Virginia Research Day 2022

Graduate Student Research Biomedical

04 Changes In Glutamatergic Neurotransmission Following Impact Traumatic Brain Injury

Caiti-Erin Talty 1 ; Michelle Dickerson 2 ; Pamela VandeVord, PhD 2,3 Corresponding author: caitierin@vt.edu

1 Graduate Program in Translational Biology, Medicine & Health, Virginia Tech 2 Biomedical Engineering & Mechanics, Virginia Tech 3 Veterans Affairs Medical Center

cortices of sham-injured and CCI animals were analyzed for expression of GLAST. Significant downregulation of GLAST was observed in the prefrontal cortex (p=0.0014) of CCI animals when compared with shams. However, no significant expressional changes were observed in the motor cortex (p=0.1370). These findings support the hypothesis that glutamatergic dysfunction occurs following concussion and may target regions involved in the manifestation of depressive mood. Further investigation into expressional and functional changes in synaptic glutamate transporters and receptors in these and other corticolimbic structures is needed to evaluate the link between concussion and depression.

disorder (MDD) with similar downregulation of astrocytic glutamate transporters being observed. Changes in mood are commonly reported following a concussion and the development of mood disorders occurs in some individuals. The contribution of glutamatergic dysfunction to the development of mood alterations and disorders following concussion is not well understood and requires further investigation. The goal of this study was to evaluate changes in glutamate transporter expression in brain regions involved in depression, specifically the prefrontal and motor cortices. A closed-head controlled cortical impact (CCI) was used to model mild TBI in rats. Seven days post-injury, tissue was collected and immunohistochemistry was performed. The prefrontal and motor

Concussions represent a significant source of injury and disability in the United States with an estimated 300,000 sport-related concussions occurring each year in addition to those resulting from other recreational activities. Dysfunction of glutamatergic circuitry in the brain has been observed in animal models of traumatic brain injury (TBI) with several groups observing the downregulation of astrocytic glutamatergic transporters responsible for removing glutamate from the synapse. Specifically, GLAST and GLT-1 have been found to be downregulated following TBI, causing extracellular glutamate levels to increase, ultimately leading to dysfunctional neurotransmission. Glutamatergic synaptic transmission is also known to be compromised in mood disorders such as major depressive

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