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- Title
Increased cerebral (R)-[(11)C]PK11195 uptake and glutamate release in a rat model of traumatic brain injury: a longitudinal pilot study.
- Authors
Folkersma, Hedy; Foster Dingley, Jessica C; van Berckel, Bart N M; Rozemuller, Annemieke; Boellaard, Ronald; Huisman, Marc C; Lammertsma, Adriaan A; Vandertop, W Peter; Molthoff, Carla F M
- Abstract
<bold>Background: </bold>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.<bold>Procedures: </bold>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.<bold>Results: </bold>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.<bold>Conclusions: </bold>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.
- Publication
Journal of Neuroinflammation, 2011, Vol 8, Issue 1, p67
- ISSN
1742-2094
- Publication type
journal article
- DOI
10.1186/1742-2094-8-67