Extinction learning with social support depends on protein synthesis in prefrontal cortex but not hippocampus

• Published in: Proceedings of the National Academy of Sciences - PNAS 2019-01, Vol.116 (5), p.1765-1769
• Main Authors: Farias, Clarissa Penha, Furini, Cristiane Regina Guerino, Nachtigall, Eduarda Godfried, Behling, Jonny Anderson Kielbovicz, de Assis Brasil, Eduardo Silva, Bühler, Letícia, Izquierdo, Ivan, de Carvalho Myskiw, Jociane
• Format: Article
• Language: English
• Subjects: Animals; Anisomycin; Anisomycin - pharmacology; Biological Sciences; Brain; Cellular structure; Extinction, Psychological - drug effects; Extinction, Psychological - physiology; Fear; Fear - drug effects; Fear - physiology; Fear conditioning; Gene expression; Gene Expression - drug effects; Hippocampus; Hippocampus - drug effects; Hippocampus - physiology; Learning - drug effects; Learning - physiology; Male; Memory - drug effects; Memory - physiology; Prefrontal cortex; Prefrontal Cortex - drug effects; Prefrontal Cortex - physiology; Protein biosynthesis; Protein Biosynthesis - drug effects; Protein Biosynthesis - physiology; Protein synthesis; Proteins; Rapamycin; Rats, Wistar; Sirolimus - pharmacology; Social behavior; Social discrimination learning; Social interactions; Social Support; TOR protein; Training
• ISSN: 0027-8424; 1091-6490; 1091-6490
• DOI: 10.1073/pnas.1815893116

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.