Abstract
Androgen excess is a hallmark feature of polycystic ovary syndrome (PCOS), the most common form of anovulatory infertility. Clinical and preclinical evidence links developmental exposure to hyperandrogenism with programming the reproductive traits of PCOS. While the critical androgen targets remain to be determined, GABAergic neurons in the brain are postulated to be involved. GABA levels are elevated in the cerebrospinal fluid of PCOS patients, and both GABA transmission and innervation to gonadotrophin relseasing hormone (GnRH) neurons are elevated in prenatally androgenised models of PCOS. Here, we tested the hypothesis that androgen signalling in GABAergic neurons is critical in PCOS pathogenesis in a well-characterised, hyperandrogenic mouse model of PCOS.