Spinal Cord Injury
We have demonstrated extensively that SUR1/TRPM4 channels are upregulated following spinal cord injury (SCI) in rodents. Importantly, we have shown that pathological opening of the SUR1/TRPM4 channel mediates progressive hemorrhagic necrosis following SCI. Gene suppression of SUR1 blocks expression of functional TRPM4 channels and improves outcome in a spinal cord injury while eliminating secondary hemorrhage. When the channels are blocked by low-dose glibenclamide, it reduces lesion size and hemorrhage while improving neurobehavioral function.
- Spinal cord injury with unilateral versus bilateral primary hemorrhage--effects of glibenclamide.
- Comparative effects of glibenclamide and riluzole in a rat model of severe cervical spinal cord injury.
- Brief suppression of Abcc8 prevents autodestruction of spinal cord after trauma.
- De novo expression of Trpm4 initiates secondary hemorrhage in spinal cord injury.
- Endothelial sulfonylurea receptor 1-regulated NC Ca-ATP channels mediate progressive hemorrhagic necrosis following spinal cord injury.