Bisphenol-A has been extensively evaluated for toxicity in a variety of tests as the most common environmental endocrine disruptors. In a previous study, we reported that exposure to bisphenol-A affects the development of the central dopaminergic system in the mouse limbic area. The present study was undertaken to investigate the relationship between the developmental toxicity of bisphenol-A and its exposure period. The exposure to bisphenol-A during either organogenesis or lactation, but not implantation and parturition, significantly enhanced the morphine-induced hyperlocomotion and rewarding effects. Furthermore, exposure to bisphenol-A during either organogenesis or lactation also produced an up-regulation of dopamine receptor function to activate G-protein in the mouse limbic forebrain. These results indicate that both organogenesis and lactation are more sensitive to the bisphenol-A-induced developmental neuronal toxicology than any other periods. In conclusion, the present data suggest that the organogenesis and lactation are the most important period to cause the alternation of dopaminergic system by bisphenol-A exposure in the mouse.
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