BOSTON (March 11, 2014) Traumatic brain injury is a risk factor for epilepsy, though the relationship is not understood. A new study in mice, published in Cerebral Cortex, identifies increased levels of a specific neurotransmitter as a contributing factor connecting traumatic brain injury (TBI) to post-traumatic epilepsy. The findings suggest that damage to brain cells called interneurons disrupts neurotransmitter levels and plays a role in the development of epilepsy after a traumatic brain injury.
The research team, led by David Cantu and Chris Dulla, studied the effect of traumatic brain injury on the levels of the neurotransmitter gamma-aminobutyric acid (GABA) in the cerebral cortex, the portion of the brain associated with higher level functions such as information processing.
Normally, GABA inhibits neurotransmission in the brain, while its precursor, glutamate, stimulates neurotransmission. When the cortex is damaged by brain injury, however, the cells that create GABA, called interneurons, die. This leads to a toxic buildup of glutamate, which overstimulates brain activity. The study identifies this disrupted balance of GABA and glutamate as a factor in increased epileptic brain activity. The findings suggest that traumatic brain injuries cause damage to the interneurons responsible for creating GABA.
"If we can preserve these important cells, we may be able to decrease the negative impacts of traumatic brain injury," said first author David Cantu, Ph.D., a postdoctoral scholar at Tufts University School of Medicine, and member of the NIH-funded Institutional Research Career and Academic Development Awards (IRACDA) Program, Training in Education and Critical Research Skills (TEACRS), at the Sackler School of Graduate Biomedical Sciences at Tufts. "Interneurons play a critical role in preventing seizures from starting."
"This research increases our basic understanding of the effects of head trauma, particu
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Tufts University, Health Sciences Campus