Fasting increases aggression and differentially modulates local and systemic steroid levels in male zebra finches.

Aggression enables individuals to obtain and retain limited resources. Studies of the neuroendocrine regulation of aggression have focused on territorial and reproductive contexts. By contrast, little is understood concerning the neuroendocrine regulation of aggression over other resources, such as food. Here, we developed a paradigm to examine the role of steroids in food-related aggression. In groups of male zebra finches, a 6-hour fast decreased body mass and increased aggressive interactions among subjects that competed for a point source feeder. Fasting also dramatically altered circulating steroid levels by decreasing plasma testosterone but not estradiol (E2). By contrast, both plasma corticosterone and dehydroepiandrosterone (DHEA) concentrations were elevated with fasting. Interestingly, short-term access to food (15 minutes) after fasting normalized circulating steroid levels. Fasting increased corticosterone levels in a wide range of peripheral tissues but increased DHEA levels specifically in adrenal glands and liver; these effects were quickly normalized with refeeding. DHEA can be metabolized within specific brain regions to testosterone and E2, which promote the expression of aggression. We measured E2 in microdissected brain regions and found that fasting specifically increased local E2 levels in 3 regions: the periaqueductal gray, ventral tegmental area, and ventromedial nucleus of the hypothalamus. These regions are part of the vertebrate social behavior network and regulate the expression of aggression. Together, these data suggest that fasting stimulates secretion of DHEA from the adrenals and liver and subsequent conversion of DHEA to E2 within specific brain regions, to enable individuals to compete for limited food resources.