Maternal exposure to low doses of bisphenol A affects learning and memory in male rat offspring with abnormal N -methyl- d -aspartate receptors in the hippocampus
Abstract
Bisphenol A (BPA), a component of polycarbonate and epoxy resins, has been reported to induce learning and memory deficits. However, the mechanisms have not been fully elucidated. Growing evidence has suggested that N -methyl-d-aspartate receptors (NMDARs) are involved in cognitive impairments. In this study, BPA was administered to female Sprague-Dawley rats (six per dose group) at concentrations of 0 (control), 4, 40, and 400 μg/kg·body weight/day from gestation day 1 through lactation day 21. Spatial learning was evaluated using the Morris water maze on postnatal day 22. Expression levels of NMDARs were determined using real-time polymerase chain reaction and Western blot. The results showed that male offspring exposed to BPA exhibited increased latency in reaching the platform and reduced time in the target quadrant, and the number of crossing the platform was less, as compared with the control group. The mRNA and protein expression levels of NMDARs in the hippocampus were significantly downregulated when compared with the control group of male offspring. The data showed that maternal exposure to BPA at low dosage can cause cognitive deficits in male rat offspring, probably due to a decrease in NMDARs in the hippocampus.
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Bisphenols interfere with glutamate receptor-dependent processes, and disturbances in AMPA and NMDA receptor expression, phosphorylation, or membrane localization are particularly damaging because these receptors are essential for excitatory synaptic transmission and plasticity.
“Bisphenols also interfere with glutamate receptor-dependent processes, and disturbances in AMPA and NMDA receptor expression, phosphorylation, or membrane localization are particularly damaging because these receptors are essential for excitatory synaptic transmission and plasticity (Hyun et al., 2022; Wang et al., 2021).”
From Environmental endocrine disruptors at the synapse: mechanisms linking chemical exposure to cognitive and behavioral dysfunction (2026) · cites this paper as Wang et al., 2021
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The essential role of hippocampal CA1 NMDA receptor-dependent synaptic plasticity in spatial memory.
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“Mice with a deletion of the GluN1 gene in the CA1 pyramidal cells of the hippocampus displayed impaired excitatory postsynaptic potential and LTP in the CA1 synapses and deficit in spatial memory (Tsien et al., 1996).”
BackgroundMethodInfluentialTian, Y., Baek, J., Lee, S., & Jang, C. (2010) · Synapse · doi:10.1002/syn.20746 · Cited by 197 · see citing works
Perinatal Exposure to Low-Dose Bisphenol A Impairs Spatial Learning and Memory in Male Rats
Kuwahara, R., Kawaguchi, S., Kohara, Y., Cui, H., & Yamashita, K. (2013) · Journal of Pharmacological Sciences · doi:10.1254/jphs.13093fp · Cited by 52 · see citing works
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Jocsak, G., Kiss, D. S., Alymbaeva, D., Diebald, A., Zsarnovszky, A., Heinzlmann, A., & Bartha, T. (2026) · Frontiers in Behavioral Neuroscience · doi:10.3389/fnbeh.2026.1821381 · Cited by 1 · see citing works
“…with glutamate receptor-dependent processes, and disturbances in AMPA and NMDA receptor expression, phosphorylation, or membrane localization are particularly damaging because these receptors are essential for excitatory synaptic transmission and plasticity (Hyun et al., 2022; Wang et al., 2021).”
- Authors
- Wang, C., Shu, Y., Xu, L., Liu, Q., Zhang, B., & Zhang, H.
- Affiliations
- Shaanxi University of Chinese Medicine (CN)
- Corresponding author
- Zhang, Hong
- Venue
- Toxicology and Industrial Health
- Publisher
- SAGE Publications
- Published
- 2021-04-21
- Volume
- 37
- Issue
- 6
- Pages
- 303-313
- ISSN
- 0748-2337 (ISSN-L)
- 1477-0393
- OpenAlex
- W3156507346
- Cited by
- 8
- References
- 3
- Citations by year
- 2026: 1 · 2025: 1 · 2024: 2 · 2023: 3 · 2021: 1
- FWCI
- 0.60
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Toxicology and Industrial Health (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Natural Science Foundation of China (81602892)
- Topics
- Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Effects and risks of endocrine disrupting chemicals
- Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Pharmacological Effects and Toxicity Studies
- Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Toxic Organic Pollutants Impact
- Keywords
- bisphenol A, maternal exposure, developmental neurotoxicity, NMDA receptor, hippocampus, learning and memory impairment, spatial learning, cognitive impairment, endocrine disruptors, low-dose exposure, male offspring, prenatal exposure
- MeSH terms
- Adult, Animals, Benzhydryl Compounds, Dose-Response Relationship, Drug, Female, Humans, Male, Memory Disorders, Phenols, Pregnancy, Prenatal Exposure Delayed Effects, Sex Factors, Receptors, N-Methyl-D-Aspartate, Rats, Sprague-Dawley, Receptors, Glutamate, Models, Animal, Rats
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