A recent mouse model suggests that high levels of a specific neurotransmitter may be a contributing factor linking traumatic brain injury (TBI) to post-traumatic epilepsy. According to the study, the damage to interneurons may disrupt neurotransmitter levels and contributes to the development of epilepsy following TBI.

During the study, David Cantu, PhD, and Chris Dulla, PhD, led a team that investigated the impact of TBI on the levels of the neurotransmitter gamma-aminobutyric acid (GABA) in the cerebral cortex.

Cantu, the first author of the study, explains in a news release from Tufts University, Health Sciences Campus, that “If we can preserve these important cells, we may be able to decrease the negative impacts of traumatic brain injury.” Cantu is a postdoctoral scholar at Tufts University School of Medicine, and member of the NIH-funded Institutional Research Center and Academic Development Awards (IRACDA) Program, Training in Education and Critical Research Skills, (TEACRS), the Sackler School of Graduate Biomedical Sciences at Tufts.

In the release, Naomi Rosenberg, PhD, dean of the Sacker School, vice dean for research at Tufts University School of Medicine, adds that the research helps increase the basic understanding of head trauma’s effects, “particularly for those severe single injuries that can and do happen in military service and contact sports.”

Senior author Chris Dulla, PhD, echoes Rosenburg’s sentiments, calling brain injury the “signature injury” of those in the military who served in Iraq and Afghanistan. “There are also many sports-related brain injuries. Fall-related injuries can develop the brain development of children, and upset the delicate brain systems among the elderly,” Dulla points out. Dulla is an assistant professor of neuroscience at Tufts University School of Medicine, and member of the Cell, Molecular & Developmental Biology, and Neuroscience program faculties, the Sackler School.

As stated in the release, the study is a key step in identifying the mechanistic relationship between TBI and post-traumatic epilepsy, according to Cantu.

“The study describes a potential outline of what happens after brain injury to trigger epilepsy, but the neurological causes of how TBI kills interneurons specifically after the initial injury are still unknown,” Cantu says.

Cantu concludes that developing an understanding of how brain injury disrupts normal brain function will help set the stage for scientists and physicians to develop new treatments and therapies to help individuals recover from post-traumatic epilepsy.

Source: Tufts University, Health Sciences Campus