Cited by 92Effects and risks of endocrine disrupting chemicalsNeuroscience and Neuropharmacology ResearchMemory and Neural Mechanisms

Abnormal synaptic plasticity in basolateral amygdala may account for hyperactivity and attention-deficit in male rat exposed perinatally to low-dose bisphenol-A

Zhou, Rong, Bai, Yinyang, Yang, Rong, Zhu, Ying, Chi, Xia, Li, Lin, Chen, Lei, Sokabe, Masahiro +1 more·2011·Neuropharmacology

Abstract

If the pregnant and lactating female rats are exposed to environmental levels of bisphenol-A (BPA), their male offspring will display hyperactivity and attention-deficit. In patients with attention-deficit/hyperactivity disorder (ADHD), the size of the amygdala is reported to be reduced. This study examined functional alterations in the basolateral amygdala (BLA) of the postnatal 28-day-old male offspring exposed perinatally to BPA (BPA-rats). We specifically focused on the synaptic properties of GABAergic/dopaminergic systems in the BLA. A single electrical stimulation of the capsule fibers evoked multispike responses with an enhanced primary population spikes (1st-PS) in the BPA-rats. A single train of high-frequency stimulation of the fibers induced NMDA receptor (NMDAR) dependent long-term potentiation (LTP) in BPA-rats, but not in control rats. Also, paired-pulse inhibition (PPI, GABA-dependent) in control rats was reversed to paired-pulse facilitation (PPF) in BPA-rats. Perfusion of slices obtained from BPA-rats with the GABA(A) receptor (GABA(A)R) agonist muscimol blocked the multispike responses and LTP, and recovered PPI. By contrast, the dopamine D1 receptor antagonist SCH23390 abolished LTP and attenuated the increased amplitude of 1st-PS in BPA-rats. Conversely, blockade of GABA(A)R by bicuculline could produce the multispike responses and PPF in BLA in control rats. Furthermore, in BLA the infusion of SCH23390, muscimol or the NMDAR blocker MK801 ameliorated the…

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Crossref · 10.1016/j.neuropharm.2011.01.031

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Authors
Zhou, R., Bai, Y., Yang, R., Zhu, Y., Chi, X., Li, L., Chen, L., Sokabe, M., & Chen, L.
Affiliations
  • Nanjing Medical University (CN)
  • Nagoya University (JP)
Corresponding author
Chen, Ling
Venue
Neuropharmacology
Publisher
Elsevier BV
Published
2011-04
Volume
60
Issue
5
Pages
789-798
ISSN
0028-3908 (ISSN-L)
OpenAlex
W1972025902
Cited by
92
References
66
Citations by year
2026: 5 · 2025: 7 · 2024: 7 · 2023: 5 · 2022: 4 · 2021: 7 · 2020: 5 · 2019: 3 · 2018: 8 · 2017: 10 · 2016: 5 · 2015: 7 · 2014: 2 · 2013: 11 · 2012: 5
FWCI
4.37
Type
journal article
Language
en
Open access
closed
Locations
  • Neuropharmacology (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • Program for Changjiang Scholars and Innovative Research Team in University (IRT0631)
  • National Natural Science Foundation of China (30872725, 81000482, 81071027)
  • Ministry of Education of the People's Republic of China (200803120006)
  • Major State Basic Research Development Program of China (2009CB941701)
Topics
  • Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Effects and risks of endocrine disrupting chemicals
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
  • Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
Keywords
bisphenol A, perinatal exposure, attention deficit hyperactivity disorder, basolateral amygdala, synaptic plasticity, paired-pulse inhibition, paired-pulse facilitation, GABAergic disinhibition, dopamine D1 receptor, GABAA receptor, muscimol, SCH 23390, MK-801, hyperactivity, attention deficits, endocrine disruptors
MeSH terms
Bisphenol A Compounds, Air Pollutants, Occupational, Amygdala, Animals, Attention Deficit Disorder with Hyperactivity, Benzazepines, Benzhydryl Compounds, Bicuculline, Disease Models, Animal, Female, Glutamate Decarboxylase, Male, Muscimol, Neuronal Plasticity, Phenols, Pregnancy, Receptors, N-Methyl-D-Aspartate, Dizocilpine Maleate, Rats, Sprague-Dawley, Long-Term Potentiation, Dopamine Antagonists, Rats, GABA-A Receptor Agonists, GABA-A Receptor Antagonists

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