Keywords: 
• bisphenol A /
• zebrafish /
• neurobehavior /
• neurotransmitter

Abstract: Toxic effects of bisphenol A (BPA) on organisms after exposure to environmentally relevant concentrations have received great concerns. In this study, embryos of zebrafish were exposed to series of concentrations (0, 1, 3, 10 and 30 mg·L^-1) of BPA, and changes in behavior and the underlying mechanisms were studied. Our results indicated that embryonic exposure to BPA caused a significant decrease in average swimming speed of larval zebrafish. Specifically, larval activity was significantly decreased in a continuous light period in groups of lower concentrations and in the next dark stimulating period in groups of higher concentrations after exposure to BPA. Transcriptional changes of htr1a and d1r indicated these receptors might be responsible for the effects observed above. HPLC analysis showed exposure to BPA increased the contents of dopamine and 5-HT at all treatments examined. Further results of expression of genes and proteins related to neurodevelopment of monoamine neurons (wnt1, lmx1a, lmx1a, nr4a2, syn2a) and rate limiting enzymes for synthesis of dopamine and 5-HT (th, tph1b) provided evidences for our hypothesis that BPA could accelerate neurogenesis and neural differentiation thus resulting in increased number of monoamine neurons. Generally, exposure to environmental relevant levels of BPA could affect neurodevelopment and result in behavioral changes in zebrafish larvae, indicating potential risks for wild animals and human due to BPA pollution.