ArticleBiomolecules2025
Prenatal Hyperhomocysteinemia Leads to Synaptic Dysfunction and Structural Alterations in the CA1 Hippocampus of Rats.
Article in Biomolecules, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Triangulating the Neuroprotective Mechanisms of Pterostilbene in Hyperhomocysteinemia Induced Cognitive Impairment: Insights from In Silico, Proteomics, and Experimental Validation.Neuromolecular medicine · 2026Article
- High-dose folic acid therapy ameliorates gut microbiota dysbiosis in reproductive-aged women with hyperhomocysteinemia.Frontiers in nutrition · 2026Article
- Homocysteine enhances the excitability of cultured hippocampal neurons without altering the gene expression of voltage-gated ion channels.Molecular brain · 2025Article
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7 authors.
Funding
Abstract
Prenatal hyperhomocysteinemia (HCY) is associated with neurodevelopmental deficits, yet its long-term impact on hippocampal synaptic function remains poorly understood. This study examines the effects of moderate maternal HCY on excitatory synaptic transmission in the CA1 region of the dorsal hippocampus in rat offspring at juvenile (P21) and adult (P90) stages. Using field postsynaptic potential (fPSP) recordings, electron microscopy, and Western blot analysis, we observed a significant age-dependent decline in the efficiency of excitatory synaptic transmission in HCY-exposed rats. Electron microscopy revealed structural alterations, including synaptic vesicle agglutination in the stratum radiatum, suggesting impaired neurotransmitter release. Additionally, a significant reduction in pyramidal neuron density was observed in the CA1 region, although seizure susceptibility remained unchanged. Western blot analysis showed altered expression of Synapsin I, indicating presynaptic dysfunction. These findings suggest that moderate prenatal HCY leads to persistent deficits in synaptic transmission and structural integrity, potentially contributing to cognitive impairments in adulthood. Our results highlight the importance of maternal homocysteine levels in shaping hippocampal function and could offer insights into neurodevelopmental disorders associated with metabolic disturbances.
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