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By Kainat Lungani, Neuroscience
Advisor: Matthew Robson
Presentation ID: PM_B24
Abstract: Traumatic Brain Injury (TBI) is a leading cause of death, and disability in the United States accounting for more than 2.5 million emergency department visits yearly. TBI results in acute neuroinflammation as well as an increased likelihood of chronic neuropsychiatric disorders such as social withdrawal, depression, and anxiety. These behaviors have been linked to irregularities in serotonergic signaling in the Central Nervous System (CNS). However, little study has been done on possible changes in serotonergic signaling following TBI. The goal of the present study was to examine the relationship between blast-induced TBI and functional changes of CNS serotonin (5-HT) signaling. High-performance liquid chromatography (HPLC) revealed increased levels of 5-HT 10 days post-injury. Administration of 5-HTP; a precursor of serotonin, 10 days post-injury, indicated an increase in serotonin receptor sensitivity. DOI head twitch assays demonstrated increased 5HT-2A receptor sensitivity in TBI subjects as compared to sham controls. This potentiation was blocked by using a 5-HT2A antagonist, M100907. Further, we discovered decreased sociability 10 days following injury as demonstrated by Crawley Three Chamber sociability test. Collectively, these studies suggest increases in 5-HT2A receptor sensitivity, driven by increased serotonin levels in the raphe nucleus, contribute to abnormal neuropsychiatric behaviors 10 days following TBI.