Doctor of Philosophy (PhD)


Comparative Biomedical Sciences

Document Type



Post-traumatic stress disorder (PTSD) is associated with elevated allostatic load, nearly double the risk for metabolic syndrome, reduced hippocampal volume, and contextual memory processing deficits. Emerging evidence suggests that these stress effects may predispose individuals to the development of PTSD, and there is a known relationship between chronic stress and metabolic dysfunction. In this work, we utilized two rat models of PTSD to explore these connections. We used an acute predator odor stressor to investigate the relationship between PTSD-like behaviors and mitochondrial dysfunction in the hippocampus of rats, and we observed that conditioned place avoidance was associated with reduced mitochondrial spare capacity and ROS production. In a separate multiple stressor + chronic psychosocial stress model, we observed increased cholesterol, triglycerides, and ROS production, fundamental allostatic load factors, in the hippocampus. In the same model, we also tested an experimental 5-HT2A agonist and known psychoplastogen and observed that it reduced ROS production in the cortex and hippocampus and normalized gene expression overlapping with human PTSD. Here, we show an association between mitochondrial dysfunction in the brain, the development of PTSD-like behaviors, and the induction of known allostatic load factors in the rat hippocampus after predator exposure + chronic psychosocial stress. Together these data support emerging models that suggest metabolic and allostatic characteristics of PTSD are related to functional changes in the hippocampus.



Committee Chair

Francis, Joseph