Mitochondrial function shows deficits post-injury in a controlled cortical impact mouse model
Abstract
A traumatic brain injury, a result of insult to the head, can induce seizure activity. This occurrence has come to be known as post-traumatic epilepsy (PTE), While traumatic brain injury and epilepsy are well-studied as separate conditions, truly little is known about the onset of PTE and the process of how epilepsy is initiated (also known as epileptogenesis). Due to mitochondria’s responsibility to produce energy, mitochondrial respiration has been shown to be affected by both traumatic brain injuries and epilepsy. Namely, oxidative phosphorylation is one example of altered mitochondrial function post-injury and post-seizure. In normal conditions, oxidative phosphorylation involves the movement of electrons through protein complexes to facilitate the eventual production of adenosine triphosphate (ATP). In stress conditions, this process is disrupted and mitochondrial deficits occur. Our lab and others have previously shown mitochondrial deficits in both post-injury and post-seizure models. This project focuses on examining these deficits in a controlled cortical impact adult mouse model. In doing this, we believe that we can reveal some of the processes of epileptogenesis within mitochondria and connect traumatic brain injury to seizure activity. 6 to 8-week-old male and female mice were impacted on the cerebral cortex and observed for seizure activity over a 6-month period. To determine the longitudinal role of mitochondria in epileptogenesis a subset of animals, acute changes in mitochondrial function were investigated at 2,24, and 72 hours as well as 7 days post injury. Cortical and hippocampal tissue were separated and ipsa- and contralateral mitochondrial function was assessed via respirometry. The results of these experiments imply that mitochondrial deficits can persist even chronically after the injury. Specifically, Complex I-led respiration tends to deplete while Complex II-led respiration appears to take over.
Start Time
15-4-2026 10:00 AM
End Time
15-4-2026 11:00 AM
Room Number
303
Presentation Type
Oral Presentation
Presentation Subtype
Grad/Comp Orals
Presentation Category
Health
Student Type
Graduate
Faculty Mentor
Chad Frasier
Mitochondrial function shows deficits post-injury in a controlled cortical impact mouse model
303
A traumatic brain injury, a result of insult to the head, can induce seizure activity. This occurrence has come to be known as post-traumatic epilepsy (PTE), While traumatic brain injury and epilepsy are well-studied as separate conditions, truly little is known about the onset of PTE and the process of how epilepsy is initiated (also known as epileptogenesis). Due to mitochondria’s responsibility to produce energy, mitochondrial respiration has been shown to be affected by both traumatic brain injuries and epilepsy. Namely, oxidative phosphorylation is one example of altered mitochondrial function post-injury and post-seizure. In normal conditions, oxidative phosphorylation involves the movement of electrons through protein complexes to facilitate the eventual production of adenosine triphosphate (ATP). In stress conditions, this process is disrupted and mitochondrial deficits occur. Our lab and others have previously shown mitochondrial deficits in both post-injury and post-seizure models. This project focuses on examining these deficits in a controlled cortical impact adult mouse model. In doing this, we believe that we can reveal some of the processes of epileptogenesis within mitochondria and connect traumatic brain injury to seizure activity. 6 to 8-week-old male and female mice were impacted on the cerebral cortex and observed for seizure activity over a 6-month period. To determine the longitudinal role of mitochondria in epileptogenesis a subset of animals, acute changes in mitochondrial function were investigated at 2,24, and 72 hours as well as 7 days post injury. Cortical and hippocampal tissue were separated and ipsa- and contralateral mitochondrial function was assessed via respirometry. The results of these experiments imply that mitochondrial deficits can persist even chronically after the injury. Specifically, Complex I-led respiration tends to deplete while Complex II-led respiration appears to take over.
