Developmental exposure to bisphenol a (BPA) and ethinyl estradiol (EE) and effects on F1 parental care and F2 pup parameters in California mice (Peromyscus californicus)
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[ACCESS RESTRICTED TO THE UNIVERSITY OF MISSOURI AT AUTHOR'S REQUEST.] Environmental exposure during the perinatal period can promote health and disease in offspring, otherwise coined developmental origins of health and disease (DOHaD). Endocrine disruptors, such as bisphenol A (BPA, widely used in many household items) may induce profound DOHaD effects. The overarching goal of this work was to determine whether developmental exposure affected parental responses in the F1 generation and resulted in multigenerational effects in F2 offspring. In Chapter 2, consequences of developmental exposure to bisphenol A (BPA) or ethinyl estradiol (estrogen present in birth control pills, EE) were examined on later parental behaviors in California mice (Peromyscus californicus), which are monogamous and biparental. In Chapter 3, hypothalamus of BPA/EE and control parents were assessed to determine if gene expression changes in this brain region might also account for the compromised biparental care. In Chapter 4, ultrasonic and audible vocalization parameters were measured in F2 offspring derived from BPA/EE treated F1 parents and control parents to determine if pups tailored their communication depending on the exposure status of the parents. Current findings suggest that early exposure to BPA and EE disrupts later parental care responses in terms of nursing for females and time spent in the nest for both parents. Early treatment with BPA increased later adult expression of Esr1, Esr2, and Kiss1 in the hypothalamus of parenting California mice. In contrast, parents exposed to EE had reduced expression of Esr2. Finally, F2 pups derived from BPA or EE-exposed parents had had altered vocalization parameters. Enhancement of some aspects of F2 pup vocalizations in the BPA and EE groups could be reflective of the general F1 parental neglect. More research will be needed in the future to understand the mechanisms underlying effects observed in California mice with an ancestral history of BPA or EE exposure. Notably, current findings suggest BPA and EE can induce neurobehavioral effects in a rodent model with a similar social structure as humans, and thus, there is cause for concern that these EDCs may induce similar responses in humans.
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