Children born to mothers with high urinary Bisphenol A (BPA) levels in the second trimester of gestation are hyperactive during childhood. However, the physiological insults incurred by prenatal exposure to endocrine disruptors like BPA remain poorly understood. Since neurogenesis (birth of neurons) is the main neurodevelopmental step occurring during the second trimester, we investigated whether prenatal BPA exposure could cause neurogenic perturbations within the hypothalamus, the brain region controlling all neuroendocrine signaling and physiologies. Given that neural progenitors are estrogen responsive, we reasoned that estrogenic BPA might influence the maintenance of the hypothalamic progenitor pool and affect timing of neuronal birth, perturbing establishment of key circuitry, and ultimately transducing into hyperactive behavior. By using the developmentally similar zebrafish as a model, we eliminated variables such as degree of placental transfer and maternal metabolic dynamics, which are observed in mammalian models. Significantly, exposure of embryonic zebrafish to a very low dose of BPA (0.0068uM) resulted in a 180% increase in hypothalamic neurogenesis with a concomitant hyperactive phenotype. Exposure to Bisphenol S (BPS), the main BPA analogue used in the production of BPA-free products, had similar neurogenic and locomotor effects. Mechanistically, our findings show Bisphenol-induced effects are not mediated by predicted estrogen receptor signaling pathways, but through a novel pathway contingent on androgen receptor-mediated increases in aromatase, the key enzyme for estrogen biosynthesis. Thus, by altering local estrogen synthesis, BPA/BPS may play a previously unappreciated role in inducing precocious cell cycle exit in hypothalamic progenitors. Our study is the first to mechanistically link prenatal BPA/BPS exposure with changes in brain development (neurogenesis) and altered behavior. Additionally, our results suggest that use of BPS, termed the ‘safe alternative’ of BPA-free products, is equally harmful to developing brains and calls for continued societal push to eliminate all Bisphenol analogues from consumer goods production.