James McGovern
Research Mentor: Joseph Wider
Mentor Department: Emergency Medicine, Medicine
Author(s): James McGovern, Joseph Wider, Reagan Speas, Sarita Raghunayakula
Session: Session 4 (1:00 PM – 1:50 PM)
Presentation Type: Poster 71
Abstract
Traumatic Brain Injury (TBI) is a neurological condition caused by blunt force trauma to the head that is characterized by cognitive and sensory dysfunction as well as emotional dysregulation. TBI remains one of the leading causes of death and disability with around 20 million cases a year. TBI has two injuries phases: primary, immediate damage caused by initial impact to the head, and secondary damage caused by molecular processes which includes ROS, energy dysregulation, and neuronal death. Previous research suggests that TBI is associated with excessive production of glutamate, an excitatory neurotransmitter, which leads to excitotoxicity. Excitotoxicity, excessive neuronal stimulation from excitatory neurotransmitters, causes a significant increase in energy demand for neurons. To meet energy demands, neuronal mitochondria attempt to produce ATP more rapidly, but doing so creates reactive oxygen species (ROS) as a byproduct at higher rates than normal. Excessive ROS production during the excitotoxic cascade leads to an increase in oxidative stress and neuronal cell death, which are major contributors to secondary injury cascades in TBI patients. Although glutamate is known to be associated with ROS, through what mechanisms glutamate impacts the production of ROS remains unclear. We hypothesize that glutamate will have a direct effect on the production of ROS through mitochondrial membrane (MM) hyperpolarization. To isolate the effect of glutamate, we used HT22 hippocampal neurons treated with glutamate to induce excitotoxicity. Live cell imaging was utilized to track ROS production through MitoSox and MM polarization through TMRE. We found that [TBD].
