{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Kim JW"],"funding":["NICHD NIH HHS","NIMH NIH HHS","U.S. Department of Health & Human Services | NIH | National Institute of Mental Health","Elisabeth and Alfred Ahlqvist foundation within the Swedish Pharmaceutical Society and the Swedish Society for Medical Research","National Research Foundation of Korea (NRF) funded by the Ministry of Education"],"pagination":["1100-1109"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8338784"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["24(8)"],"pubmed_abstract":["The rapidly acting antidepressants ketamine and scopolamine exert behavioral effects that can last from several days to more than a week in some patients. The molecular mechanisms underlying the maintenance of these antidepressant effects are unknown. Here we show that methyl-CpG-binding protein 2 (MeCP2) phosphorylation at Ser421 (pMeCP2) is essential for the sustained, but not the rapid, antidepressant effects of ketamine and scopolamine in mice. Our results reveal that pMeCP2 is downstream of BDNF, a critical factor in ketamine and scopolamine antidepressant action. In addition, we show that pMeCP2 is required for the long-term regulation of synaptic strength after ketamine or scopolamine administration. These results demonstrate that pMeCP2 and associated synaptic plasticity are essential determinants of sustained antidepressant effects."],"journal":["Nature neuroscience"],"pubmed_title":["Sustained effects of rapidly acting antidepressants require BDNF-dependent MeCP2 phosphorylation."],"pmcid":["PMC8338784"],"funding_grant_id":["R56 MH081060","R01 MH066198","MH081060","P50 HD103537","MH066198","P50 HD105352","R01 MH081060","R01 MH070727"],"pubmed_authors":["Monteggia LM","Adachi M","Kavalali ET","Autry AE","Bjorkholm C","Kim JW","Na ES"],"additional_accession":[]},"is_claimable":false,"name":"Sustained effects of rapidly acting antidepressants require BDNF-dependent MeCP2 phosphorylation.","description":"The rapidly acting antidepressants ketamine and scopolamine exert behavioral effects that can last from several days to more than a week in some patients. The molecular mechanisms underlying the maintenance of these antidepressant effects are unknown. Here we show that methyl-CpG-binding protein 2 (MeCP2) phosphorylation at Ser421 (pMeCP2) is essential for the sustained, but not the rapid, antidepressant effects of ketamine and scopolamine in mice. Our results reveal that pMeCP2 is downstream of BDNF, a critical factor in ketamine and scopolamine antidepressant action. In addition, we show that pMeCP2 is required for the long-term regulation of synaptic strength after ketamine or scopolamine administration. These results demonstrate that pMeCP2 and associated synaptic plasticity are essential determinants of sustained antidepressant effects.","dates":{"release":"2021-01-01T00:00:00Z","publication":"2021 Aug","modification":"2025-04-05T10:04:22.2Z","creation":"2025-04-05T10:04:22.2Z"},"accession":"S-EPMC8338784","cross_references":{"pubmed":["34183865"],"doi":["10.1038/s41593-021-00868-8"]}}