ArticleProceedings of the National Academy of Sciences of the United States of America2019
Extinction learning with social support depends on protein synthesis in prefrontal cortex but not hippocampus.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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8 citing papers in PubMed, 17 citations in OpenAlex.
- DNA methylation regulates the extinction of fear memory.World journal of psychiatry · 2025Article
- Cpeb1 remodels cell type-specific translational program to promote fear extinction.Science advances · 2025Article
- A biopsychosocial model of MDMA-assisted therapy in application: Dyadic One Session Treatment for specific phobia.Frontiers in psychiatry · 2025Article
- The effects of parental presence on amygdala and mPFC activation during fear conditioning: An exploratory study.Developmental science · 2024Article
- Social buffering in rats reduces fear by oxytocin triggering sustained changes in central amygdala neuronal activity.Nature communications · 2024Article
- Social buffering diminishes fear response but does not equal improved fear extinction.Cerebral cortex (New York, N.Y. : 1991) · 2023Article
- A novel social fear conditioning procedure alters social behavior and mTOR signaling in differentially housed adolescent rats.Developmental psychobiology · 2021Article
- Infant Trauma Alters Social Buffering of Threat Learning: Emerging Role of Prefrontal Cortex in Preadolescence.Frontiers in behavioral neuroscience · 2019Article
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Authors and funding
8 authors at 2 institutions in 1 country.
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Abstract
Extinction of contextual fear conditioning (CFC) in the presence of a familiar nonfearful conspecific (social support), such as that of others tasks, can occur regardless of whether the original memory is retrieved during the extinction training. Extinction with social support is blocked by the protein synthesis inhibitors anisomycin and rapamycin and by the inhibitor of gene expression 5,6-dichloro-1-β-d-ribofuranosylbenzimidazole infused immediately after extinction training into the ventromedial prefrontal cortex (vmPFC) but unlike regular CFC extinction not in the CA1 region of the dorsal hippocampus. So social support generates a form of learning that differs from extinction acquired without social support in terms of the brain structures involved. This finding may lead to a better understanding of the brain mechanisms involved in the social support of memories and in therapies for disorders related to dysfunctional fear memories. Thus, here we show that the consolidation of extinction memory with social support relies on vmPFC rather than hippocampus gene expression and ribosomal- and mammalian target of rapamycin-dependent protein synthesis. These results provide additional knowledge about the cellular mechanisms and brain structures involved on the effect of social support in changing behavior and fear extinction memory.
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