@article{baldwin_phillips_horman_arambula_rebuli_stapleton_patisaul_2017, title={Sex Specific Placental Accumulation and Behavioral Effects of Developmental Firemaster 550 Exposure in Wistar Rats}, volume={7}, ISSN={["2045-2322"]}, DOI={10.1038/s41598-017-07216-6}, abstractNote={Abstract}, journal={SCIENTIFIC REPORTS}, author={Baldwin, Kylie R. and Phillips, Allison L. and Horman, Brian and Arambula, Sheryl E. and Rebuli, Meghan E. and Stapleton, Heather M. and Patisaul, Heather B.}, year={2017}, month={Aug} }
 @article{rebuli_patisaul_2016, title={Assessment of sex specific endocrine disrupting effects in the prenatal and pre-pubertal rodent brain}, volume={160}, ISSN={["0960-0760"]}, DOI={10.1016/j.jsbmb.2015.08.021}, abstractNote={Brain sex differences are found in nearly every region of the brain and fundamental to sexually dimorphic behaviors as well as disorders of the brain and behavior. These differences are organized during gestation and early adolescence and detectable prior to puberty. Endocrine disrupting compounds (EDCs) interfere with hormone action and are thus prenatal exposure is hypothesized to disrupt the formation of sex differences, and contribute to the increased prevalence of pediatric neuropsychiatric disorders that present with a sex bias.Available evidence for the ability of EDCs to impact the emergence of brain sex differences in the rodent brain was reviewed here, with a focus on effects detected at or before puberty.The peer-reviewed literature was searched using PubMed, and all relevant papers published by January 31, 2015 were incorporated. Endpoints of interest included molecular cellular and neuroanatomical effects. Studies on behavioral endpoints were not included because numerous reviews of that literature are available.The hypothalamus was found to be particularly affected by estrogenic EDCs in a sex, time, and exposure dependent manner. The hippocampus also appears vulnerable to endocrine disruption by BPA and PCBs although there is little evidence from the pre-pubertal literature to make any conclusions about sex-specific effects. Gestational EDC exposure can alter fetal neurogenesis and gene expression throughout the brain including the cortex and cerebellum. The available literature primarily focuses on a few, well characterized EDCs, but little data is available for emerging contaminants.The developmental EDC exposure literature demonstrates evidence of altered neurodevelopment as early as fetal life, with sex specific effects observed throughout the brain even before puberty.}, journal={JOURNAL OF STEROID BIOCHEMISTRY AND MOLECULAR BIOLOGY}, author={Rebuli, Meghan E. and Patisaul, Heather B.}, year={2016}, month={Jun}, pages={148–159} }
 @article{hicks_sullivan_cao_sluzas_rebuli_patisaul_2016, title={Interaction of bisphenol A (BPA) and soy phytoestrogens on sexually dimorphic sociosexual behaviors in male and female rats}, volume={84}, ISSN={["1095-6867"]}, DOI={10.1016/j.yhbeh.2016.06.010}, abstractNote={Concerns have been raised regarding the potential for endocrine disrupting compounds (EDCs) to alter brain development and behavior. Developmental exposure to bisphenol A (BPA), a ubiquitous EDC, has been linked to altered sociosexual and mood-related behaviors in various animal models and children but effects are inconsistent across laboratories and animal models creating confusion about potential risk in humans. Exposure to endocrine active diets, such as soy, which is rich in phytoestrogens, may contribute to this variability. Here, we tested the individual and combined effects of low dose oral BPA and soy diet or the individual isoflavone genistein (GEN; administered as the aglycone genistin (GIN)) on rat sociosexual behaviors with the hypothesis that soy would obfuscate any BPA-related effects. Social and activity levels were unchanged by developmental exposure to BPA but soy diet had sex specific effects including suppressed novelty preference, and open field exploration in females. The data presented here reinforce that environmental factors, including anthropogenic chemical exposure and hormone active diets, can shape complex behaviors and even reverse expected sex differences.}, journal={HORMONES AND BEHAVIOR}, author={Hicks, Kimani D. and Sullivan, Alana W. and Cao, Jinyan and Sluzas, Emily and Rebuli, Meghan and Patisaul, Heather B.}, year={2016}, month={Aug}, pages={121–126} }
 @article{rebuli_gibson_rhodes_cushing_patisaul_2016, title={Sex differences in microglial colonization and vulnerabilities to endocrine disruption in the social brain}, volume={238}, ISSN={["1095-6840"]}, DOI={10.1016/j.ygcen.2016.04.018}, abstractNote={During development, microglia, the resident immune cells of the brain, play an important role in synaptic organization. Microglial colonization of the developing brain is sexually dimorphic in some regions, including nuclei critical for the coordination of social behavior, suggesting steroid hormones have an influencing role, particularly estrogen. By extension, microglial colonization may be vulnerable to endocrine disruption. Concerns have been raised regarding the potential for endocrine disrupting compounds (EDCs) to alter brain development and behavior. Developmental exposure to Bisphenol A (BPA), a ubiquitous EDC, has been associated with altered sociosexual and mood-related behaviors in various animal models and children. Through a comparison of the promiscuous Wistar rat (Rattus norvegicus) and the socially monogamous prairie vole (Microtus ochrogaster), we are the first to observe that developmental exposure to the synthetic estrogen ethinyl estradiol (EE) or BPA alters the sex-specific colonization of the hippocampus and amygdala by microglia.}, journal={GENERAL AND COMPARATIVE ENDOCRINOLOGY}, author={Rebuli, Meghan E. and Gibson, Paul and Rhodes, Cassie L. and Cushing, Bruce S. and Patisaul, Heather B.}, year={2016}, month={Nov}, pages={39–46} }
 @article{rebuli_camacho_adonay_reif_aylor_patisaul_2015, title={Impact of Low-Dose Oral Exposure to Bisphenol A (BPA) on Juvenile and Adult Rat Exploratory and Anxiety Behavior: A CLARITY-BPA Consortium Study}, volume={148}, ISSN={["1096-0929"]}, url={http://www.scopus.com/inward/record.url?eid=2-s2.0-84952932385&partnerID=MN8TOARS}, DOI={10.1093/toxsci/kfv163}, abstractNote={Bisphenol A (BPA) is a high volume production chemical and has been identified as an endocrine disruptor, prompting concern that developmental exposure could impact brain development and behavior. Rodent and human studies suggest that early life BPA exposure may result in an anxious, hyperactive phenotype but results are conflicting and data from studies using multiple doses below the no-observed-adverse-effect level are limited. To address this, the present studies were conducted as part of the CLARITY-BPA (Consortium Linking Academic and Regulatory Insights on BPA Toxicity) program. The impact of perinatal BPA exposure (2.5, 25, or 2500 µg/kg body weight (bw)/day) on behaviors related to anxiety and exploratory activity was assessed in juvenile (prepubertal) and adult NCTR Sprague-Dawley rats of both sexes. Ethinyl estradiol (0.5 µg/kg bw/day) was used as a reference estrogen. Exposure spanned gestation and lactation with dams gavaged from gestational day 6 until birth and then the offspring gavaged directly through weaning (n = 12/sex/group). Behavioral assessments included open field, elevated plus maze, and zero maze. Anticipated sex differences in behavior were statistically identified or suggested in most cases. No consistent effects of BPA were observed for any endpoint, in either sex, at either age compared to vehicle controls; however, significant differences between BPA-exposed and ethinyl estradiol-exposed groups were identified for some endpoints. Limitations of this study are discussed and include suboptimal statistical power and low concordance across behavioral tasks. These data do not indicate BPA-related effects on anxiety or exploratory activity in these developmentally exposed rats.}, number={2}, journal={TOXICOLOGICAL SCIENCES}, author={Rebuli, Meghan E. and Camacho, Luisa and Adonay, Maria E. and Reif, David M. and Aylor, David L. and Patisaul, Heather B.}, year={2015}, month={Dec}, pages={341–354} }
 @article{rebuli_cao_sluzas_delclos_camacho_lewis_vanlandingham_patisaul_2014, title={Investigation of the Effects of Subchronic Low Dose Oral Exposure to Bisphenol A (BPA) and Ethinyl Estradiol (EE) on Estrogen Receptor Expression in the Juvenile and Adult Female Rat Hypothalamus}, volume={140}, ISSN={["1096-0929"]}, DOI={10.1093/toxsci/kfu074}, abstractNote={Concerns have been raised regarding the long-term impacts of early life exposure to the ubiquitous environmental contaminant bisphenol A (BPA) on brain organization. Because BPA has been reported to affect estrogen signaling, and steroid hormones play a critical role in brain sexual differentiation, there is also concern that BPA exposure could alter neural sex differences. Here, we examine the impact of subchronic exposure from gestation to adulthood to oral doses of BPA below the current no-observed-adverse-effect level (NOAEL) of 5 mg/kg body weight (bw)/day on estrogen receptor (ESR) expression in sexually dimorphic brain regions of prepubertal and adult female rats. The dams were gavaged daily with vehicle (0.3% carboxymethylcellulose), 2.5, 25, 260, or 2700 μg BPA/kg bw/day, or 0.5 or 5.0 μg ethinyl estradiol (EE)/kg bw/day from gestational day 6 until labor began. Offspring were then gavaged directly from the day after birth until the day before scheduled sacrifice on postnatal days 21 or 90. Using in situ hybridization, one or more BPA doses produced significant decreases in Esr1 expression in the juvenile female rat anteroventral periventricular nucleus (AVPV) of the hypothalamus and significant decreases in Esr2 expression in the adult female rat AVPV and medial preoptic area (MPOA), relative to vehicle controls. BPA did not simply reproduce EE effects, indicating that BPA is not acting solely as an estrogen mimic. The possible consequences of long-term changes in hypothalamic ESR expression resulting from subchronic low dose BPA exposure on neuroendocrine effects are discussed and being addressed in ongoing, related work.}, number={1}, journal={TOXICOLOGICAL SCIENCES}, author={Rebuli, Meghan E. and Cao, Jinyan and Sluzas, Emily and Delclos, K. Barry and Camacho, Luisa and Lewis, Sherry M. and Vanlandingham, Michelle M. and Patisaul, Heather B.}, year={2014}, month={Jul}, pages={190–203} }
 @article{patisaul_sullivan_radford_walker_adewale_winnik_coughlin_buckley_gore_2012, title={Anxiogenic Effects of Developmental Bisphenol A Exposure Are Associated with Gene Expression Changes in the Juvenile Rat Amygdala and Mitigated by Soy}, volume={7}, ISSN={["1932-6203"]}, DOI={10.1371/journal.pone.0043890}, abstractNote={Early life exposure to Bisphenol A (BPA), a component of polycarbonate plastics and epoxy resins, alters sociosexual behavior in numerous species including humans. The present study focused on the ontogeny of these behavioral effects beginning in adolescence and assessed the underlying molecular changes in the amygdala. We also explored the mitigating potential of a soy-rich diet on these endpoints. Wistar rats were exposed to BPA via drinking water (1 mg/L) from gestation through puberty, and reared on a soy-based or soy-free diet. A group exposed to ethinyl estradiol (50 µg/L) and a soy-free diet was used as a positive estrogenic control. Animals were tested as juveniles or adults for anxiety-like and exploratory behavior. Assessment of serum BPA and genistein (GEN), a soy phytoestrogen, confirmed that internal dose was within a human-relevant range. BPA induced anxiogenic behavior in juveniles and loss of sexual dimorphisms in adult exploratory behavior, but only in the animals reared on the soy-free diet. Expression analysis revealed a suite of genes, including a subset known to mediate sociosexual behavior, associated with BPA-induced juvenile anxiety. Notably, expression of estrogen receptor beta (Esr2) and two melanocortin receptors (Mc3r, Mc4r) were downregulated. Collectively, these results show that behavioral impacts of BPA can manifest during adolescence, but wane in adulthood, and may be mitigated by diet. These data also reveal that, because ERβ and melanocortin receptors are crucial to their function, oxytocin/vasopressin signaling pathways, which have previously been linked to human affective disorders, may underlie these behavioral outcomes.}, number={9}, journal={PLOS ONE}, author={Patisaul, Heather B. and Sullivan, Alana W. and Radford, Meghan E. and Walker, Deena M. and Adewale, Heather B. and Winnik, Bozena and Coughlin, Janis L. and Buckley, Brian and Gore, Andrea C.}, year={2012}, month={Sep} }