We have previously shown that male and female Siberian hamsters increase serum dehydroepiandrosterone (DHEA) and elevate aggressive behavior during the short-day (SD) photoperiods of the non-breeding season, despite gonadal regression and reduced levels of circulating testosterone (T) and estradiol. In addition, we found that in vitro melatonin administration elevates DHEA secretion from cultured adrenals in SD females, but not females housed in long-day (LD) photoperiods. While these findings suggest that hamsters elevate DHEA levels in circulation during SDs, it is unclear how melatonin acts locally to influence adrenal steroidogenesis and, ultimately, increase non-breeding aggression.
DHEA is synthesized in the adrenal cortex via the enzyme CYP17A1 and can be converted to more potent androgens, such as androstenedione (AE) and T, via the steroidogenic enzymes 3β-hydroxysteroid dehydrogenase (3β-HSD) and 17β-HSD, respectively. Thus, it is possible that melatonin mediates SD increases in aggression by upregulating local 3β-HSD activity. The goal of this study is to test whether melatonin signaling induces increased non-breeding aggression by upregulating 3β-HSD activity peripherally and/or centrally. Because 3β-HSD is responsible for catalyzing two separate steroidogenic reactions: the conversion of pregnenolone to progesterone and the conversion of DHEA to AE, this study will allow me to compare DHEA synthesis and metabolism both within and across tissues.