MicroRNA miR124 is required for the expression of homeostatic synaptic plasticity
Homeostatic synaptic plasticity is a compensatory response to alterations in neuronal activity. Chronic deprivation of neuronal activity results in an increase in synaptic AMPA receptors (AMPARs) and postsynaptic currents. The biogenesis of GluA2-lacking, calcium-permeable AMPARs (CP-AMPARs) plays a...
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description | Homeostatic synaptic plasticity is a compensatory response to alterations in neuronal activity. Chronic deprivation of neuronal activity results in an increase in synaptic AMPA receptors (AMPARs) and postsynaptic currents. The biogenesis of GluA2-lacking, calcium-permeable AMPARs (CP-AMPARs) plays a crucial role in the homeostatic response; however, the mechanisms leading to CP-AMPAR formation remain unclear. Here we show that the microRNA, miR124, is required for the generation of CP-AMPARs and homeostatic plasticity. miR124 suppresses GluA2 expression via targeting its 3′-UTR, leading to the formation of CP-AMPARs. Blockade of miR124 function abolishes the homeostatic response, whereas miR124 overexpression leads to earlier induction of homeostatic plasticity. miR124 transcription is controlled by an inhibitory transcription factor EVI1, acting by association with the deacetylase HDAC1. Our data support a cellular cascade in which inactivity relieves EVI1/HDAC-mediated inhibition of miR124 gene transcription, resulting in enhanced miR124 expression, formation of CP-AMPARs and subsequent induction of homeostatic synaptic plasticity.
GluA2-lacking AMPA receptors are known to play a role in homeostatic plasticity. Here, the authors show that spiking activity blockade disinhibits mir124 transcription, which in turn suppresses GluA2 mRNA translation, thereby contributing to synaptic upscaling in hippocampal cells. |
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GluA2-lacking AMPA receptors are known to play a role in homeostatic plasticity. Here, the authors show that spiking activity blockade disinhibits mir124 transcription, which in turn suppresses GluA2 mRNA translation, thereby contributing to synaptic upscaling in hippocampal cells.</description><identifier>ISSN: 2041-1723</identifier><identifier>EISSN: 2041-1723</identifier><identifier>DOI: 10.1038/ncomms10045</identifier><identifier>PMID: 26620774</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>13 ; 13/109 ; 13/89 ; 631/337/384/331 ; 631/378/2591 ; 631/80/86 ; 82 ; 82/51 ; 9/74 ; Animals ; Hippocampus - cytology ; Hippocampus - metabolism ; Homeostasis ; Humanities and Social Sciences ; Humans ; MicroRNAs - genetics ; MicroRNAs - metabolism ; multidisciplinary ; Neuronal Plasticity ; Neurons - metabolism ; Rats, Sprague-Dawley ; Receptors, AMPA - genetics ; Receptors, AMPA - metabolism ; Science ; Science (multidisciplinary)</subject><ispartof>Nature communications, 2015-12, Vol.6 (1), p.10045-10045, Article 10045</ispartof><rights>The Author(s) 2015</rights><rights>Copyright Nature Publishing Group Dec 2015</rights><rights>Copyright © 2015, Nature Publishing Group, a division of Macmillan Publishers Limited. All Rights Reserved. 2015 Nature Publishing Group, a division of Macmillan Publishers Limited. All Rights Reserved.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c554t-5d8c9dd5053bf693c4e8434d739a9bd63129c280fc70583f91744cfa512ba10c3</citedby><cites>FETCH-LOGICAL-c554t-5d8c9dd5053bf693c4e8434d739a9bd63129c280fc70583f91744cfa512ba10c3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4686673/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4686673/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,27924,27925,41120,42189,51576,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26620774$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hou, Qingming</creatorcontrib><creatorcontrib>Ruan, Hongyu</creatorcontrib><creatorcontrib>Gilbert, James</creatorcontrib><creatorcontrib>Wang, Guan</creatorcontrib><creatorcontrib>Ma, Qi</creatorcontrib><creatorcontrib>Yao, Wei-Dong</creatorcontrib><creatorcontrib>Man, Heng-Ye</creatorcontrib><title>MicroRNA miR124 is required for the expression of homeostatic synaptic plasticity</title><title>Nature communications</title><addtitle>Nat Commun</addtitle><addtitle>Nat Commun</addtitle><description>Homeostatic synaptic plasticity is a compensatory response to alterations in neuronal activity. Chronic deprivation of neuronal activity results in an increase in synaptic AMPA receptors (AMPARs) and postsynaptic currents. The biogenesis of GluA2-lacking, calcium-permeable AMPARs (CP-AMPARs) plays a crucial role in the homeostatic response; however, the mechanisms leading to CP-AMPAR formation remain unclear. Here we show that the microRNA, miR124, is required for the generation of CP-AMPARs and homeostatic plasticity. miR124 suppresses GluA2 expression via targeting its 3′-UTR, leading to the formation of CP-AMPARs. Blockade of miR124 function abolishes the homeostatic response, whereas miR124 overexpression leads to earlier induction of homeostatic plasticity. miR124 transcription is controlled by an inhibitory transcription factor EVI1, acting by association with the deacetylase HDAC1. Our data support a cellular cascade in which inactivity relieves EVI1/HDAC-mediated inhibition of miR124 gene transcription, resulting in enhanced miR124 expression, formation of CP-AMPARs and subsequent induction of homeostatic synaptic plasticity.
GluA2-lacking AMPA receptors are known to play a role in homeostatic plasticity. Here, the authors show that spiking activity blockade disinhibits mir124 transcription, which in turn suppresses GluA2 mRNA translation, thereby contributing to synaptic upscaling in hippocampal cells.</description><subject>13</subject><subject>13/109</subject><subject>13/89</subject><subject>631/337/384/331</subject><subject>631/378/2591</subject><subject>631/80/86</subject><subject>82</subject><subject>82/51</subject><subject>9/74</subject><subject>Animals</subject><subject>Hippocampus - cytology</subject><subject>Hippocampus - metabolism</subject><subject>Homeostasis</subject><subject>Humanities and Social Sciences</subject><subject>Humans</subject><subject>MicroRNAs - genetics</subject><subject>MicroRNAs - metabolism</subject><subject>multidisciplinary</subject><subject>Neuronal Plasticity</subject><subject>Neurons - metabolism</subject><subject>Rats, Sprague-Dawley</subject><subject>Receptors, AMPA - genetics</subject><subject>Receptors, AMPA - metabolism</subject><subject>Science</subject><subject>Science (multidisciplinary)</subject><issn>2041-1723</issn><issn>2041-1723</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNptkctLxDAQxoMoKuuevEvAi6DVpEma9CIs4gt8oOg5pGnqRtqmJq24_71Zd5VVnMsMzI9vHh8AuxgdY0TESatd0wSMEGVrYDtFFCeYp2R9pd4C4xBeUQySY0HpJthKsyxFnNNt8HBrtXePdxPY2EecUmgD9OZtsN6UsHIe9lMDzUfnTQjWtdBVcOoa40KveqthmLWqmxddrULMtp_tgI1K1cGMl3kEni_On86ukpv7y-uzyU2iGaN9wkqh87JkiJGiynKiqRGU0JKTXOVFmRGc5joVqNIcMUGqHHNKdaUYTguFkSYjcLrQ7YaiMaU2be9VLTtvG-Vn0ikrf3daO5Uv7l3STGQZJ1HgYCng3dtgQi8bG7Spa9UaNwSJORECU4qziO7_QV_d4Nt43hcVP8s4jdThgoofDcGb6mcZjOTcLbniVqT3Vvf_Yb-9icDRAgix1b4YvzL0H71PMh6f1Q</recordid><startdate>20151201</startdate><enddate>20151201</enddate><creator>Hou, Qingming</creator><creator>Ruan, Hongyu</creator><creator>Gilbert, James</creator><creator>Wang, Guan</creator><creator>Ma, Qi</creator><creator>Yao, Wei-Dong</creator><creator>Man, Heng-Ye</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</general><scope>C6C</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QL</scope><scope>7QP</scope><scope>7QR</scope><scope>7SN</scope><scope>7SS</scope><scope>7ST</scope><scope>7T5</scope><scope>7T7</scope><scope>7TM</scope><scope>7TO</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>RC3</scope><scope>SOI</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20151201</creationdate><title>MicroRNA miR124 is required for the expression of homeostatic synaptic plasticity</title><author>Hou, Qingming ; Ruan, Hongyu ; Gilbert, James ; Wang, Guan ; Ma, Qi ; Yao, Wei-Dong ; Man, Heng-Ye</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c554t-5d8c9dd5053bf693c4e8434d739a9bd63129c280fc70583f91744cfa512ba10c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>13</topic><topic>13/109</topic><topic>13/89</topic><topic>631/337/384/331</topic><topic>631/378/2591</topic><topic>631/80/86</topic><topic>82</topic><topic>82/51</topic><topic>9/74</topic><topic>Animals</topic><topic>Hippocampus - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Nature communications</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hou, Qingming</au><au>Ruan, Hongyu</au><au>Gilbert, James</au><au>Wang, Guan</au><au>Ma, Qi</au><au>Yao, Wei-Dong</au><au>Man, Heng-Ye</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>MicroRNA miR124 is required for the expression of homeostatic synaptic plasticity</atitle><jtitle>Nature communications</jtitle><stitle>Nat Commun</stitle><addtitle>Nat Commun</addtitle><date>2015-12-01</date><risdate>2015</risdate><volume>6</volume><issue>1</issue><spage>10045</spage><epage>10045</epage><pages>10045-10045</pages><artnum>10045</artnum><issn>2041-1723</issn><eissn>2041-1723</eissn><abstract>Homeostatic synaptic plasticity is a compensatory response to alterations in neuronal activity. Chronic deprivation of neuronal activity results in an increase in synaptic AMPA receptors (AMPARs) and postsynaptic currents. The biogenesis of GluA2-lacking, calcium-permeable AMPARs (CP-AMPARs) plays a crucial role in the homeostatic response; however, the mechanisms leading to CP-AMPAR formation remain unclear. Here we show that the microRNA, miR124, is required for the generation of CP-AMPARs and homeostatic plasticity. miR124 suppresses GluA2 expression via targeting its 3′-UTR, leading to the formation of CP-AMPARs. Blockade of miR124 function abolishes the homeostatic response, whereas miR124 overexpression leads to earlier induction of homeostatic plasticity. miR124 transcription is controlled by an inhibitory transcription factor EVI1, acting by association with the deacetylase HDAC1. Our data support a cellular cascade in which inactivity relieves EVI1/HDAC-mediated inhibition of miR124 gene transcription, resulting in enhanced miR124 expression, formation of CP-AMPARs and subsequent induction of homeostatic synaptic plasticity.
GluA2-lacking AMPA receptors are known to play a role in homeostatic plasticity. Here, the authors show that spiking activity blockade disinhibits mir124 transcription, which in turn suppresses GluA2 mRNA translation, thereby contributing to synaptic upscaling in hippocampal cells.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>26620774</pmid><doi>10.1038/ncomms10045</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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subjects | 13 13/109 13/89 631/337/384/331 631/378/2591 631/80/86 82 82/51 9/74 Animals Hippocampus - cytology Hippocampus - metabolism Homeostasis Humanities and Social Sciences Humans MicroRNAs - genetics MicroRNAs - metabolism multidisciplinary Neuronal Plasticity Neurons - metabolism Rats, Sprague-Dawley Receptors, AMPA - genetics Receptors, AMPA - metabolism Science Science (multidisciplinary) |
title | MicroRNA miR124 is required for the expression of homeostatic synaptic plasticity |
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