Traumatic brain injury (TBI) survivors experience long, term post-traumatic morbidities. In diffuse brain injured rats, a chronic sensory sensitivity to whisker stimulation models agitation in brain injury survivors and provides anatomical landmarks across the whisker-barrel circuit to evaluate traumatic neuropathology. As a consequence of TBI, acute and chronic microglial activation can contribute to degenerative and reparative events underlying post-traumatic morbidity. Here, we hypothesize that delayed microglial activation is concomitant with neuroplastic change after diffuse brain injury in the rat, by examining differential microglial activation states and neuroplasticity through gene and protein expression. Adult male, Sprague-Dawley rats were subjected to a single moderate midline fluid percussion (FPI) or sham injury. Microglial activation was determined by immunohistochemistry, receptor autoradiography, and quantitative real-time PCR in the primary somatosensory barrel field (S1 BF) and ventral posteromedial nucleus of the thalamus (VPM) at seven and 28 days following FPI. At seven days post-injury in both relays of the whisker circuit, classical activation (CD45) and acquired deactivation (TGFl, TGF R2) gene expression were elevated significantly above uninjured sham levels. Evidence for alternative activation (arginase I) was not observed. Daily anti-inflammatory ibuprofen administration (20 mg/kg, i . p.) significantly reduced evidence of classical activation, but had no effect on neuroplastic (GAP-43, synaptophysin) compared to saline vehicle. These data confirm concomitant classical activation and de-activation phenotypes of microglia after diffuse TBI, which are unlikely to impact injury-induced neuroplasticity that is typically associated with alternative microglial activation.

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