Rw. Colburn et al., DISSOCIATION OF MICROGLIAL ACTIVATION AND NEUROPATHIC PAIN BEHAVIORS FOLLOWING PERIPHERAL-NERVE INJURY IN THE RAT, Journal of neuroimmunology, 79(2), 1997, pp. 163-175
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.