Evidence map›Paper›PMID 31251963›Full record

ArticleNeurotoxicology2019

Perinatal bisphenol A (BPA) exposure alters brain oxytocin receptor (OTR) expression in a sex- and region- specific manner: A CLARITY-BPA consortium follow-up study.

Shannah K Witchey, Joelle Fuchs, Heather B Patisaul

Open access · greenAbstract read
In one paragraph

Article in Neurotoxicology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.6field-weighted citation impact, top 11% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

20 citing papers in PubMed, 40 citations in OpenAlex.

  1. Article
  2. Article
  3. Postnatal maternal care impacts hypothalamicbioRxiv : the preprint server for biology · 2025
    Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Shannah K WitcheyDepartment of Biological Sciences, NC State University, Raleigh, NC, 27695, United States.
Joelle FuchsDepartment of Biological Sciences, NC State University, Raleigh, NC, 27695, United States.
Heather B PatisaulDepartment of Biological Sciences, NC State University, Raleigh, NC, 27695, United States; Center for Human Health and the Environment, NC State University, Raleigh, NC, 27695, United States. Electronic address: hbpatisa@ncsu.edu.
North Carolina State University · US

Funding

Translational Research Support CoreP30ES025128 · NIEHS · NORTH CAROLINA STATE UNIVERSITY RALEIGH · PI Sue Fenton · 2015 to 2026
$18.3M
Neurobehavioral effects of Bisphenol A Across age and sexU01ES020929 · NIEHS · NORTH CAROLINA STATE UNIVERSITY RALEIGH · PI PATISAUL, HEATHER B, ROSENFELD, CHERYL SUSAN · 2011 to 2014
$775k
NIEHS NIH HHS P30 ES025128NIEHS NIH HHS U01 ES020929
6 · The paper itself

Abstract

Bisphenol A (BPA) is a well-characterized endocrine disrupting chemical (EDC) used in plastics, epoxy resins and other products. Neurodevelopmental effects of BPA exposure are a major concern with multiple rodent and human studies showing that early life BPA exposure may impact the developing brain and sexually dimorphic behaviors. The CLARITY-BPA (Consortium Linking Academic and Regulatory Insights on BPA Toxicity) program was established to assess multiple endpoints, including neural, across a wide dose range. Studies from our lab as part of (and prior to) CLARITY-BPA have shown that BPA disrupts estrogen receptor expression in the developing brain, and some evidence of oxytocin (OT) and oxytocin receptor (OTR) disruption in the hypothalamus and amygdala. While BPA disruption of steroid hormone function is well documented, less is known about its capacity to alter nonapeptide signals. In this CLARITY-BPA follow up study, we used remaining juvenile rat tissues to test the hypothesis that developmental BPA exposure affects OTR expression across the brain. Perinatal BPA exposure (2.5, 25, or 2500 μg/kg body weight (bw)/day) spanned gestation and lactation with dams gavaged from gestational day 6 until birth and then the offspring gavaged directly through weaning. Ethinyl estradiol (0.5 μg/kg bw/day) was used as a reference estrogen. Animals of both sexes were sacrificed as juveniles and OTR expression assessed by receptor binding. Our results demonstrate prenatal exposure to BPA can eliminate sex differences in OTR expression in three hypothalamic regions, and that male OTR expression may be more susceptible. Our data also identify a sub-region of the BNST with sexually dimorphic OTR expression not previously reported in juvenile rats that is also susceptible to BPA.

Indexed as

AnimalsAnimals, NewbornBenzhydryl CompoundsBisphenol A CompoundsBrain ChemistryEndocrine DisruptorsEthinyl EstradiolFemaleHypothalamusMaleOxytocinPhenolsPregnancyPrenatal Exposure Delayed EffectsRatsRats, Sprague-DawleyBenzhydryl Compoundsbisphenol ABisphenol A CompoundsEndocrine DisruptorsEthinyl EstradiolOxytocinoxytocin receptor, ratPhenolsReceptors, OxytocinBehaviorEndocrine disruptionEstrogenNeuroendocrineOxytocinSexual differentiation

Identifiers

PMID31251963
PMCPMC6750986
OpenAlexW2955860096

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.