Evidence map›Paper›PMID 26934298›Full record

ArticleEndocrinology2016

BPA Directly Decreases GnRH Neuronal Activity via Noncanonical Pathway.

Ulrike Klenke, Stephanie Constantin, Susan Wray

Open access · greenAbstract read
In one paragraph

Article in Endocrinology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
3.5field-weighted citation impact, top 9% 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

21 citing papers in PubMed, 44 citations in OpenAlex.

  1. Article
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  7. Article
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  11. Review
  12. Review
  13. Bisphenol A Activates Calcium Influx in Immortalized GnRH Neurons.International journal of molecular sciences · 2019
    Article
  14. Neuro-toxic and Reproductive Effects of BPA.Current neuropharmacology · 2019
    Review
  15. Review
  16. Perinatal BPA exposure and reproductive axis function in CD-1 mice.Reproductive toxicology (Elmsford, N.Y.) · 2018
    Article
  17. Article
  18. Article
  19. Review
  20. Review
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 2 institutions in 1 country.

Ulrike KlenkeCellular and Developmental Neurobiology Section (U.K., S.C., S.W.), National Institute of Neurological Disorders and Stroke/National Institutes of Health, Bethesda, Maryland 20892-3703.
Stephanie ConstantinCellular and Developmental Neurobiology Section (U.K., S.C., S.W.), National Institute of Neurological Disorders and Stroke/National Institutes of Health, Bethesda, Maryland 20892-3703.
Susan WrayCellular and Developmental Neurobiology Section (U.K., S.C., S.W.), National Institute of Neurological Disorders and Stroke/National Institutes of Health, Bethesda, Maryland 20892-3703.
National Institutes of Health · USNational Institute of Neurological Disorders and Stroke · US

Funding

Development And Regulation Of The Luteinizing Hormone Releasing Hormone SystemZIANS002824 · NINDS · NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE · PI WRAY, SUSAN · 2009 to 2025
$41.2M
Intramural NIH HHS ZIA NS002824
6 · The paper itself

Abstract

Peripheral feedback of gonadal estrogen to the hypothalamus is critical for reproduction. Bisphenol A (BPA), an environmental pollutant with estrogenic actions, can disrupt this feedback and lead to infertility in both humans and animals. GnRH neurons are essential for reproduction, serving as an important link between brain, pituitary, and gonads. Because GnRH neurons express several receptors that bind estrogen, they are potential targets for endocrine disruptors. However, to date, direct effects of BPA on GnRH neurons have not been shown. This study investigated the effects of BPA on GnRH neuronal activity using an explant model in which large numbers of primary GnRH neurons are maintained and express many of the receptors found in vivo. Because oscillations in intracellular calcium have been shown to correlate with electrical activity in GnRH neurons, calcium imaging was used to assay the effects of BPA. Exposure to 50μM BPA significantly decreased GnRH calcium activity. Blockage of γ-aminobutyric acid ergic and glutamatergic input did not abrogate the inhibitory BPA effect, suggesting direct regulation of GnRH neurons by BPA. In addition to estrogen receptor-β, single-cell RT-PCR analysis confirmed that GnRH neurons express G protein-coupled receptor 30 (G protein-coupled estrogen receptor 1) and estrogen-related receptor-γ, all potential targets for BPA. Perturbation studies of the signaling pathway revealed that the BPA-mediated inhibition of GnRH neuronal activity occurred independent of estrogen receptors, GPER, or estrogen-related receptor-γ, via a noncanonical pathway. These results provide the first evidence of a direct effect of BPA on GnRH neurons.

Indexed as

AnimalsBenzhydryl CompoundsBisphenol A CompoundsCalciumCalcium SignalingEndocrine DisruptorsEstradiolGonadotropin-Releasing HormoneMiceNeuronsPhenolsReceptors, EstrogenReproductionSignal TransductionBenzhydryl Compoundsbisphenol ABisphenol A CompoundsCalciumEndocrine DisruptorsEstradiolGonadotropin-Releasing HormonePhenolsReceptors, Estrogen

Identifiers

PMID26934298
PMCPMC4870872
OpenAlexW2314711281

What OpenQuestion holds

Textmetadata
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.