Student: Sarah DeWolf*
Mentor: Rachel Bowman
Bisphenol-A (BPA), one of the most common environmental endocrine disruptors, is known to modulate estrogenic, androgenic, and anti-androgenic effects throughout the lifespan. The effects of BPA exposure during early organizational periods of development have been well documented. In order to better understand the mechanisms responsible for BPA’s effects on the adolescent brain, male and female rats were exposed to BPA during adolescence (postnatal days [PND] 42-49) and spine density in the medial prefrontal cortex (mPFC) and CA1 region of the hippocampus (CA1) assessed immediately on day 49 (7 weeks of age), and later in adulthood, at 11 weeks of age. In addition, because perinatal exposure to low-dose BPA alters corticosterone levels under both basal and stress conditions in adolescence, we examined whether adolescent BPA exposure altered serum corticosterone levels in response to a restraint stress challenge at 7 and 11 weeks of age, immediately prior to sacrifice. Stress dependent corticosterone responses were not altered by adolescent BPA exposure at either 7 or 11 weeks of age; however, BPA caused a significant decrease in spine density on apical and basal dendrites of pyramidal cells in both the mPFC and CA1. There was also a sex difference in spine density: females had greater spine density than males on basal dendrites of the mPFC and CA1. This sex difference was further augmented by both age and treatment, with overall results indicating that BPA-dependent decreases in spine density were more pronounced in males than females. These results are the first demonstrating that BPA, at levels below the current U.S.E.P.A. recommended safe daily limit, given during adolescence leads to enduring effects on neural morphology in adulthood. Given that humans are routinely exposed to low levels of BPA through a variety of sources, the decreased spine density reported in both male and female rats after BPA exposure warrants further investigation.