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Do fish feel pain? For over 50 years, this question has been the focus of multiple scientific careers and consumed countless hours of research, debate, and reflection. But a different [...]

Octopuses stand out among invertebrates for their complex behavior. They are capable of problem-solving, mimicking their surroundings using color changes that take place on a scale of seconds, outwitting predatory [...]

Bisphenol A (BPA) is an estrogenic endocrine disruptor widely used in the production of plastics. Increasing evidence indicates that in utero BPA exposure affects sexual differentiation and behavior; however, the mechanisms underlying these effects are unknown. We hypothesized that BPA may disrupt epigenetic programming of gene expression in the brain. Here, we provide evidence that maternal exposure during pregnancy to environmentally relevant doses of BPA (2, 20, and 200 μg/kg/d) in mice induces sex-specific, dose-dependent (linear and curvilinear), and brain region-specific changes in expression of genes encoding estrogen receptors (ERs; ERα and ERβ) and estrogen-related receptor-γ in juvenile offspring. Concomitantly, BPA altered mRNA levels of epigenetic regulators DNA methyltransferase (DNMT) 1 and DNMT3A in the juvenile cortex and hypothalamus, paralleling changes in estrogen-related receptors. Importantly, changes in ERa and DNMT expression in the cortex (males) and hypothalamus (females) were associated with DNA methylation changes in the ERa gene. BPA exposure induced persistent, largely sex-specific effects on social and anxiety-like behavior, leading to disruption of sexually dimorphic behaviors. Although postnatal maternal care was altered in mothers treated with BPA during pregnancy, the effects of in utero BPA were not found to be mediated by maternal care. However, our data suggest that increased maternal care may partially attenuate the effects of in utero BPA on DNA methylation. Overall, we demonstrate that low-dose prenatal BPA exposure induces lasting epigenetic disruption in the brain that possibly underlie enduring effects of BPA on brain function and behavior, especially regarding sexually dimorphic phenotypes. [ABSTRACT FROM AUTHOR]

Paternal environmental experiences are significant predictors of developmental outcomes in offspring and can occur even in the absence of paternal care. Although there has been a recent focus on the role of environmentally induced changes in the male germline in producing these effects, the potential mediating role of mothers has not been investigated. A role for mothers in the transmission of paternal effects has been well acknowledged in behavioral ecology, which predicts that females will dynamically adjust their reproductive investment in response to the qualities of their mate. In the present study, we show that a lifetime of socially enriched compared with impoverished housing conditions shifts anxiety-like behavior and gene expression of male mice. Females that mate with enriched-reared males exhibit increased levels of pup nursing and licking toward their offspring, which are associated with changes in gene expression within the maternal hypothalamus. Significantly, these changes in maternal behavior are correlated with the general levels of anxiety exhibited by their male mates. Further, we show that paternal environmental enrichment results in increased growth of their offspring. These results suggest that maternal-paternal interactions at mating may guide offspring development, with significant implications for the transgenerational transmission of paternal environmental experiences. [ABSTRACT FROM AUTHOR]