ZFIN ID: ZDB-PUB-110520-22
17alpha-Ethinylestradiol and nonylphenol affect the development of forebrain GnRH neurons through an estrogen receptors-dependent pathway
Vosges, M., Kah, O., Hinfray, N., Chadili, E., Le Page, Y., Combarnous, Y., Porcher, J.M., and Brion, F.
Date: 2012
Source: Reproductive toxicology (Elmsford, N.Y.)   33(2): 198-204 (Journal)
Registered Authors: Kah, Olivier
Keywords: gonadotropin-releasing hormone (GnRH), aromatase B (cyp19a1b), zebrafish, danio rerio, 17α-Ethinylestradiol, nonylphenol, endocrine disruption
MeSH Terms:
  • Animals
  • Aromatase/metabolism
  • Embryo, Nonmammalian/drug effects
  • Endocrine Disruptors/toxicity
  • Estradiol/analogs & derivatives
  • Estradiol/pharmacology
  • Estrogen Antagonists/pharmacology
  • Estrogens/toxicity*
  • Ethinyl Estradiol/toxicity*
  • Gonadotropin-Releasing Hormone/physiology
  • Neurons/drug effects*
  • Neurons/physiology
  • Phenols/toxicity*
  • Prosencephalon/physiology
  • Receptors, Estrogen/antagonists & inhibitors
  • Receptors, Estrogen/physiology*
  • Zebrafish
PubMed: 21549831 Full text @ Reprod. Toxicol.
There is growing evidence that neuroendocrine circuits controlling development and reproduction are targeted by EDCs. We have previously demonstrated that low concentrations of 17α-ethinylestradiol (EE2) disrupt the development of forebrain GnRH neurons during zebrafish development. The objectives of the present study were to determine whether the weak estrogenic compound, nonylphenol (NP), could elicit similar effects to EE2 and to what extent the estrogen receptors are involved in mediating these effects. Using immunohistochemistry, we confirmed that EE2 exposure induces an increase in the number of GnRH-ir neurons and we demonstrated that NP is able to produce similar effects in a concentration-dependent manner. The effects of both NP and EE2 were shown to be blocked by the estrogen receptors (ERs) antagonist ICI 182-780, demonstrating the involvement of functional ERs in mediating their effects. Altogether, these results highlight the need to consider neuroendocrine networks as critical endpoints in the field of endocrine disruption.