Bisphenol A enhances kisspeptin neurons in anteroventral periventricular nucleus of female mice.

@article{Wang2014BisphenolAE,
  title={Bisphenol A enhances kisspeptin neurons in anteroventral periventricular nucleus of female mice.},
  author={Xiaoli Wang and Fei Chang and Yinyang Bai and Fang Chen and Jun Zhang and Ling Chen},
  journal={The Journal of endocrinology},
  year={2014},
  volume={221 2},
  pages={
          201-13
        }
}
Bisphenol-A (BPA), an environmental estrogen, adversely affects female reproductive health. However, the underlying mechanisms remain largely unknown. We found that oral administration (p.o.) of BPA (20  μg/kg) to adult female mice at proestrus, but not at estrus or diestrus, significantly increased the levels of plasma E₂, LH and FSH, and Gnrh mRNA within 6  h. The administration of BPA at proestrus, but not at diestrus, could elevate the levels of Kiss1 mRNA and kisspeptin protein in… 

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References

SHOWING 1-10 OF 127 REFERENCES
Kiss1 Neurons in the Forebrain as Central Processors for Generating the Preovulatory Luteinizing Hormone Surge
TLDR
Kisspeptins are neuropeptides encoded by the Kiss1 gene, which have been implicated in the neuroendocrine regulation of gonadotropin-releasing hormone (GnRH) secretion, and most Kiss1 neurons in the AVPV and Arc express estrogen receptor α mRNA, suggesting that E acts directly on these neurons.
Neonatal Exposure to Bisphenol A Alters Reproductive Parameters and Gonadotropin Releasing Hormone Signaling in Female Rats
TLDR
It is demonstrated for the first time that neonatal in vivo BPA permanently affects GnRH pulsatility and pituitary GnRH signaling.
Regulation of Kiss1 gene expression in the brain of the female mouse.
The Kiss1 gene encodes a family of neuropeptides called kisspeptins, which activate the receptor G protein-coupled receptor-54 and play a role in the neuroendocrine regulation of GnRH secretion. We
A role for kisspeptins in the regulation of gonadotropin secretion in the mouse.
TLDR
Kisspeptins are products of the KiSS-1 gene, which bind to a G protein-coupled receptor known as GPR54, and it is concluded that kisspeptin-GPR54 signaling may be part of the hypothalamus circuitry that governs the hypothalamic secretion of GnRH.
Involvement of anteroventral periventricular metastin/kisspeptin neurons in estrogen positive feedback action on luteinizing hormone release in female rats.
TLDR
It is demonstrated that preoptic area (POA) infusion of the anti-rat metastin/kisspeptin monoclonal antibody blocked the estrogen-induced LH surge, indicating that endogenous metastIn/kissPeptin released around the POA mediates the estrogen positive feedback effect on GnRH/LH release.
Regulation of Kiss1 and Dynorphin Gene Expression in the Murine Brain by Classical and Nonclassical Estrogen Receptor Pathways
TLDR
The effects of E2 on Kiss1 and Dyn mRNAs in the brains of mice bearing targeted alterations in the ERα signaling pathways were studied and it was found that stimulation of Kiss1 expression by E2 in the AVPV and inhibition of Dyn in the Arc required an ERE-dependent pathway, whereas the inhibition of Kiss 1 expression by NLP involved Ere-independent mechanisms.
Minireview: kisspeptin neurons as central processors in the regulation of gonadotropin-releasing hormone secretion.
TLDR
Observations demonstrate that kisspeptin-GPR54 signaling in the brain serves as an important conduit for controlling GnRH secretion in the developing and adult animal.
...
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3
4
5
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