Article published by Medical Xpress
Traumatic brain injury is a leading cause of epilepsy, a chronic neurological disorder characterized by recurrent seizures that affects around 50 million people. A research team led by Bret Smith, professor and head of the Department of Biomedical Sciences, discovered specific neuronal processes that could help advance future preventative treatments for post-traumatic epilepsy.
The findings, published in The Journal of Neuroscience, show that activation of a subset of hippocampal neurons plays a key role in the changes that occur during the development of post-traumatic epilepsy and may be restorative.
“We know that trauma induces a cascade of events that can cause epilepsy,” says Smith. “We want to understand exactly what is occurring, and what the endpoints are, and then work backwards to try and stop epilepsy from developing after a brain injury.”
Neuroscience research in Smith’s lab focuses on two distinct programs; one is aimed at identifying neural changes related to the development of epilepsy, which the team has created leading models in the field to study, and the other examines how the brain is influenced by and contributes to hyperglycemia in diabetes.
For this study, Smith’s team looked at neurons called dentate granule cells, which continuously regenerate in areas of the brain that are crucial for learning and memory and are also commonly impacted by epilepsy. The team was surprised to find that when they were activated, the activity of other brain cells involved in epilepsy were inhibited. And that the cells that were formed just prior to a traumatic brain injury were much more likely to activate this circuit than those generated at other points in time.