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

• Main Authors: Lammertsma Adriaan A, Huisman Marc C, Boellaard Ronald, Rozemuller Annemieke, van Berckel Bart NM, Foster Dingley Jessica C, Folkersma Hedy, Vandertop W Peter, Molthoff Carla FM
• Format: Article
• Language: English
• Published: BMC 2011-06-01
• Series: Journal of Neuroinflammation
• Online Access: http://www.jneuroinflammation.com/content/8/1/67

<p>Abstract</p> <p>Background</p> <p>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.</p> <p>Procedures</p> <p>Sequential dynamic <it>(R)</it>-[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.</p> <p>Results</p> <p>Ten days after TBI, <it>(R)</it>-[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.</p> <p>Conclusions</p> <p>Increased cerebral uptake of <it>(R)</it>-[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.</p>