Consistent with a crucial role for PNA as a major driver of these PCOS-like traits, protracted changes in GnRH neuronal morphology (increased dendritic spine density) and increased excitatory (GABAergic) appositions onto GnRH neurons in adult PAMH offspring have been reported (107), closely mimicking the aberrant neurocircuitry of PNA mice (93, 95, 97) and further reinforcing the notion of hypothalamic GABAergic activation as a programmed driver of LH hypersecretion. This evidence concerns the gene PLOD1 and polycystic ovary syndrome.