Polycystic ovary syndrome (PCOS) has recently been renamed polyendocrine metabolic ovarian syndrome (PMOS) to more accurately reflect the breadth of endocrine, metabolic and reproductive systems affected in roughly 1 in 10 women. Reflecting the ‘polyendocrine’ component of the new name, neuroendocrine dysfunction is a hallmark feature of PMOS, including persistently elevated GnRH/LH pulses and impaired central sensitivity to estrogen and progesterone negative feedback. The research in our laboratory, largely employing mouse models of PMOS and transgenic neuroscience tools, is focused on understanding the specific brain mechanisms involved in PMOS neuroendocrine dysfunction. In this talk, I will discuss how early exposure to androgen excess shapes the developing female brain to program PMOS-like reproductive features in adulthood and the likely role of GABA neurons in the arcuate nucleus of the hypothalamus. I will also talk about our recent published and unpublished work investigating the critical brain circuits required for progesterone negative feedback regulation of the reproductive axis.