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Updated: Jan 20, 2026
Learning and Memory: Types; Behavioral Tests & Techniques
Published on: April 30, 2023
Low-dose bisphenol A exposure impairs learning and memory ability with alterations of neuromorphology and
Haibin Zhang1, Hongxuan Kuang1, Yifan Luo1
1Guangdong Provincial Engineering Technology Research Center for Drug and Food Biological Resources Processing and Comprehensive Utilization, School of Life Sciences, South China Normal University, Guangzhou 510631, China.
Insights
Postnatal exposure to bisphenol A (BPA) impairs infant and child neurodevelopment, affecting learning, memory, and brain structure. BPA disrupts hippocampal development and neurotransmitter balance in a sex- and dose-dependent manner.
Area of Science:
- Environmental Health
- Neuroscience
- Toxicology
Background:
- Environmental bisphenol A (BPA) exposure is a growing concern for infant and child neurodevelopment.
- Understanding the specific neurotoxic effects of BPA during critical developmental windows is crucial.
Purpose of the Study:
- To investigate the developmental neurotoxicity of postnatal bisphenol A (BPA) exposure in a rat model.
- To assess the impact of varying BPA concentrations on learning, memory, hippocampal morphology, and neurotransmitter levels.
Main Methods:
- Postnatal rats were exposed to different BPA concentrations (0, 0.5, 50, 5000 μg/kg·bw/day) from postnatal days 7 to 21.
- Y-maze tests evaluated learning and memory.
- Golgi-Cox assays examined hippocampal neuromorphology.
- Liquid chromatography-tandem mass spectrometry (LC/MS/MS) measured neurotransmitter levels.
Main Results:
- BPA exposure, particularly at low and high doses, impaired learning and memory in rats.
- Decreased dendritic complexity in the DG and reduced spine densities in CA1 and DG regions of the hippocampus were observed.
- Low-dose BPA significantly altered hippocampal neurotransmitter levels, including glutamic acid (Glu), acetylcholine, 5-hydroxytryptamine (5-HT), and γ-aminobutyric acid (GABA), in a sex-dependent manner.
Conclusions:
- Postnatal BPA exposure disrupts hippocampal dendritic development and neurotransmitter homeostasis in a sex- and dose-dependent manner.
- Impaired spatial learning and memory in rats exposed to low-dose BPA are linked to disrupted hippocampal development and neurotransmitter balance.
- These findings highlight the potential neurodevelopmental risks of environmental BPA exposure in early life.
Abstract:
To investigate the developmental neurotoxicity of environmental bisphenol A (BPA) exposure for infants and children, postnatal rats were used as the animal model and were divided into four groups. Then, they were treated with different concentrations of BPA (i.e., 0, 0.5, 50, or 5000 μg/kg·bw/day of BPA as the control, low-, medium- and high-exposed group) from postnatal days 7 to 21. Y-maze tests, Golgi-Cox assays and liquid chromatography-tandem mass spectrometry (LC/MS/MS) were performed to test the changes of learning and memory ability, hippocampal neuromorphology and neurotransmitter levels, respectively. The results showed that the BPA-exposed rats, especially the low- and high-exposed rats, needed more trials and longer times to qualify for the learned criterion than the control rats. Additionally, rats after low- or high-exposure to BPA exhibited decreased DG dendritic complexity and reduced CA1 and DG dendritic spine densities in the hippocampus. Low-dosage BPA treatment could significantly alter the neurotransmitter contents in the hippocampus. In male rats, the levels of glutamic acid (Glu) and acetylcholine increased, while the 5-hydroxytryptamine (5-HT) and γ-aminobutyric acid (GABA) levels decreased, which lead to an unbalanced Glu/GABA ratio. However, in female rats, only 5-HT levels decreased. In conclusion, postnatal exposure to BPA could sex- and dose-dependently disrupt dendritic development and neurotransmitter homeostasis in the rat hippocampus. The impaired spatial learning and memory ability of rats induced by low-dose BPA is associated with both disrupted dendritic development and neurotransmitter homeostasis in the hippocampus.
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