Sustained effects of rapidly acting antidepressants require BDNF-dependent MeCP2 phosphorylation
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 (...
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| Veröffentlicht in: | Nature neuroscience 2021-08, Vol.24 (8), p.1100-1109 |
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| creator | Kim, Ji-Woon Autry, Anita E. Na, Elisa S. Adachi, Megumi Björkholm, Carl Kavalali, Ege T. Monteggia, Lisa M. |
| 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.
How ketamine and scopolamine produce sustained antidepressant effects remains unknown. Kim et al. show that BDNF-dependent MeCP2 phosphorylation drives sustained antidepressant effects of ketamine and scopolamine with distinct synaptic plasticity changes. |
| doi_str_mv | 10.1038/s41593-021-00868-8 |
| format | Article |
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How ketamine and scopolamine produce sustained antidepressant effects remains unknown. Kim et al. show that BDNF-dependent MeCP2 phosphorylation drives sustained antidepressant effects of ketamine and scopolamine with distinct synaptic plasticity changes.</description><identifier>ISSN: 1097-6256</identifier><identifier>EISSN: 1546-1726</identifier><identifier>DOI: 10.1038/s41593-021-00868-8</identifier><identifier>PMID: 34183865</identifier><language>eng</language><publisher>New York: Nature Publishing Group US</publisher><subject>631/378 ; 631/378/1689/1414 ; 631/378/2591 ; 692/699 ; Animal Genetics and Genomics ; Animals ; Antidepressants ; Antidepressive Agents - pharmacology ; Behavioral Sciences ; Biological Techniques ; Biomedical and Life Sciences ; Biomedicine ; Brain - drug effects ; Brain - metabolism ; Brain-derived neurotrophic factor ; Brain-Derived Neurotrophic Factor - metabolism ; Chemical properties ; Ketamine ; Ketamine - pharmacology ; MeCP2 protein ; Methyl-CpG binding protein ; Methyl-CpG-Binding Protein 2 - metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Molecular modelling ; Neurobiology ; Neuronal Plasticity - drug effects ; Neuronal Plasticity - physiology ; Neurosciences ; Pharmacology, Experimental ; Phosphorylation ; Physiological aspects ; Plasticity ; Psychological aspects ; Scopolamine ; Scopolamine - pharmacology ; Synaptic plasticity ; Synaptic strength ; Transcription factors</subject><ispartof>Nature neuroscience, 2021-08, Vol.24 (8), p.1100-1109</ispartof><rights>The Author(s), under exclusive licence to Springer Nature America, Inc. 2021</rights><rights>2021. The Author(s), under exclusive licence to Springer Nature America, Inc.</rights><rights>COPYRIGHT 2021 Nature Publishing Group</rights><rights>The Author(s), under exclusive licence to Springer Nature America, Inc. 2021.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c641t-ca82527c3a24b175af8a010571f0488e65f5eb61007fc474785eb507eaafbcfe3</citedby><cites>FETCH-LOGICAL-c641t-ca82527c3a24b175af8a010571f0488e65f5eb61007fc474785eb507eaafbcfe3</cites><orcidid>0000-0003-3933-1977 ; 0000-0003-2730-789X ; 0000-0003-0018-501X ; 0000-0001-7236-9868</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/34183865$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kim, Ji-Woon</creatorcontrib><creatorcontrib>Autry, Anita E.</creatorcontrib><creatorcontrib>Na, Elisa S.</creatorcontrib><creatorcontrib>Adachi, Megumi</creatorcontrib><creatorcontrib>Björkholm, Carl</creatorcontrib><creatorcontrib>Kavalali, Ege T.</creatorcontrib><creatorcontrib>Monteggia, Lisa M.</creatorcontrib><title>Sustained effects of rapidly acting antidepressants require BDNF-dependent MeCP2 phosphorylation</title><title>Nature neuroscience</title><addtitle>Nat Neurosci</addtitle><addtitle>Nat Neurosci</addtitle><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.
How ketamine and scopolamine produce sustained antidepressant effects remains unknown. Kim et al. show that BDNF-dependent MeCP2 phosphorylation drives sustained antidepressant effects of ketamine and scopolamine with distinct synaptic plasticity changes.</description><subject>631/378</subject><subject>631/378/1689/1414</subject><subject>631/378/2591</subject><subject>692/699</subject><subject>Animal Genetics and Genomics</subject><subject>Animals</subject><subject>Antidepressants</subject><subject>Antidepressive Agents - pharmacology</subject><subject>Behavioral Sciences</subject><subject>Biological Techniques</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Brain - drug effects</subject><subject>Brain - metabolism</subject><subject>Brain-derived neurotrophic factor</subject><subject>Brain-Derived Neurotrophic Factor - metabolism</subject><subject>Chemical properties</subject><subject>Ketamine</subject><subject>Ketamine - pharmacology</subject><subject>MeCP2 protein</subject><subject>Methyl-CpG binding protein</subject><subject>Methyl-CpG-Binding Protein 2 - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Nature neuroscience</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kim, Ji-Woon</au><au>Autry, Anita E.</au><au>Na, Elisa S.</au><au>Adachi, Megumi</au><au>Björkholm, Carl</au><au>Kavalali, Ege T.</au><au>Monteggia, Lisa M.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Sustained effects of rapidly acting antidepressants require BDNF-dependent MeCP2 phosphorylation</atitle><jtitle>Nature neuroscience</jtitle><stitle>Nat Neurosci</stitle><addtitle>Nat Neurosci</addtitle><date>2021-08-01</date><risdate>2021</risdate><volume>24</volume><issue>8</issue><spage>1100</spage><epage>1109</epage><pages>1100-1109</pages><issn>1097-6256</issn><eissn>1546-1726</eissn><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.
How ketamine and scopolamine produce sustained antidepressant effects remains unknown. Kim et al. show that BDNF-dependent MeCP2 phosphorylation drives sustained antidepressant effects of ketamine and scopolamine with distinct synaptic plasticity changes.</abstract><cop>New York</cop><pub>Nature Publishing Group US</pub><pmid>34183865</pmid><doi>10.1038/s41593-021-00868-8</doi><tpages>10</tpages><orcidid>https://orcid.org/0000-0003-3933-1977</orcidid><orcidid>https://orcid.org/0000-0003-2730-789X</orcidid><orcidid>https://orcid.org/0000-0003-0018-501X</orcidid><orcidid>https://orcid.org/0000-0001-7236-9868</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | 631/378 631/378/1689/1414 631/378/2591 692/699 Animal Genetics and Genomics Animals Antidepressants Antidepressive Agents - pharmacology Behavioral Sciences Biological Techniques Biomedical and Life Sciences Biomedicine Brain - drug effects Brain - metabolism Brain-derived neurotrophic factor Brain-Derived Neurotrophic Factor - metabolism Chemical properties Ketamine Ketamine - pharmacology MeCP2 protein Methyl-CpG binding protein Methyl-CpG-Binding Protein 2 - metabolism Mice Mice, Inbred C57BL Mice, Knockout Molecular modelling Neurobiology Neuronal Plasticity - drug effects Neuronal Plasticity - physiology Neurosciences Pharmacology, Experimental Phosphorylation Physiological aspects Plasticity Psychological aspects Scopolamine Scopolamine - pharmacology Synaptic plasticity Synaptic strength Transcription factors |
| title | Sustained effects of rapidly acting antidepressants require BDNF-dependent MeCP2 phosphorylation |
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