Journal
TOXICOLOGY RESEARCH
Volume 5, Issue 3, Pages 828-835Publisher
OXFORD UNIV PRESS
DOI: 10.1039/c5tx00449g
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Funding
- National Program on Key Basic Research Project of China (973 Program) [2012CB722401]
- National Natural Science Foundation of China [21437002]
- R&D Special Fund for Public Welfare Industry (Environment) [201309048]
- National Basic Research Development Program of China [2008CB418206]
- Fundamental Research Funds for the Central Universities, HUST [2012QN240, 2012TS072]
- Ministry of Education of China [20120142120017]
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Developmental exposure to bisphenol A (BPA) has been indicated to pose long-lasting effects on brain development and behaviors in adulthood. Previous studies have also shown that BPA may disrupt the epigenetic programming of genes in the brain. Here, we focused on investigating the effects of perinatal exposure to low-dose BPA on learning/memory function and emotional regulation, as well as the associated molecular events. Pregnant Sprague-Dawley (SD) rats were treated with control corn oil or BPA (40 mu g kg(-1) per day) throughout gestation and lactation. Morris water maze (MWM) and elevated plus maze (EPM) were used to evaluate learning/memory and anxiety-like behaviors at postnatal day (PND) 60 and 85 respectively. The expression level of mRNA for estrogen receptors (ER), ER alpha and ER beta, in the hippocampus and the serum corticosterone level were determined, as well as the DNA methylation status of the ERa gene promoter. Perinatal exposure to BPA prolonged the escape latency independent of gender, and decreased the percentage of time spent in the target quadrant when examined in the MWM task. While no substantial alteration was observed in the EPM test, the serum corticosterone level was altered in a gender-specific manner. BPA also decreased the expression of mRNA for ERa in the hippocampus, along with elevated DNA methylation of the ERa gene promoter. These results suggest that perinatal exposure to BPA impairs learning/memory function and elevated DNA methylation of the ERa gene in the hippocampus may be involved.
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