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By Macy Urig, Biological Sciences - Biomedical Sciences Concentration
Advisor: Nathan Evanson
Award: Excellence in Research Communication
Presentation ID: 106
Abstract: Not only does adolescence represent a critical period for development, but also a period of increased vulnerability to stress that is known to further increase in situations of chronic illness. One such chronic condition is traumatic brain injury (TBI), to which adolescents are particularly at risk. We hypothesized that chronic stress potentiates the neurodegenerative effects of TBI in a murine model. Using adolescent, male C57BL/6J mice, we induced a closed-head weight drop TBI, then subjected them to a chronic variable stress (CVS) paradigm (exposure to two daily stressors like cage tilt or wet bedding in an unpredictable pattern) for two weeks. Tissue collection occurred 2-, 5-, 20-, or 28- weeks post injury. We stained tissue with the neurodegeneration stain FlouroJade-B. Regions examined included the hypothalamic paraventricular nucleus (PVN), lateral geniculate nucleus (LGN), optic tract (OT), and superior colliculi (SC). We previously found evidence of persistent degeneration in vision-associated brain regions (LGN, OT, SC). However, we have not examined stress regions like the PVN, which serves as the major integrator of brain stress responses. In the PVN there were no significant differences between any of the groups. Degeneration was persistently increased in vision-associated regions up to 20 weeks. In contrast to our hypothesis, CVS had a protective effect when examined at 5 and 20 weeks with degeneration only present in the most severely injured region, the OT, by 28 weeks. Based on these findings, CVS after TBI is not detrimental, and may be protective against chronic brain degenerative injury after TBI.