ArticleMolecular neurobiology2021
Prenatal Stress Leads to the Altered Maturation of Corticostriatal Synaptic Plasticity and Related Behavioral Impairments Through Epigenetic Modifications of Dopamine D2 Receptor in Mice.
Article in Molecular neurobiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.
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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.
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Who cites it
10 citing papers in PubMed, 1 synthesis or guideline pooled it, 15 citations in OpenAlex.
- Pooled it
- Epigenetic Regulation of Inflammation by Dopamine in Primary Human Macrophages.bioRxiv : the preprint server for biology · 2026Article
- Epigenetic regulation of inflammation by dopamine in primary human macrophages.Frontiers in immunology · 2026Article
- Tactile stimulation reverses painful stimuli outcomes via PVN-VTA oxytocin circuitry and dopaminergic regulation.Communications biology · 2025Article
- The Promise of Epigenetic Editing for Treating Brain Disorders.Sub-cellular biochemistry · 2025Review
- PRKCB methylation: a potential biomarker of MDD with childhood chronic stress, a cross-sectional study in drug-naive, first-episode adolescent MDD.Epigenetics · 2024Observational
- S-ketamine alleviates depression-like behavior and hippocampal neuroplasticity in the offspring of mice that experience prenatal stress.Scientific reports · 2024Article
- Melatonin improves maternal sleep deprivation-induced learning and memory impairment, inflammation, and synaptic dysfunction in murine male adult offspring.Brain and behavior · 2024Article
- The effect of epigenetic aging on neurodegenerative diseases: a Mendelian randomization study.Frontiers in endocrinology · 2024Article
- Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Prenatal stress (PRS) had a long-term adverse effect on motor behaviors. Corticostriatal synaptic plasticity, a cellular basis for motor controlling, has been proven to participate in the pathogenesis of many behavior disorders. Based on the reports about the involvement of epigenetic DNA alterations in PRS-induced long-term effects, this research investigated the influence of PRS on the development and maturation of corticostriatal synaptic plasticity and related behaviors and explored the underlying epigenetic mechanism. Subjects were male offspring of dams that were exposed to stress three times per day from the 10th day of pregnancy until delivery. The development and maturation of plasticity at corticostriatal synapses, dopamine signaling, behavioral habituation, and DNA methylation were examined and analyzed. Control mice expressed long-term potentiation (LTP) at corticostriatal synapses during postnatal days (PD) 12-14 and produced long-term depression (LTD) during PD 20-60. However, PRS mice exhibited sustained LTP during PD 12-60. The treatment with dopamine 2 receptor (D2R) agonist quinpirole recovered striatal LTD and improved the impaired behavioral habituation in PD 45 adult PRS mice. Additionally, adult PRS mice showed reduced D2R, excess DNA methyltransferase 1 (DNMT1), increased binding of DNMT1 to D2R promoter, and hypermethylation at D2R promoter in the striatum. The DNMT1 inhibitor 5-aza-deoxycytidine restored striatal synaptic plasticity and improved behavioral habituation in adult PRS mice via D2R-mediated dopamine signaling. DNMT1-associated D2R hypermethylation is responsible for altering the maturation of plasticity at corticostriatal synapses and impairing the behavioral habituation in PRS mice.
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Registered trials
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