Nearly one in ten New Zealand women suffer from polycystic ovarian syndrome (PCOS), which is the leading cause of female infertility worldwide. Patients with PCOS often present with both reproductive and metabolic symptoms and have a higher incidence of diabetes, atherosclerosis and uterine cancer. PCOS, therefore, represents a major health and cost burden to the people of New Zealand. Although the syndrome's aetiology is not clear, prenatal exposure to androgens is strongly implicated. While its name indicates an ovarian disorder, we hypothesise that prenatal androgen exposure causes PCOS via actions on the brain centres that regulate reproductive function. We propose to combine transgenic and molecular approaches with classical neuroendocrine techniques to advance our limited knowledge of the neuroendocrine pathophysiology of PCOS in a well-established mouse model of PCOS. By identifying and understanding the central defects that result from prenatal androgen exposure, we will generate new knowledge to guide future development of therapeutic and preventative strategies for PCOS.