{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Chen B"],"funding":["Massachusetts Institute of Technology","NIDCR NIH HHS","Jane Coffin Childs Memorial Fund for Medical Research","NIH"],"pagination":["4261-4271.e5"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12093384"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["34(18)"],"pubmed_abstract":["Placebo analgesia is a widely observed clinical phenomenon. Establishing a robust mouse model of placebo analgesia is needed for careful dissection of the underpinning circuit mechanisms. However, previous studies failed to observe consistent placebo effects in rodent models of chronic pain. We wondered whether strong placebo analgesia can be reverse engineered using general-anesthesia-activated neurons in the central amygdala (CeA<sub>GA</sub>) that can potently suppress pain. Indeed, in both acute and chronic pain models, pairing a context with CeA<sub>GA</sub>-mediated pain relief produced robust context-dependent analgesia, exceeding that produced by morphine in the same paradigm. CeA<sub>GA</sub> neurons receive monosynaptic inputs from temporal lobe areas that could potentially relay"],"journal":["Current biology : CB"],"pubmed_title":["Reverse-engineering placebo analgesia."],"pmcid":["PMC12093384"],"funding_grant_id":["DE029342","R01 DE029342"],"pubmed_authors":["Choi S","Zhao S","Dziubek J","Wang F","Chen B","Goldstein N","Harrahill A","Sundai A","Prevosto V"],"additional_accession":[]},"is_claimable":false,"name":"Reverse-engineering placebo analgesia.","description":"Placebo analgesia is a widely observed clinical phenomenon. Establishing a robust mouse model of placebo analgesia is needed for careful dissection of the underpinning circuit mechanisms. However, previous studies failed to observe consistent placebo effects in rodent models of chronic pain. We wondered whether strong placebo analgesia can be reverse engineered using general-anesthesia-activated neurons in the central amygdala (CeA<sub>GA</sub>) that can potently suppress pain. Indeed, in both acute and chronic pain models, pairing a context with CeA<sub>GA</sub>-mediated pain relief produced robust context-dependent analgesia, exceeding that produced by morphine in the same paradigm. CeA<sub>GA</sub> neurons receive monosynaptic inputs from temporal lobe areas that could potentially relay","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Sep","modification":"2026-06-03T16:54:59.137Z","creation":"2026-06-03T03:07:39.306Z"},"accession":"S-EPMC12093384","cross_references":{"pubmed":["39241777"],"doi":["10.1016/j.cub.2024.08.004"]}}