Targeted Over-Expression of Glutamate Transporter 1 (GLT-1) Reduces Ischemic Brain Injury in a Rat Model of Stroke
2011

Targeted Over-Expression of Glutamate Transporter 1 Reduces Ischemic Brain Injury in a Rat Model of Stroke

Sample size: 16 publication 10 minutes Evidence: high

Author Information

Author(s): Harvey Brandon K., Airavaara Mikko, Hinzman Jason, Wires Emily M., Chiocco Matthew J., Howard Douglas B., Shen Hui, Gerhardt Greg, Hoffer Barry J., Wang Yun

Primary Institution: Intramural Research Program, National Institute on Drug Abuse, National Institutes of Health, Baltimore, Maryland, United States of America

Hypothesis

Does overexpression of the glutamate transporter GLT-1 reduce ischemic brain injury in a rat model of stroke?

Conclusion

Overexpression of GLT-1 significantly reduces ischemia-induced glutamate overflow, decreases cell death, and improves behavioral recovery in a rat model of stroke.

Supporting Evidence

  • Animals receiving AAV-GLT1 showed significant decreases in extracellular glutamate during the stroke.
  • A significant reduction in brain infarction was observed in the region of AAV-GLT1 injection.
  • Behavioral recovery was significantly improved in animals treated with AAV-GLT1 compared to controls.
  • TUNEL staining showed a significant reduction in cell death in the AAV-GLT1 group.

Takeaway

This study shows that giving a special treatment to increase a brain protein can help protect the brain from damage during a stroke and help the rats recover better.

Methodology

The study used a rat model where an adeno-associated viral vector expressing GLT-1 was injected before inducing a stroke, and various assessments were made on brain injury and recovery.

Limitations

The study was conducted in a rat model, which may not fully replicate human stroke conditions.

Participant Demographics

Adult male Fischer 344 and Sprague-Dawley rats were used.

Statistical Information

P-Value

<0.0001

Statistical Significance

p<0.05

Digital Object Identifier (DOI)

10.1371/journal.pone.0022135

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