ArticleScientific reports2018
Dnmt3a in the dorsal dentate gyrus is a key regulator of fear renewal.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed, 11 citations in OpenAlex.
- MicroRNA-29 acutely regulates memory stability, expression of synaptic genes, and DNA methylation in the mouse adult hippocampus.Cellular and molecular life sciences : CMLS · 2026Article
- Profiling fear-extinction learning induced small ncRNAs landscape and identifying miR-29b-3p as a promising biomarker for PTSD.Journal of translational medicine · 2025Article
- DNA methylation regulates the extinction of fear memory.World journal of psychiatry · 2025Article
- DNA Methylation in Long-Term Memory.Physiology (Bethesda, Md.) · 2025Review
- Study on the Role ofAlpha psychiatry · 2024Article
- L-methionine and the L-type CaFrontiers in neural circuits · 2024Article
- Article
- Elevated activity in the dorsal dentate gyrus reduces expression of fear memory after fear extinction training.Journal of psychiatry & neuroscience : JPN · 2021Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Renewal of extinguished fear memory in an altered context is widely believed to be a major limiting issue for exposure therapy in treating various psychiatric diseases. Effective prevention of fear renewal will significantly improve the efficacy of exposure therapy. DNA methyltransferase (DNMTs) mediated epigenetic processes play critical roles in long term memory, but little is known about their functions in fear memory extinction or renewal. Here we investigated whether DNMTs regulate fear renewal after extinction. We found that elevated Dnmt3a level in the dorsal dentate gyrus (dDG) of hippocampus was associated with the absence of fear renewal in an altered context after extinction training. Overexpression and knockdown of Dnmt3a in the dDG regulated the occurrence of fear renewal in a bi-directional manner. In addition, Dnmt3a overexpression was associated with elevated expression of c-Fos in the dDG during extinction training. Furthermore, we found that renewal of remote fear memory can be prevented, and the absence of renewal was concurrent with an elevated Dnmt3a level. Our results indicate that Dnmt3a in the dDG is a key regulator of fear renewal after extinction, and Dnmt3a may play a critical role in controlling fear memory return and thus has therapeutic values.
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