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

H. Folkersma, J.C. Foster Dingley, B.N.M. van Berckel, A. Rozemuller, R. Boellaard, M.C. Huisman, A.A. Lammertsma, W.P. Vandertop, C.F.M. Molthoff, J.M. Rozemuller

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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. Sequential dynamic (R)-[(11)C]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. Ten days after TBI, (R)-[(11)C]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. Increased cerebral uptake of (R)-[(11)C]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
Original languageEnglish
Article number67
Pages (from-to)67
Number of pages7
JournalJournal of neuroinflammation
Issue number1
Publication statusPublished - 2011

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