ZFIN ID: ZDB-PUB-171216-2
Opening the black box of endocrine disruption of brain development: Lessons from the characterization of Bisphenol A
Nesan, D., Sewell, L.C., Kurrasch, D.M.
Date: 2017
Source: Hormones and behavior   101: 50-58 (Review)
Registered Authors: Kurrasch, Deborah
Keywords: none
MeSH Terms:
  • Animals
  • Anura
  • Benzhydryl Compounds/pharmacology
  • Benzhydryl Compounds/toxicity*
  • Brain/drug effects*
  • Brain/embryology*
  • Endocrine Disruptors/pharmacology
  • Endocrine Disruptors/toxicity*
  • Female
  • Humans
  • Mental Disorders/chemically induced
  • Neurogenesis/drug effects*
  • Phenols/pharmacology
  • Phenols/toxicity*
  • Pregnancy
  • Zebrafish
PubMed: 29241697 Full text @ Horm. Behav.
ABSTRACT
Bisphenol A (BPA) is among the best-studied endocrine disrupting chemicals, known to act via multiple steroid hormone receptors to mediate a myriad of cellular effects. Pre-, peri-, and postnatal BPA exposure have been linked to a variety of altered behaviors in multiple model organisms, ranging from zebrafish to frogs to mammalian models. Given that BPA can cross the human placental barrier and has been found in the serum of human fetuses during gestation, BPA has been postulated to adversely affect ongoing neurodevelopment, ultimately leading to behavioral disorders later in life. Indeed, the brain has been identified as a key developmental target for BPA disruption. Despite these known associations between gestational BPA exposure and adverse developmental outcomes, as well as an extensive body of evidence existing in the literature, the mechanisms by which BPA induces its cellular- and tissue-specific effects on neurodevelopmental processes still remains poorly understood at a mechanistic level. In this review we will briefly summarize the effects of gestational BPA exposure on neural developmental mechanisms and resulting behaviors, and then present suggestions for how we might address gaps in our knowledge to develop a fuller understanding of endocrine neurodevelopmental disruption to better inform governmental policy against the use of BPA or other endocrine disruptors.
ADDITIONAL INFORMATION No data available