Prenatal and neonatal exposure to low-dose of bisphenol-A enhance the morphine-induced hyperlocomotion and rewarding effect.

Bisphenol-A has been extensively evaluated for toxicity in a variety of tests as the most common environmental endocrine disruptors. In the previous study, we reported that prenatal and neonatal exposure to high-dose of bisphenol-A affects the development of central dopaminergic system in the mouse limbic area. The present study was then undertaken to investigate whether prenatal and neonatal exposure to lower dose of bisphenol-A could change the morphine-induced several pharmacological actions such as rewarding effect and hyperlocomotion in mice. Prenatal and neonatal exposure to low-dose of bisphenol-A enhanced the morphine-induced hyperlocomotion and rewarding effect. Additionally, the treatment with bisphenol-A produced an up-regulation of dopamine receptor function to activate G-protein in the mouse limbic forebrain, which is thought to play a critical role for hyperlocomotion and rewarding effects by drugs of abuse. These findings suggest that prenatal and neonatal exposure to low-dose of bisphenol-A can potentiate the central dopamine receptor-dependent neurotransmission, resulting in the supersensitivity of the morphine-induced hyperlocomotion and rewarding effects in the mouse.