Very broadly, I am interested in the hypothalamic-pituitary-adrenal (HPA) axis and how it functions in both basal and post-stress scenarios. The HPA axis is a highly conserved neuroendocrine system and its hormonal end products, the glucocorticoids (e.g., cortisol and corticosterone), play an important role in many physiological and behavior processes (e.g., reproductive physiology and behavior, immune response and inflammation, energy metabolism and partitioning, memory and cognition, cardiac function, etc.). Additionally, many human diseases and psychopathologies (e.g., major depression, post-traumatic stress disorder, Alzheimer’s disease, Parkinson’s disease, anorexia nervosa) present with HPA axis dysregulation for unknown reasons and by unknown mechanisms.
My prior work at UCR focused on the role stress and the HPA axis play in the trade-off between current vs. future reproduction in the monogamous California mouse (Peromyscus californicus). Traditionally, stress is hypothesized to promote future reproduction at the cost of a current reproductive bout. In light of this, I addressed and the bi-directional interaction between the HPA axis and fatherhood by asking 1) does being a father alter HPA axis activity and reactivity, and 2) does stress and HPA axis activation alter paternal behavior. Additionally, because older individuals should theoretically invest more in reproduction as compared to younger individuals, I investigated the effect of age on HPA axis function.
In addition to trade-offs, I am also interested in how variation in HPA axis activity (basal function) and reactivity (post-stress response) impacts organisms. Traditionally, HPA axis function is assessed by measuring concentrations of hormones (e.g., cortisol, corticosterone) in the blood, saliva, urine or feces; however, glucocorticoid action and HPA axis function is modulated by binding proteins (e.g., CBG), intracellular enzymes (e.g., 11-beta HSD), receptor number, type and density, and by interactions with other hormones (e.g., the reproductive axis). Function of the HPA axis relies on multiple levels of regulation and feedback, and variation at any level can alter behavioral or physiological processes resulting in functional consequences for an organism. Along with Drs. Carr (biology) and Littlefield (psychology), I am currently investigating how allostatic load (a measure of cumulative stress) and polymorphisms in stress-associated genes impact cognitive function and onset of mild cognitive impairment (a precursor to Alzheimer’s disease) in a human population.