as a tool to suppress microglial activation and challenge the putative role of mic roglia in initiating or potentiating pain behaviors which result from nerve injury. (C) 1997 Elsevier Science B.V.