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