Cited by 197Effects and risks of endocrine disrupting chemicalsNeuroendocrine regulation and behaviorPharmacological Effects and Toxicity Studies

Prenatal and postnatal exposure to bisphenol a induces anxiolytic behaviors and cognitive deficits in mice

Tian, Yu‐Hua, Baek, Joung‐Hee, Lee, Seok‐Yong, Jang, Choon‐Gon·2010·Synapse

Abstract

Bisphenol A (BPA), an environmental endocrine‐disrupting chemical, has been extensively evaluated for reproductive toxicity and carcinogenicity. However, little is known about the behavioral and neurochemical effects of BPA exposure. This study examined whether chronic daily exposure to an environmental endocrine‐disrupting chemical, bisphenol A [(BPA); 100 μg/kg/day or 500 μg/kg/day, p.o.], from prenatal Day 7 to postnatal Day 36 would lead to changes in anxiety and memory in mice. First, we observed the behavioral alterations of BPA‐treated mice using two anxiety‐related models, the open field test and elevated plus maze (EPM) test. In the open field test, BPA treatment (100 μg/kg/day) increased movement in the central zone. BPA treatment (500 μg/kg/day) also increased the time spent in the open arms in the EPM test. Second, we measured cognitive ability in the Y‐maze test and novel object test. BPA‐treated mice showed decreased alternation behavior in the Y‐maze at both of doses, indicating working memory impairment. BPA‐treated mice (100 μg/kg/day) also showed decreased novel object recognition as expressed by central locomotion and frequency in the central zone, showing recognition memory impairment. Finally, to measure changes in the dopaminergic and NMDAergic systems in the brain, we performed autoradiographic receptor binding assays for dopamine D 1 and D 2 receptors, the NMDA receptor, and the dopamine transporter. BPA treatment increased D 2 receptor binding in the caudate putamen (CPu) but decreased DAT binding. BPA treatment also decreased NMDA receptor binding in the frontal cortex and CA1, CA3, and DG of the hippocampus. Taken together, our results suggest that long‐term BPA exposure in mice can induce anxiolytic behaviors, cognitive deficits and changes in the dopaminergic and NMDAergic systems. Synapse 64:432–439, 2010. © 2010 Wiley‐Liss, Inc.

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Authors
Tian, Y., Baek, J., Lee, S., & Jang, C.
Affiliations
  • Ministry of Food and Drug Safety (KR)
  • Sungkyunkwan University (KR)
Corresponding author
Jang, Choon‐Gon
Venue
Synapse
Publisher
Wiley
Published
2010-02-18
Volume
64
Issue
6
Pages
432-439
ISSN
  • 0887-4476 (ISSN-L)
  • 1098-2396
OpenAlex
W1986018940
Cited by
197
References
50
Citations by year
2026: 8 · 2025: 9 · 2024: 6 · 2023: 10 · 2022: 15 · 2021: 17 · 2020: 12 · 2019: 12 · 2018: 16 · 2017: 11 · 2016: 13 · 2015: 16 · 2014: 12 · 2013: 11 · 2012: 11
FWCI
9.53
Type
journal article
Language
en
Open access
closed
Locations
  • Synapse (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Effects and risks of endocrine disrupting chemicals
  • Social Sciences › Psychology › Social Psychology › Neuroendocrine regulation and behavior
  • Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Pharmacological Effects and Toxicity Studies
Keywords
bisphenol A, endocrine disruptors, prenatal exposure, postnatal exposure, anxiety-like behavior, cognitive impairment, working memory, recognition memory, dopamine D2 receptor, dopamine transporter, NMDA receptor, caudate-putamen, hippocampus, neurobehavioral effects
MeSH terms
Bisphenol A Compounds, Animals, Animals, Newborn, Behavior, Animal, Mental Disorders, Benzhydryl Compounds, Brain, Cognition Disorders, Disease Models, Animal, Estrogens, Non-Steroidal, Female, Frontal Lobe, Hippocampus, Memory Disorders, Mice, Inbred ICR, Phenols, Pregnancy, Prenatal Exposure Delayed Effects, Anti-Anxiety Agents, Receptors, N-Methyl-D-Aspartate, Receptors, Dopamine D1, Receptors, Dopamine D2, Maze Learning, Dopamine Plasma Membrane Transport Proteins, Mice

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