DISSERTATION RESEARCH: Neuroendocrine Mechanisms of Seasonal Aggression in Female Siberian Hamsters (Phodopus sungorus)

Indiana University, Bloomington IN

Investigators

Abstract

Aggression is a widespread naturally-occurring behavior serving a range of adaptive functions including access to mates and resources. Testosterone produced by the gonads is frequently associated with high levels of aggression. However, in seasonal breeding animals aggression can be both intense and widespread during the non-breeding season when testosterone levels are undetectable. This means that aggression is regulated by more than one mechanism and there is little understanding of how non-breeding aggression is regulated. This research seeks to understand the physiological mechanisms that underlie seasonal variation of aggression using female Siberian hamsters as a model. This work is highly integrative and unlike most other studies that examine single factors it will consider many relevant endocrine parameters and their interactions to understand how the brain and hormones function to control seasonal aggression in females. These studies will provide important insights into the physiological mechanisms mediating aggression, and social behavior more broadly. Additionally, this proposal will allow for the continued mentorship of undergraduates and high school students in research directly related to this work. Communication of these research findings will include public lectures and scientific conferences, and journal articles, as well as specialized regional symposia and organizations focused on the advancement of underrepresented minorities in the sciences. The researchers' data so far show that melatonin, the hormonal signal encoding photoperiod, drives seasonal changes in aggression, and further that adrenal hormones, such as DHEA, rather than gonadal hormones, may indirectly regulate aggression via conversion to active androgens or estrogens during periods when animals are non-reproductive. To examine seasonal switching from a gonadal to adrenal source of hormone, the proposed research tests the hypotheses that DHEA mediates non-breeding season aggression and that melatonin regulates DHEA release and its conversion to active hormones, which can then act on neural receptors. Specific Aim 1 will link seasonal changes in aggression and seasonal melatonin cues to neural receptor profiles (androgen and estrogen receptors) as well as a converting enzyme (aromatase, the enzyme that converts T to estradiol), via immunocytochemistry. Specific Aim 2 will determine whether changes in DHEA levels predict aggression among individuals across seasons by challenging animals in different photoperiods with ACTH, and assessing DHEA release. Lastly, Specific Aim 3 will test the hypothesis that short-day increases in melatonin mediate seasonal changes in DHEA by isolating the adrenal gland from other organs responsible for DHEA release and by using an in vitro bioassay to address localized action of melatonin on this organ and its subsequent production of DHEA. Collectively, the proposed work takes a whole organism approach and examines direct hormonal action on multiple tissues to determine the mechanisms underlying seasonal aggression in female hamsters using multiple levels of analysis. To facilitate proper storage and access of data, manuscripts will be published in open-access format, when possible, and on the lab website. Presentations will be made at international and national conferences, as well as in local venues to lay audiences, including high schools. Following processing of samples for the primary project, samples will be archived, and made accessible for collaborations from interested parties. Lastly, the PI will work with Indiana University Information Technology Services to archive data on the Research Data Complex (RDC), a dedicated server for hosting databases.