Thus far, our lab has mainly focused on how gonadal and adrenal steroidogenesis vary seasonally to influence aggressive behavior. However, because seasonal shifts in social behavior are ultimately determined by local changes in steroid synthesis, metabolism, and signaling mechanisms within the brain, it is important to examine how these processes differ between brain regions and across seasonal phenotypes. In a recent study, our group showed that female hamsters housed in short-day photoperiods (SDs, characteristic of non-breeding season) increase the abundance of estrogen receptor α (ERα) in brain nuclei of the social behavior network that are associated with aggressive, but not reproductive behaviors. While these data suggest that localized variation in neural ERα abundance mediates seasonal changes in aggression, the concentrations of androgens and estrogens in these regions, which are a critical component of hormonal signaling, have yet to be determined.
Studies in seasonally-breeding animals suggest a few potential neuroendocrine pathways by which androgens and estrogens could act on neural circuits to elevate aggression during the non-breeding season. These mechanisms include uptake of circulating hormone precursors [e.g., dehydroepiandrosterone (DHEA)] and local conversion to bioactive steroids, such as testosterone and estradiol; and/or neurosteroid synthesis de novo from cholesterol in regions that possess the appropriate steroidogenic enzymes (reviewed in Munley et al., 2018). The goals of this study are to determine: 1) whether seasonal changes in melatonin signaling facilitate region-specific changes in neural hormone synthesis, and 2) whether these local shifts in hormone levels are associated with increased aggression during the non-breeding season.