Effects of bisphenol A (BPA) during neural development using Xenopus laevis as a model

Bisphenol A (BPA) is widely used in industry to produce polycarbonate plastics associated with everyday consumption. It has been suggested that it acts as an endocrine disruptor and is associated with developmental disorders. The amphibian Xenopus laevis is a widely used model for studying vertebrate development. Unlike the most used amniote models, its external development facilitates the study of vertebrate embryogenesis and its alterations by chemical and environmental agents from the outset. Studies conducted in this model showed that BPA causes malformations in tadpoles and is capable of inhibiting γ-secretase. However, there are no previous studies investigating BPA exposure during the early stages of development. We previously found that the treatment with 20 µM BPA of X. laevis embryos from the onset of gastrulation to the onset of neurulation delays neural plate folding and increases the density of differentiated neurons at neurula stage. Now, we performed a new treatment window: from the beginning of development to mid-blastula transition. We found that BPA impairs the specification of neural precursors (sox2 expression), neural plate, neural border and embryonic midline (hes 4). Also, our results indicate that BPA disrupts early steps, critical for cephalic development.