ArticleFrontiers in integrative neuroscience2024
Prenatal low-dose Bisphenol A exposure impacts cortical development via cAMP-PKA-CREB pathway in offspring.
Article in Frontiers in integrative neuroscience, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
4 citing papers in PubMed.
- Prenatal and Lactation Exposure to Bisphenol A (BPA) at the Global Mean Daily Intake Level Leads to Sex-Dependent Changes in Microglial State, Gene Expression, and Behavioral Patterns in Newborn and Juvenile Wistar Rat Offspring.Life (Basel, Switzerland) · 2026Article
- Kelulut honey (Toxicology reports · 2026Review
- Prenatal exposure to Bisphenol-A as a risk factor for infant neurodevelopment.Frontiers in endocrinology · 2025Review
- Short-Term Exposure of Bisphenol A Deteriorates the Quality of Rabbit Milk by Impairing Milk Fat Synthesis.Food science & nutrition · 2024Article
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
Bisphenol A (BPA) is a widely used plasticizer known to cause various disorders. Despite a global reduction in the use of BPA-containing products, prenatal exposure to low-dose BPA, even those below established safety limits, has been linked to neurological and behavioral deficits in childhood. The precise mechanisms underlying these effects remain unclear. In the present study, we observed a significant increase in the number of cortical neurons in offspring born to dams exposed to low-dose BPA during pregnancy. We also found that this prenatal exposure to low-dose BPA led to increased proliferation but reduced migration of cortical neurons. Transcriptomic analysis via RNA sequencing revealed an aberrant activation of the cAMP-PKA-CREB pathway in offspring exposed to BPA. The use of H89, a selective PKA inhibitor, effectively rescued the deficits in both proliferation and migration of cortical neurons. Furthermore, offspring from dams exposed to low-dose BPA exhibited manic-like behaviors, including hyperactivity, anti-depressant-like responses, and reduced anxiety. While H89 normalized hyperactivity, it didn't affect the other behavioral changes. These results suggest that the overactivation of PKA plays a causative role in BPA-induced changes in neuronal development. Our data also indicate that manic-like behaviors induced by prenatal low-dose BPA exposure may be influenced by both altered neuronal development and abnormal PKA signaling in adulthood.
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Registered trials
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