Maternal and paternal origin differentially affect prosocial behavior and neural mechanisms in prairie voles.

This study tested the hypotheses that maternal and paternal effects differentially influence expression of their offspring's adult behavior and underlying neural mechanisms. We predicted that maternal influences would be greater than paternal influences on male offspring. We tested these hypotheses by cross-breeding two phenotypically-, behaviorally- and neuroanatomically-distinct populations of prairie voles (Microtus ochrogaster) from Illinois, which are highly prosocial, and Kansas, which are significantly less prosocial. Females from each population were crossed with males from the other population. F1 crosses were tested as adults to determine the effect of parentage on the expression of prosocial behavior and aggression, using a same-sex dyadic encounter and a heterosexual partner preference test, and for the expression of oxytocin (OT) and arginine vasopressin (AVP) in the paraventricular nucleus of the hypothalamus (PVN). As predicted, all significant differences in males, behavioral, OT and AVP immunoreactivity, were associated exclusively with maternal influences. There was a significant effect of treatment in the OT immunoreactivity of females. The effect of treatment in females' OT was associated with an interaction of population and sex, while same-sex social interactions differences were associated with population. Finally, in females, paternity influenced heterosexual bonds, with females with Illinois sires forming a partner preference. The results indicate that maternal influences dominate in male offspring, suggesting a parent-of-origin effect, while paternal effects are limited to selected prosocial behavioral expression in daughters.

Bisphenol A alters the cardiovascular response to hypoxia in Danio rerio embryos.

The purpose of this study was to determine if the cardiovascular response to hypoxia was altered by the presence of bisphenol A (BPA) in Danio rerio embryos. It was expected that BPA exposure would affect cardiovascular parameters during hypoxia more than normoxia due to an interaction between BPA and the hypoxia-inducible factor (HIF-1α) pathway. We demonstrate that BPA exposure has a minimal effect during normoxia but can severely affect the cardiovascular system during a hypoxic event. Cardiovascular response was measured in vivo using video microscopy and digital motion analysis. RBC density increased 35% in hypoxia alone but decreased 48% with addition of 0.25mg/L BPA. Tissue vascularization (% coverage) was unaffected by hypoxia alone but decreased 37% with addition of 0.25mg/L BPA. The diameter and RBC velocity of arteries were more sensitive than veins to BPA exposure during both normoxia and hypoxia. Arterial RBC velocity decreased 42% during normoxia and 52% during hypoxia with 1mg/L BPA. This decrease in velocity may in part be due to the 86% decrease in heart rate (ƒH) observed during co-exposure to hypoxia and 5mg/L BPA. While stroke volume (SV) was unaffected by treatment, cardiac output (Q) decreased by 69% with co-exposure. ƒH and Q were not affected by BPA exposure during normoxia. Development ultimately slowed by 146% and mortality rates were 95% during hypoxia when exposed to 5mg/L BPA. Our results show for the first time that BPA exposure alters the cardiovascular system during hypoxia more so than normoxia.