Date of Presentation
5-2-2024 12:00 AM
College
Rowan-Virtua School of Osteopathic Medicine
Poster Abstract
Traumatic Brain Injury (TBI) is a common cause of death and disability in the United States, and it can occur due to varied reasons including motor vehicle accidents, gunshot wounds, and falls. Following TBIs, patients are often left with lifelong disabilities and cognitive problems that can lead to increased risk-taking behaviors. The main goal of my research was to understand the neural mechanisms that drive increased risk-taking behaviors due to TBIs. The specific areas of the brain I was interested in looking at were the medial prefrontal cortex (mPFC), orbitofrontal cortex (OFC), and/or anterior cingulate cortex (ACC) of the prefrontal cortex (PFC). Higher order executive functions that guide complex decision-making are regulated by the PFC and are most often impacted by TBIs. During my summer research fellowship, I studied noradrenergic innervation of the OFC by performing a fiber analysis study. In order to do this, my plan was to investigate the relative density of Dopamine beta-hydroxylase (DBH) fibers and norepinephrine transporter fibers (NET) within the OFC at week 1 versus week 4 post-experimental repetitive mild traumatic brain injury (rmTBI) or sham surgery of adult male and female Long Evans rats (n=4/group, 4 groups).
Keywords
Traumatic Brain Injury, Orbitofrontal cortex, Dopaminergic neurons, norepinephrine transporter fibers, risk-taking behaviors, prefrontal cortex, Risk-Taking
Disciplines
Behavioral Neurobiology | Behavior and Behavior Mechanisms | Medical Neurobiology | Medicine and Health Sciences | Neurology | Neuroscience and Neurobiology | Neurosciences | Physiological Processes | Trauma
Document Type
Poster
DOI
10.31986/issn.2689-0690_rdw.stratford_research_day.159_2024
Included in
Behavioral Neurobiology Commons, Behavior and Behavior Mechanisms Commons, Medical Neurobiology Commons, Neurology Commons, Neurosciences Commons, Physiological Processes Commons, Trauma Commons
The Impact of Traumatic Brain Injury on Noradrenergic Innervation of the Prefrontal Cortex
Traumatic Brain Injury (TBI) is a common cause of death and disability in the United States, and it can occur due to varied reasons including motor vehicle accidents, gunshot wounds, and falls. Following TBIs, patients are often left with lifelong disabilities and cognitive problems that can lead to increased risk-taking behaviors. The main goal of my research was to understand the neural mechanisms that drive increased risk-taking behaviors due to TBIs. The specific areas of the brain I was interested in looking at were the medial prefrontal cortex (mPFC), orbitofrontal cortex (OFC), and/or anterior cingulate cortex (ACC) of the prefrontal cortex (PFC). Higher order executive functions that guide complex decision-making are regulated by the PFC and are most often impacted by TBIs. During my summer research fellowship, I studied noradrenergic innervation of the OFC by performing a fiber analysis study. In order to do this, my plan was to investigate the relative density of Dopamine beta-hydroxylase (DBH) fibers and norepinephrine transporter fibers (NET) within the OFC at week 1 versus week 4 post-experimental repetitive mild traumatic brain injury (rmTBI) or sham surgery of adult male and female Long Evans rats (n=4/group, 4 groups).