作者: Sarah A. Johnson , William G. Spollen , Lindsey K. Manshack , Nathan J. Bivens , Scott A. Givan
DOI: 10.14814/PHY2.13133
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摘要: Abstract Bisphenol A (BPA) is an endocrine‐disrupting chemical (EDC) prevalent in many household items. Rodent models and human epidemiological studies have linked this to neurobehavior impairments. In California mice, developmental exposure BPA results sociosexual disorders at adulthood, including communication biparental care deficits, behaviors that are primarily regulated by the hypothalamus. Thus, we sought examine transcriptomic profile brain region of juvenile male female mice offspring exposed from periconception through lactation or ethinyl estradiol (EE, estrogen present birth control pills considered a positive for studies). Two weeks prior breeding, P 0 females were fed diet, diet supplemented with 50 mg BPA/kg feed weight 0.1 ppb EE, continued on diets lactation. At weaning, brains collected, hypothalamic RNA isolated, RNA‐seq analysis performed. Results indicate EE groups clustered separately controls leading unique set signature gene profiles. Kcnd3 was downregulated hypothalamus BPA‐ EE‐exposed females, whereas Tbl2 , Topors Kif3a Phactr2 upregulated these groups. Comparison transcripts differentially expressed revealed significant enrichment ontology terms associated microtubule‐based processes. Current show perinatal can result several alterations, those microtubule functions, mice. It remains be determined whether genes mediate BPA‐induced behavioral disruptions.