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Research Mentor Name

Dr. Alana Conti

Research Mentor Email Address


Institution / Department

Department of Psychiatry and Behavioral Neurosciences, WSUSOM

Document Type

Research Abstract

Research Type


Level of Research



Traumatic brain injury (TBI) affects approximately 3 million people annually, with 70-80% presenting with pain symptoms. Research has shown that increased reactive oxygen species (ROS) and neuroinflammation play a role in both pain and TBI, but the roles and interaction of oxidative stress and inflammation in TBI-related pain remain unclear. The purpose of the current study is to establish molecular data supporting proposed alterations in ROS and neuroinflammation in a mouse model of TBI in pain-related brain regions and to quantify how levels of these mediators change over time. Once the time course is determined, it will allow for optimal use of various interventions such as antioxidant and anti-inflammatory treatment. Male (n=54) and female (n=27) mice ages 7-14 weeks were exposed to moderate level TBI or sham control surgery. Microdissections from pain-related brain regions, such as anterior cingulate cortex, amygdala, and periaqueductal gray were taken at 24 hours (n= 26 males, 9 females), 7 days (n= 13 males, 9 females), and 14 days (n= 15 males, 9 females) post-TBI and used to quantify ROS and inflammatory cytokine levels using a cell-based fluorescence assay and an enzyme-linked absorbance assay, respectively. Data demonstrated complex patterns of ROS and cytokine activation that varied with region and time post-injury. These data will provide information leading to optimal intervention strategies to mitigate the increased oxidative stress and neuroinflammation post-TBI.


Medicine and Health Sciences | Psychiatry and Psychology