ArticleAlpha psychiatry2025
Prenatal Exposure to Valproic Acid may Alter CD200/CD200R Signaling Pathways in a Rat Model of Autism Spectrum Disorder.
Article in Alpha psychiatry, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed.
- PEGylated Liposomal Resveratrol Induces Region-Specific Redox Modulation Without Behavioral or Neurotrophin Recovery in a VPA Model of Autism.Journal of molecular neuroscience : MN · 2026Article
- Redox System Dysfunction as a Key Mechanism in Autism Spectrum Disorder Pathogenesis.International journal of molecular sciences · 2025Review
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objective: To investigate the potential toxic effects of prenatal exposure to valproic acid (VPA) on microglia-neuron communication in the brain, with a specific focus on the alterations in key molecules involved in this process, namely CX3CL1/CX3CR1 and CD200/CD200R, during the early stages of life in a rat model of autism. Methods: Pregnant female rats were administered either sterile saline or VPA on embryonic day 12.5. The brains of the rat offspring were collected on postnatal day 30 for analysis. Immunohistochemical techniques and enzyme-linked immunosorbent assay (ELISA) were employed to assess changes in microglia-neuron crosstalk. Results: The study revealed a significant reduction in CD200 levels within the hippocampus of rats on postnatal day 30 following prenatal exposure to VPA, indicating an impairment in CD200/CD200R signaling. Additionally, there was no observed increase in microglial numbers or any pathological alterations in the hippocampus. Additionally, no significant changes in the levels of CX3CL1 and CX3CR1 were noted in the VPA-exposed rats compared with the control group. Conclusion: Prenatal exposure to VPA resulted in a decrease in CD200 expression within the hippocampus, potentially disrupting the communication between microglia and neurons. The findings suggest that VPA may modify the interactions between microglia and neurons, which could lead to neuroinflammation due to hyperactivated microglia. These disruptions have the potential to affect synaptic connectivity and contribute to the development of neurodevelopmental disorders, including autism. Further research is necessary to clarify the underlying mechanisms and implications for pathological conditions associated with autism spectrum disorder (ASD).
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Registered trials
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