Gestational Exposure to Low Dose Bisphenol A Alters Social Behavior in Juvenile Mice

Abstract

Bisphenol A (BPA) is a man-made compound used to make polycarbonate plastics and epoxy resins; public health concerns have been fueled by findings that BPA exposure can reduce sex differences in brain and some behaviors. We asked if a low BPA dose, within the range measured in humans, ingested during pregnancy, would affect social behaviors in prepubertal mice. We noted sex differences in social interactions whereby females spent more time sitting side-by-side, while males engaged in more exploring and sitting alone. In addition BPA increased display of nose-to-nose contacts, play solicitations and approaches in both sexes. Interactions between sex and diet were found for self grooming, social interactions while sitting side-by-side and following the other mouse. In all these cases interactions were produced by differences between control and BPA females. We examined brains from embryos during late gestation to determine if gene expression differences might be correlated with some of the sexually dimorphic or BPA affected behaviors we observed. Because BPA treatments ended at birth we took the brains during embryogenesis to increase the probability of discovering BPA mediated effects. We also selected this embryonic age (E18.5) because it coincides with the onset of sexual differentiation of the brain. Interestingly, mRNA for the glutamate transporter, Slc1a1, was enhanced by exposure to BPA in female brains. Also we noted that BPA changed the expression of two of the three DNA methyltransferase genes, Dnmt1 and Dnmt3a. We propose that BPA affects DNA methylation of Sc1a1 during neural development. Sex differences in juvenile social interactions are affected by BPA and in particular this compound modifies behavior in females.

Loss of Hippocampal Oligodendrocytes Contributes to the Deficit of Contextual Fear Learning in Adult Rats Experiencing Early Bisphenol A Exposure

“…Continuous BPA exposure during this period has been shown to have profound effects on the brain and behavior [8], leading to altered learning and memory [9][10][11], hyperactivity [12], increased expression of anxiety, and aggression [11]. As such, early BPA exposure (EBE) has been linked to the development of some neuropsychiatric disorders such as autism, schizophrenia in the later life [12][13][14]. Studies in the past decade have demonstrated that many of its adverse effects on the brain are associated with the ability of BPA to disrupt estrogen receptor (ER) signaling in developing neurons leading to aberrant neuronal proliferation and differentiation [15].…”

Bisphenol A: Human exposure and neurobehavior

“…Results obtained in animals (mostly rodents) have shown that low doses of BPA 538 can disrupt the development of sexually dimorphic behaviors, including anxiety, social 539 interaction, aggression, and spatial memory, and that this disruption has distinct effects 540 on males and females (Adriani et al 2003;Gioiosa et al 2013;Palanza et al 2008;541 Rubin et al 2006;Rosenfeld et al 2012;Wolstenholme et al 2011a and2011b).…”

Bisfenol A Verilen Ratlarda Kuersetinin Kortizol ve Oksitosin Seviyeleri İle Oksitosin Reseptör Gen Ekspresyonu ve Uterus Morfometrisi Üzerine Etkileri

“…Brains from 18.5 days post-coitus male mice exposed to BPA express less oxytocin, oxytocin receptor gene expression, and vasopressin than control males [28] . In their study, expression of oxytocin receptor gene in brain of female mice was higher than control that is consistent with our finding in uterine.…”