Date of Presentation
5-5-2022 12:00 AM
College
School of Osteopathic Medicine
Poster Abstract
Traumatic brain injury (TBI) resulting from impact to the head can cause long lasting impairments of cognitive processes that lead to increased risk-taking behavior in clinical populations. Our laboratory has recently shown that female, but not age-matched male, rats increase preference for risky choices after multiple experimentally-induced mild TBI’s. Our overarching goal is to understand the neural mechanisms underlying TBI-induced increases in risk-taking behavior.
The prefrontal cortex (PFC) plays a prominent role in risk-based decision making. Sub[1]regions of the PFC include the medial PFC (mPFC), the orbitofrontal cortex (OFC), and the anterior cingulate cortex (ACC), and these sub[1]regions play specific roles in decision-making processes. Catecholamine neurotransmitter circuits, such as the dopamine (DA) and norepinephrine (NE) systems, project to the PFC and modulate the PFC’s control over executive functions. Previous studies have demonstrated that both dopamine (DA) and norepinephrine (NE) transmitter levels are increased in the PFC immediately following TBI, which is then followed by a persistent hypo-catecholaminergic state. These results suggest that an imbalance of catecholamine levels within the PFC may underlie aberrant decision-making behavior following TBI; however, it is not presently known what processes contribute to TBI-induced catecholamine imbalance.
Here we examined how levels of catecholamine neurotransmitter regulatory proteins responsible for packaging (VMAT2) and degrading (COMT and MAO) are altered to explain chronic decreases in DA and NE levels observed in the PFC following TBI. Age-matched adult male and female Long Evans rats (n=6-8) were exposed to either a single or a series of three closed head controlled cortical impact (CH-CCI) injuries over the course of one week. Rats were sacrificed and brain tissue (mPFC, OFC, and ACC) were collected and standard western blotting protocols were used to measure the levels of VMAT2, COMT, and MAO in each sub-region.
Keywords
Catecholamines, Traumatic Brain Injuries, Head Injury, Decision Making
Disciplines
Behavioral Neurobiology | Cell Biology | Laboratory and Basic Science Research | Medical Cell Biology | Medicine and Health Sciences | Nervous System | Neurosciences
Document Type
Poster
Included in
Behavioral Neurobiology Commons, Cell Biology Commons, Laboratory and Basic Science Research Commons, Medical Cell Biology Commons, Nervous System Commons, Neurosciences Commons
Examining Levels of Catecholamine Neurotransmitter Regulatory Proteins Within the Prefrontal Cortex of Rodents Following Traumatic Brain Injury
Traumatic brain injury (TBI) resulting from impact to the head can cause long lasting impairments of cognitive processes that lead to increased risk-taking behavior in clinical populations. Our laboratory has recently shown that female, but not age-matched male, rats increase preference for risky choices after multiple experimentally-induced mild TBI’s. Our overarching goal is to understand the neural mechanisms underlying TBI-induced increases in risk-taking behavior.
The prefrontal cortex (PFC) plays a prominent role in risk-based decision making. Sub[1]regions of the PFC include the medial PFC (mPFC), the orbitofrontal cortex (OFC), and the anterior cingulate cortex (ACC), and these sub[1]regions play specific roles in decision-making processes. Catecholamine neurotransmitter circuits, such as the dopamine (DA) and norepinephrine (NE) systems, project to the PFC and modulate the PFC’s control over executive functions. Previous studies have demonstrated that both dopamine (DA) and norepinephrine (NE) transmitter levels are increased in the PFC immediately following TBI, which is then followed by a persistent hypo-catecholaminergic state. These results suggest that an imbalance of catecholamine levels within the PFC may underlie aberrant decision-making behavior following TBI; however, it is not presently known what processes contribute to TBI-induced catecholamine imbalance.
Here we examined how levels of catecholamine neurotransmitter regulatory proteins responsible for packaging (VMAT2) and degrading (COMT and MAO) are altered to explain chronic decreases in DA and NE levels observed in the PFC following TBI. Age-matched adult male and female Long Evans rats (n=6-8) were exposed to either a single or a series of three closed head controlled cortical impact (CH-CCI) injuries over the course of one week. Rats were sacrificed and brain tissue (mPFC, OFC, and ACC) were collected and standard western blotting protocols were used to measure the levels of VMAT2, COMT, and MAO in each sub-region.