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 two treatment windows: i) from the start to the end of gastrulation and ii) during primary neurogenesis. We found that the genes involved in the neurogenesis cascade, like zic2, xmyt1 and n-tubulin; in the neural border/neural crest and those involved in the Notch pathway, like hes4 and dll1, change their expression differently between the windows treatments which strongly suggest that the BPA affects in a different way the developmental steps.