Increased cerebral (R)-[11C]PK11195 uptake and glutamate release in a rat model of traumatic brain injury: a longitudinal pilot study
2011

Increased Brain Activity After Injury in Rats

Sample size: 12 publication Evidence: moderate

Author Information

Author(s): Hedy Folkersma, Jessica C. Foster Dingley, Bart N.M. van Berckel, Annemieke Rozemuller, Ronald Boellaard, Marc C. Huisman, Adriaan A. Lammertsma, W. Peter Vandertop, Carla F.M. Molthoff

Primary Institution: VU University Medical Center

Hypothesis

The study aims to investigate microglia activation over time following traumatic brain injury (TBI) and relate these findings to glutamate release.

Conclusion

Increased cerebral uptake of (R)-[11C]PK11195 ten days after TBI points to prolonged and ongoing activation of microglia, following a significant acute posttraumatic increase in ECF glutamate levels.

Supporting Evidence

  • Ten days after TBI, (R)-[11C]PK11195 binding was significantly increased in TBI rats compared with both baseline values and sham controls.
  • ECF glutamate values were increased immediately after TBI compared to the sham procedure.
  • Significant differences were found between TBI and sham for various histological markers.

Takeaway

When rats get a brain injury, certain brain cells become more active over time, and there is a spike in a chemical called glutamate right after the injury.

Methodology

Rats underwent controlled cortical impact or sham procedures, followed by PET scans and microdialysis to measure glutamate levels.

Limitations

Some rats died during the study, which may affect the results.

Participant Demographics

Male Wistar rats, approximately 300 g.

Statistical Information

P-Value

p = 0.006

Statistical Significance

p<0.05

Digital Object Identifier (DOI)

10.1186/1742-2094-8-67

Want to read the original?

Access the complete publication on the publisher's website

View Original Publication