Cited by 48Neuroscience and Neuropharmacology ResearchEffects and risks of endocrine disrupting chemicalsMemory and Neural Mechanisms

Deficits in development of synaptic plasticity in rat dorsal striatum following prenatal and neonatal exposure to low-dose bisphenol A.

Zhou, R., Zhang, Z., Zhu, Y., Chen, L., Sokabe, M., Chen, L.·2009·Neuroscience

Abstract

Prenatal and neonatal exposure to relatively low-dose bisphenol-A (BPA, 20 microg/kg/day) causes hyper-locomotion of male rat offspring. This research investigated the developmental pattern of activity-dependent synaptic plasticity in dorsolateral (DL) striatum, a cellular basis for motor controlling, in male rat offspring with hyper-locomotion. High frequency stimulation (four-pulse bursts at 100 Hz) was undertaken to induce long-term potentiation (LTP) and long-term depression (LTD) in corticostriatal synapse during postnatal day (PD) 10-32. Herein, we show that in control rats HFS induces LTP during PD12-14 and LTD during PD24-32. Strikingly, the prenatal and neonatal exposure to low-dose BPA resulted in delay of LTP induction during PD21-32, showing a reversal of LTD induction. In addition, in PD28 BPA-rats basal population spike amplitude was increased with reduction of paired-pulse facilitation (PPF) compared to the same age control rats. Acute application of the dopamine 1 receptor (D1R) antagonist SCH23390 in slices obtained from PD28 BPA-rats inhibited not only the PS-potentiation and PPF-induction but also the induction of LTP. Furthermore, the dopamine 2 receptor (D2R) agonist quinpirole recovered the LTD induction in PD28 BPA-rats, which was D1R-dependent and metabotropic glutamate receptor-dependent. In PD28 control rats, the blockade of D2R by l-sulpiride reversed the D1R- and mGluR-dependent LTD to short-term potentiation. Therefore, the findings provide functi…

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Crossref · 10.1016/j.neuroscience.2008.12.028

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Authors
Zhou, R., Zhang, Z., Zhu, Y., Chen, L., Sokabe, M., & Chen, L.
Affiliations
  • Nanjing Medical University (CN)
  • Japan Science and Technology Agency (JP)
Venue
Neuroscience
Publisher
Elsevier BV
Published
2009-03
Volume
159
Issue
1
Pages
161-171
ISSN
0306-4522 (ISSN-L)
OpenAlex
W2087370445
Cited by
48
References
3
Citations by year
2026: 1 · 2024: 1 · 2022: 2 · 2020: 1 · 2019: 1 · 2018: 3 · 2017: 3 · 2016: 2 · 2015: 3 · 2014: 2 · 2013: 7 · 2012: 2
FWCI
2.88
Type
journal article
Language
en
Open access
closed
Locations
  • Neuroscience (publishedVersion)
  • PubMed (publishedVersion)
Funders
National Natural Science Foundation of China
Topics
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
  • Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Effects and risks of endocrine disrupting chemicals
  • Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
Keywords
bisphenol A, prenatal exposure, neonatal exposure, dorsal striatum, corticostriatal synapses, synaptic plasticity, long-term potentiation, long-term depression, dopamine D1 receptor, dopamine D2 receptor, metabotropic glutamate receptors, paired-pulse facilitation, population spike, developmental neurotoxicity
MeSH terms
Bisphenol A Compounds, Age Factors, Analysis of Variance, Animals, Animals, Newborn, Benzazepines, Benzhydryl Compounds, Corpus Striatum, Electric Stimulation, Evoked Potentials, Female, Male, Neuronal Plasticity, Phenols, Pregnancy, Prenatal Exposure Delayed Effects, Pyridines, Synapses, Valine, Rats, Sprague-Dawley, Dopamine Agonists, Excitatory Amino Acid Antagonists, Rats, In Vitro Techniques

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