Functional changes in dopamine D3 receptors by prenatal and neonatal exposure to an endocrine disruptor bisphenol-A in mice.

Abstract

Bisphenol-A (BPA), one of the most common environmental endocrine disrupters, has been evaluated extensively for toxicity and carcinogenicity. However, little is still known about its action on the central nervous system (CNS). In the previous study, we found that prenatal and neonatal exposure to BPA markedly enhanced the rewarding effect induced by morphine. Here we found that prenatal and neonatal exposure to BPA resulted in the attenuation of dopamine D3 receptor-mediated G-protein activation by 7-OH-DPAT in the mouse limbic forebrain. This treatment also caused a significant decrease in the B(max) value of [(3)H]PD128907, a dopamine D3 receptor ligand, in this area. Under these conditions, no change in dopamine D3 receptor mRNA expression in the limbic forebrain and lower midbrain was observed by prenatal and neonatal exposure to BPA. The present data provide further evidence that prenatal and neonatal exposure to BPA leads to the reduction of functional dopamine D3 receptors without affecting the new synthesis of dopamine D3 receptors in the mouse limbic forebrain.