Increased cerebral (R)-[11C]PK11195 uptake and glutamate release in a rat model of traumatic brain injury: A longitudinal pilot study

Background: the aim of the present study was to investigate microglia activation over time following traumatic brain injury (tbi) and to relate these findings to glutamate release.procedures: sequential dynamic (r)-[11c]pk11195 pet scans were performed in rats 24 hours before (baseline),and one and ten days after tbi using controlled cortical impact,or a sham procedure. extracellular fluid (ecf) glutamate concentrations were measured using cerebral microdialysis. brains were processed for histopathology and (immuno)-histochemistry.results: ten days after tbi,(r)-[11c]pk11195 binding was significantly increased in tbi rats compared with both baseline values and sham controls (p < 0.05). ecf glutamate values were increased immediately after tbi (27.6 ± 14.0 μmol·l-1) as compared with the sham procedure (6.4 ± 3.6 μmol·l-1). significant differences were found between tbi and sham for ed-1,ox-6,gfap,perl's,and fluoro-jade b.conclusions: increased cerebral uptake of (r)-[11c]pk11195 ten days after tbi points to prolonged and ongoing activation of microglia. this activation followed a significant acute posttraumatic increase in ecf glutamate levels. © 2011 folkersma et al; licensee biomed central ltd.