Prenatal and neonatal exposure to bisphenol-A affects the morphine-induced rewarding effect and hyperlocomotion in mice.

Bisphenol-A (BPA), one of the most common environmental endocrine disrupters, has been extensively evaluated for toxicity and carcinogenicity. However, little is still known about its action on the CNS. Here we found that prenatal and neonatal exposure to BPA resulted in the enhancement of the rewarding effect and hyperlocomotion induced by morphine in mice. Under these conditions, no change in the G-protein activation by morphine and mu-opioid receptor expression in the lower midbrain was observed by prenatal and neonatal exposure to BPA. These results suggest that chronic exposure to BPA produces the supersensitivity of the morphine-induced rewarding effect and hyperlocomotion without direct changes in mu-opioid receptor function in the lower midbrain. The present data provide further evidence that prenatal and neonatal exposure to BPA can directly influence the development of the central dopaminergic system.