Enriched environment rescues bisphenol A induced anxiety-like behavior and cognitive impairment by modulating synaptic plasticity
Bisphenol A (BPA) is an exogenous endocrine disruptor in the environmental context, garnering attention for its harmful effects on the nervous system function and behavior. Research indicates that being exposed to BPA may result in anxiety-like behavior and impairment in cognitive function. Enriched...
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Elsevier
2025-01-01
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| Series: | Ecotoxicology and Environmental Safety |
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| Online Access: | http://www.sciencedirect.com/science/article/pii/S0147651324015033 |
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| author | Jiong Li Guangyin Yu Laijian Wang Wenjun Zhang Wenya Ke Yifei Li Danlei Liu Keman Xie Yuanyuan Xu Caihui Cha Guoqing Guo Jifeng Zhang |
| author_facet | Jiong Li Guangyin Yu Laijian Wang Wenjun Zhang Wenya Ke Yifei Li Danlei Liu Keman Xie Yuanyuan Xu Caihui Cha Guoqing Guo Jifeng Zhang |
| author_sort | Jiong Li |
| collection | DOAJ |
| description | Bisphenol A (BPA) is an exogenous endocrine disruptor in the environmental context, garnering attention for its harmful effects on the nervous system function and behavior. Research indicates that being exposed to BPA may result in anxiety-like behavior and impairment in cognitive function. Enriched environment (EE) is beneficial to improve cognitive behavior, but whether EE can improve BPA-induced behavioral impairment is still unclear. This research explored the possible pathways through which EE alleviates anxiety-like behavior and cognitive impairment in mice exposed to BPA. Except for the control mice, all mice received BPA treatment. After BPA treatment, some mice were housed normally, some housed with EE, and some were given NMDA and AMPA receptor agonists. Our research revealed that exposure to BPA results in anxiety-like behavior in open field and elevated-plus maze experiments. Additionally, spatial and learning memory cognitive impairments were observed in Y-maze and water maze tests. Furthermore, exposure to BPA led to a decrease in both the density and maturity of dendritic spines, as well as a reduction in neurite length and branch numbers. PSD-95, GluA1, and NR2A expression were down-regulated, and excitatory synaptic transmission was decreased. However, EE treatment increased dendrite spine density and maturity, up-regulated PSD-95, GluA1and NR2A expression, enhanced excitatory synaptic transmission, and relieved anxiety-like behavior and cognitive impairment in BPA mice. Furthermore, administering NMDA or AMPA receptor agonists to BPA mice led to an increase in dendritic spine density and maturity, a rise in mEPSC amplitude, as well as a restoration of anxiety-like behavior and cognitive deficits induced by BPA. The findings of this study provide proof that EE has a neuroprotective effect in reducing anxiety-related behavior and cognitive decline caused by BPA. |
| format | Article |
| id | doaj-art-fed3dc4c8a5b4777bd0e19c1fcfafefb |
| institution | Kabale University |
| issn | 0147-6513 |
| language | English |
| publishDate | 2025-01-01 |
| publisher | Elsevier |
| record_format | Article |
| series | Ecotoxicology and Environmental Safety |
| spelling | doaj-art-fed3dc4c8a5b4777bd0e19c1fcfafefb2025-01-23T05:25:30ZengElsevierEcotoxicology and Environmental Safety0147-65132025-01-01289117427Enriched environment rescues bisphenol A induced anxiety-like behavior and cognitive impairment by modulating synaptic plasticityJiong Li0Guangyin Yu1Laijian Wang2Wenjun Zhang3Wenya Ke4Yifei Li5Danlei Liu6Keman Xie7Yuanyuan Xu8Caihui Cha9Guoqing Guo10Jifeng Zhang11Neuroscience Laboratory for Cognitive and Developmental Disorders, Department of Anatomy, Medical College of Jinan University, Guangzhou, Guangdong 510630, ChinaNeuroscience Laboratory for Cognitive and Developmental Disorders, Department of Anatomy, Medical College of Jinan University, Guangzhou, Guangdong 510630, ChinaNeuroscience Laboratory for Cognitive and Developmental Disorders, Department of Anatomy, Medical College of Jinan University, Guangzhou, Guangdong 510630, ChinaNeuroscience Laboratory for Cognitive and Developmental Disorders, Department of Anatomy, Medical College of Jinan University, Guangzhou, Guangdong 510630, ChinaNeuroscience Laboratory for Cognitive and Developmental Disorders, Department of Anatomy, Medical College of Jinan University, Guangzhou, Guangdong 510630, ChinaNeuroscience Laboratory for Cognitive and Developmental Disorders, Department of Anatomy, Medical College of Jinan University, Guangzhou, Guangdong 510630, ChinaNeuroscience Laboratory for Cognitive and Developmental Disorders, Department of Anatomy, Medical College of Jinan University, Guangzhou, Guangdong 510630, ChinaNeuroscience Laboratory for Cognitive and Developmental Disorders, Department of Anatomy, Medical College of Jinan University, Guangzhou, Guangdong 510630, ChinaNeuroscience Laboratory for Cognitive and Developmental Disorders, Department of Anatomy, Medical College of Jinan University, Guangzhou, Guangdong 510630, ChinaDepartment of Pediatrics, Guangzhou Women and Children’s Medical Center, Guangzhou 510120, ChinaNeuroscience Laboratory for Cognitive and Developmental Disorders, Department of Anatomy, Medical College of Jinan University, Guangzhou, Guangdong 510630, ChinaNeuroscience Laboratory for Cognitive and Developmental Disorders, Department of Anatomy, Medical College of Jinan University, Guangzhou, Guangdong 510630, China; Corresponding author.Bisphenol A (BPA) is an exogenous endocrine disruptor in the environmental context, garnering attention for its harmful effects on the nervous system function and behavior. Research indicates that being exposed to BPA may result in anxiety-like behavior and impairment in cognitive function. Enriched environment (EE) is beneficial to improve cognitive behavior, but whether EE can improve BPA-induced behavioral impairment is still unclear. This research explored the possible pathways through which EE alleviates anxiety-like behavior and cognitive impairment in mice exposed to BPA. Except for the control mice, all mice received BPA treatment. After BPA treatment, some mice were housed normally, some housed with EE, and some were given NMDA and AMPA receptor agonists. Our research revealed that exposure to BPA results in anxiety-like behavior in open field and elevated-plus maze experiments. Additionally, spatial and learning memory cognitive impairments were observed in Y-maze and water maze tests. Furthermore, exposure to BPA led to a decrease in both the density and maturity of dendritic spines, as well as a reduction in neurite length and branch numbers. PSD-95, GluA1, and NR2A expression were down-regulated, and excitatory synaptic transmission was decreased. However, EE treatment increased dendrite spine density and maturity, up-regulated PSD-95, GluA1and NR2A expression, enhanced excitatory synaptic transmission, and relieved anxiety-like behavior and cognitive impairment in BPA mice. Furthermore, administering NMDA or AMPA receptor agonists to BPA mice led to an increase in dendritic spine density and maturity, a rise in mEPSC amplitude, as well as a restoration of anxiety-like behavior and cognitive deficits induced by BPA. The findings of this study provide proof that EE has a neuroprotective effect in reducing anxiety-related behavior and cognitive decline caused by BPA.http://www.sciencedirect.com/science/article/pii/S0147651324015033Bisphenol-AAnxietyCognitive functionEnriched environmentDendritic spinemEPSC |
| spellingShingle | Jiong Li Guangyin Yu Laijian Wang Wenjun Zhang Wenya Ke Yifei Li Danlei Liu Keman Xie Yuanyuan Xu Caihui Cha Guoqing Guo Jifeng Zhang Enriched environment rescues bisphenol A induced anxiety-like behavior and cognitive impairment by modulating synaptic plasticity Ecotoxicology and Environmental Safety Bisphenol-A Anxiety Cognitive function Enriched environment Dendritic spine mEPSC |
| title | Enriched environment rescues bisphenol A induced anxiety-like behavior and cognitive impairment by modulating synaptic plasticity |
| title_full | Enriched environment rescues bisphenol A induced anxiety-like behavior and cognitive impairment by modulating synaptic plasticity |
| title_fullStr | Enriched environment rescues bisphenol A induced anxiety-like behavior and cognitive impairment by modulating synaptic plasticity |
| title_full_unstemmed | Enriched environment rescues bisphenol A induced anxiety-like behavior and cognitive impairment by modulating synaptic plasticity |
| title_short | Enriched environment rescues bisphenol A induced anxiety-like behavior and cognitive impairment by modulating synaptic plasticity |
| title_sort | enriched environment rescues bisphenol a induced anxiety like behavior and cognitive impairment by modulating synaptic plasticity |
| topic | Bisphenol-A Anxiety Cognitive function Enriched environment Dendritic spine mEPSC |
| url | http://www.sciencedirect.com/science/article/pii/S0147651324015033 |
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