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

      , , , , ,
      Journal of Neuroimmunology
      Elsevier BV

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          Abstract

          Peripheral nerve injury commonly leads to neuropathic pain states fostered, in part, by neuroimmunologic events. We used two models of neuropathic pain (L5 spinal nerve cryoneurolysis (SPCN) and chronic constriction injury (CCI)) to assess the role of spinal glial activation responses in producing pain behaviors. Scoring of glial responses subjectively encompassed changes in cell morphology, cell density and intensity 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 thermal hyperalgesia at 10 days in the CCI group. Neuropathic pain behaviors preceded and did not closely correlate with microglial responses in either model. Perineural application of bupivacaine prior to SPCN prevented spinal microglial responses but not pain behaviors. Spinal astrocytic responses to SPCN were early, robust and not altered by bupivacaine. The current findings support the use of bupivacaine as a tool to suppress microglial activation and challenge the putative role of microglia in initiating or potentiating pain behaviors which result from nerve injury.

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          Author and article information

          Journal
          Journal of Neuroimmunology
          Journal of Neuroimmunology
          Elsevier BV
          01655728
          November 1997
          November 1997
          : 79
          : 2
          : 163-175
          Article
          10.1016/S0165-5728(97)00119-7
          9394789
          d6b5d93a-1f64-47a9-ad89-9a52246c4351
          © 1997

          https://www.elsevier.com/tdm/userlicense/1.0/

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