Thesis Defense Seminar: "Effects of Chronic Stress on Avoidance Behavior in Estrogen Receptor Alpha Knockout (ERKO) Mice" - Victoria Appel

Graduate Program in Endocrinology and Animal Biosciences Thesis Defense Seminar: "Effects of Chronic Stress on Avoidance Behavior in Estrogen Receptor Alpha Knockout (ERKO) Mice"

Victoria Appel
MS Student
Graduate Program in Endocrinology and Animal Biosciences, Rutgers

Chronic stress has long been implicated in the development of mood disorders. Research has demonstrated that cisgender women are more susceptible than cisgender men to developing such conditions, and that these sex differences may, in part, be attributed to endocrine pathways. The mechanisms behind these pathways are progressively being elucidated, with focus on estrogen signaling. Using estrogen receptor alpha knockout (ERKO) mice, we examined the role of chronic stress on avoidance behavior across the sexes. Experimental mice were subjected to two different chronic stress paradigms. Chronic Variable Mild Stress (CVMS) exposes mice to physical stressors such as bedding alterations, forced swim, and cage tilting for 6 weeks. Chronic Social Instability Stress (CSIS) is a psycho-social stress model, where mice are placed with novel cage mates every three days for 7 weeks. Four behavior tests were used to assess avoidance behavior: the open field test, elevated plus maze, light-dark test, and novelty suppressed feeding. We conducted qPCR to assess the expression of stress-associated genes in the amygdala, paraventricular nucleus of the hypothalamus (PVH), and bed nucleus of the stria terminalis (BNST). We demonstrated both anxiogenic and anxiolytic effects of stress on behavior and gene expression in both sexes. When compared to our published work in wild-type mice, our findings suggest that the deletion of estrogen receptor alpha increases the susceptibility to chronic stress, which may also involve estrogen receptor beta or G-protein estrogen receptor 1 to elicit the observed avoidant responses. This work lends itself to further investigation into the intersection of chronic stress and steroid hormone signaling pathways.