Prenatal and lactational exposure to low-doses of bisphenol A alters brain monoamine concentration in adult mice.

Bisphenol A (BPA) is an endocrine-disrupting chemical, widely used in industry and dentistry. We have previously reported that BPA affects murine neocortical development by accelerating neuronal differentiation/migration resulting in abnormal neocortical architecture as well as apparent thalamocortical connections in adult mice brains. The aim of this study was to investigate whether or not prenatal and lactational BPA-exposure affects the level of neurotransmitters in mice brains. Pregnant mice were injected subcutaneously with 20μg/kg of BPA daily from embryonic day 0 (E0) until postnatal day 21 (P21). Control animals received a vehicle alone. The brains were removed and dissected into six regions for biochemical assays (n=7-8) at postnatal 3 weeks (P3W) and P10-15W. The concentration of the neurotransmitters was determined by high-performance liquid chromatography. The levels of dopamine and its metabolite significantly increased in the caudate/putamen and dorsal raphe nucleus, whereas serotonin and its metabolite increased in the caudate/putamen, dorsal raphe nucleus, thalamus and Substantia nigra in the BPA-exposure group at both P3W and/or P14-15W. These results suggested that prenatal and lactational BPA-exposure might perturb the neurotransmitter system in adult mice. Copyright 2010 Elsevier Ireland Ltd. All rights reserved.