We have developed a novel traumatic brain injury (TBI) model, named the “Maryland Model,” where impact is applied to the anterior part of the cranium and an injury is caused by anterior/posterior plus sagittal rotation acceleration inside the brain.
Repeated frontal impact and cortical contusion models are also being utilized in our investigations.
We have demonstrated that SUR1 is upregulated in TBI, and plays a critical role in expanding hemorrhagic lesions, as well as cell death in the CNS.
In our model of cortical contusion, blockade of SUR1-regulated channels using low-dose glibenclamide largely eliminated progressive secondary hemorrhage, reduced necrotic lesion size, and preserved neurobehavioral function.
- Hemorrhagic progression of a contusion after traumatic brain injury: a review
- Rodent model of direct cranial blast injury
- Glibenclamide reduces hippocampal injury and preserves rapid spatial learning in a model of traumatic brain injury
- Novel model of frontal impact closed head injury in the rat
- Key role of sulfonylurea receptor 1 in progressive secondary hemorrhage after brain contusion