Bisphenol A (BPA) is a mass produced and wide-ranging endocrine disrupting chemical (EDC). We have demonstrated sex-specific developmental vulnerability to BPA supplied through the diet to pregnant polygynous deer mice, Peromyscus maniculatus bairdii, and their related monogamous cousins, California mice (P. californicus). Exposure of BPA at the upper dose tested resulted in circulating serum concentrations of BPA in the dams comparable to those found in pregnant women unknowingly exposed to this chemical. At sexual maturity, males but not females from these pregnancies had severely compromised spatial navigational abilities needed for these polygynous males to find dispersed mates in the wild and were rejected in mate- choice experiments. In California mice, no selection for a sex difference in this trait has evolved, but high levels of paternal investment and potential sexual receptivity of female California mice to intruding males has resulted in selection for male-mate guarding and territorial defense. Our work demonstrates that developmental exposure of these males to BPA compromises the latter behavior. We seek to understand how developmental exposure to BPA impacts maternal and paternal behaviors in California mice, as biparental deprivation might account for later adult offspring behavioral deficits. Other studies have determined that early exposure to BPA disrupts maternal behaviors, but no study has examined the effects that any EDC might have on paternal behaviors, even though neural hormones controlling parenting behaviors are well-conserved across species and sex. By using an outbred monogamous and biparental species, it will provide a better model for humans, who are considered monogamous and both parents generally rear the young. An automated system with an infrared camera has permitted 24 hour video documentation and prevented any confounding effects due to observer presence. Our preliminary results indicate control females bred to developmentally BPA-exposed F1 males nurse the offspring less than pups whose both parents are controls, suggesting that females perceive the offspring fathered by BPA-exposed males to be compromised and decrease their parental investment. These latter F2 offspring also receive less overall biparental care compared to control pups.
Specific aims are: 1) To assess parenting behaviors in P1 and F1 pair bonds of male and female California mice either acutely exposed or developmentally exposed to BPA/ EE through maternal diet, respectively, relative to unexposed controls. We shall also examine how these exposures, possibly through altered parental care, influence F1 and F2 pup parameters, which will include body weight and temperature, a number of developmental parameters, and ultrasonic vocalizations (USV). Additionally, we will measure such USV between the parents to determine if one partner can influence the parental care provided by the other. 2) Determine whether developmental exposure to BPA or EE in F1 male and female California mice affects mRNA and protein expression of peptide hormones and their cognate and steroid receptors governing parenting behaviors in the hypothalamus.

Public Health Relevance

A linkage has been shown in exposure of animal models and children to mass produced endocrine disrupting chemicals (EDC), including bisphenol A (BPA), and adverse behavioral effects. Poor parenting by both mothers and fathers may in turn compromise offspring neurodevelopment, cognition, and ability to compete. Current studies will employ a monogamous and biparental species, California mice (Peromyscus californicus), where both males and females rear the young, to determine whether developmental exposure to BPA affects later maternal and paternal behaviors and how parental alterations might impact post-natal pup development.

National Institute of Health (NIH)
National Institute of Environmental Health Sciences (NIEHS)
Exploratory/Developmental Grants (R21)
Project #
Application #
Study Section
Biobehavioral Regulation, Learning and Ethology Study Section (BRLE)
Program Officer
Hollander, Jonathan
Project Start
Project End
Budget Start
Budget End
Support Year
Fiscal Year
Total Cost
Indirect Cost
University of Missouri-Columbia
Veterinary Sciences
Schools of Veterinary Medicine
United States
Zip Code