Classically, testosterone (T) was considered the principal regulator of aggression. However, recent studies in birds have found aggression and T uncoupled during the non-breeding season. Circulating testosterone comes with costs such as immunosuppression and energy expenditure. Instead, the pro-hormone, dehydroepiandrosterone (DHEA), is circulated and activated within the brain via conversion into oestradiol (E2), avoiding the costs associated with T. At present the site of DHEA synthesis is unknown. My thesis investigated the existence of an analogous pathway in non-breeding red squirrels (Tamiasciurus hudsonicus) with two studies: (a) a field study investigating the effects of E2 on aggression and (b) a laboratory study that attempted to determine the site of DHEA synthesis. I conclude that E2 regulates non-breeding aggression in red squirrels and that the adrenals are not the site of DHEA synthesis. My results suggest the existence of a mammalian analogue to the regulatory pathway found in birds.

Classically, testosterone (T) was considered the principal regulator of aggression. However, recent studies in birds have found aggression and T uncoupled during the non-breeding season. Circulating testosterone comes with costs such as immunosuppression and energy expenditure. Instead, the pro-hormone, dehydroepiandrosterone (DHEA), is circulated and activated within the brain via conversion into oestradiol (E2), avoiding the costs associated with T. At present the site of DHEA synthesis is unknown. My thesis investigated the existence of an analogous pathway in non-breeding red squirrels (Tamiasciurus hudsonicus) with two studies: (a) a field study investigating the effects of E2 on aggression and (b) a laboratory study that attempted to determine the site of DHEA synthesis. I conclude that E2 regulates non-breeding aggression in red squirrels and that the adrenals are not the site of DHEA synthesis. My results suggest the existence of a mammalian analogue to the regulatory pathway found in birds.