In rats and mice, developmental exposure to bisphenol A (BPA) increases anxiety-like behavior and hyperactivity but evidence of impacts on social and exploratory behaviors is limited and mixed. Emerging epidemiological data suggest links between prenatal BPA exposure and altered affective behaviors in children, including hyperactivity, but potential mechanisms are unclear.  Impacts on oxytocin/vasopression pathways within the mesolimbic dopamine system have been proposed, but evidence for this is minimal. To address these data gaps, we orally exposed the prairie vole (Microtus ochrogaster), a more prosocial animal model than rats or mice, to three different doses of BPA (5 mg/kg bw/day, 50 mg/kg bw/day, or 50 mg/kg bw/day) or a vehicle over postnatal days (PNDs) 8-14, and assessed effects on a suite of behaviors and related neuroendocrine pathways.  Animals were subjected to open field, novel social, and a partner preference tests to access anxiety, exploratory behavior and sociality. Immunopositive tyrosine hydroxylase (TH; as a marker for dopaminergic neurons), oxytocin (OT) and vasopressin (AVP), neurons in the paraventricular nucleus of the hypothalamus (PVN), and TH neurons in the bed nucleus of the stria terminalis (BnST) were then quantified. Females exposed to 5 mg/kg bw/day BPA showed elevated levels of activity suggestive of hyperactivity. No major behavioral effects were observed in BPA-exposed males. Females neonatally exposed to 50 mg/kg bw BPA had more AVP-ir neurons in the anterior PVN and fewer OT-ir neurons in the posterior PVN.  BPA exposure eliminated sex differences in numbers of PVN TH neurons, at the two lowest doses, and sex revered it at the highest dose.  These data support the hypothesis that BPA alters exploratory behaviors potentially via disruption of OT/AVP and related pathways and are consistent with prior data from our lab, using rats, showing that BPA can impact brain organization and sexually dimorphic behaviors.