Serotonin receptor 3A controls interneuron migration into the neocortex
Neuronal excitability has been shown to control the migration and cortical integration of reelin-expressing cortical interneurons (INs) arising from the caudal ganglionic eminence (CGE), supporting the possibility that neurotransmitters could regulate this process. Here we show that the ionotropic s...
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description | Neuronal excitability has been shown to control the migration and cortical integration of reelin-expressing cortical interneurons (INs) arising from the caudal ganglionic eminence (CGE), supporting the possibility that neurotransmitters could regulate this process. Here we show that the ionotropic serotonin receptor 3A (5-HT
3A
R) is specifically expressed in CGE-derived migrating interneurons and upregulated while they invade the developing cortex. Functional investigations using calcium imaging, electrophysiological recordings and migration assays indicate that CGE-derived INs increase their response to 5-HT
3A
R activation during the late phase of cortical plate invasion. Using genetic loss-of-function approaches and
in vivo
grafts, we further demonstrate that the 5-HT
3A
R is cell autonomously required for the migration and proper positioning of reelin-expressing CGE-derived INs in the neocortex. Our findings reveal a requirement for a serotonin receptor in controlling the migration and laminar positioning of a specific subtype of cortical IN.
During brain development, neuronal excitability controls the laminar migration of cortical interneurons from the caudal ganglionic eminences (CGEs). Here the authors identify the 5-HT
3A
receptor as a specific marker of CGE-derived cortical interneurons (cINs), and as a stimulator of cIN migration. |
doi_str_mv | 10.1038/ncomms6524 |
format | Article |
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3A
R) is specifically expressed in CGE-derived migrating interneurons and upregulated while they invade the developing cortex. Functional investigations using calcium imaging, electrophysiological recordings and migration assays indicate that CGE-derived INs increase their response to 5-HT
3A
R activation during the late phase of cortical plate invasion. Using genetic loss-of-function approaches and
in vivo
grafts, we further demonstrate that the 5-HT
3A
R is cell autonomously required for the migration and proper positioning of reelin-expressing CGE-derived INs in the neocortex. Our findings reveal a requirement for a serotonin receptor in controlling the migration and laminar positioning of a specific subtype of cortical IN.
During brain development, neuronal excitability controls the laminar migration of cortical interneurons from the caudal ganglionic eminences (CGEs). Here the authors identify the 5-HT
3A
receptor as a specific marker of CGE-derived cortical interneurons (cINs), and as a stimulator of cIN migration.</description><identifier>ISSN: 2041-1723</identifier><identifier>EISSN: 2041-1723</identifier><identifier>DOI: 10.1038/ncomms6524</identifier><identifier>PMID: 25409778</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>14/1 ; 14/19 ; 14/63 ; 38/61 ; 631/378/2571 ; 631/80/84 ; 631/80/86 ; 64/110 ; Animals ; Cell Adhesion Molecules, Neuronal - metabolism ; Cell Movement - genetics ; Extracellular Matrix Proteins - metabolism ; Gene expression ; Gene Expression Regulation, Developmental - genetics ; Humanities and Social Sciences ; Interneurons - metabolism ; Mice ; multidisciplinary ; Neocortex - embryology ; Neocortex - metabolism ; Nerve Tissue Proteins - metabolism ; Receptors, Serotonin, 5-HT3 - genetics ; Science ; Science (multidisciplinary) ; Serine Endopeptidases - metabolism ; Serotonin ; Transcription factors</subject><ispartof>Nature communications, 2014-11, Vol.5 (1), p.5524-5524, Article 5524</ispartof><rights>The Author(s) 2014</rights><rights>Copyright Nature Publishing Group Nov 2014</rights><rights>Copyright © 2014, Nature Publishing Group, a division of Macmillan Publishers Limited. All Rights Reserved. 2014 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-c442t-8f5295d526a16f654913732c0fa96f53fade74282af6139f26629f27a7db8b813</citedby><cites>FETCH-LOGICAL-c442t-8f5295d526a16f654913732c0fa96f53fade74282af6139f26629f27a7db8b813</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/PMC4263148/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4263148/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,41120,42189,51576,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25409778$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Murthy, Sahana</creatorcontrib><creatorcontrib>Niquille, Mathieu</creatorcontrib><creatorcontrib>Hurni, Nicolas</creatorcontrib><creatorcontrib>Limoni, Greta</creatorcontrib><creatorcontrib>Frazer, Sarah</creatorcontrib><creatorcontrib>Chameau, Pascal</creatorcontrib><creatorcontrib>van Hooft, Johannes A.</creatorcontrib><creatorcontrib>Vitalis, Tania</creatorcontrib><creatorcontrib>Dayer, Alexandre</creatorcontrib><title>Serotonin receptor 3A controls interneuron migration into the neocortex</title><title>Nature communications</title><addtitle>Nat Commun</addtitle><addtitle>Nat Commun</addtitle><description>Neuronal excitability has been shown to control the migration and cortical integration of reelin-expressing cortical interneurons (INs) arising from the caudal ganglionic eminence (CGE), supporting the possibility that neurotransmitters could regulate this process. Here we show that the ionotropic serotonin receptor 3A (5-HT
3A
R) is specifically expressed in CGE-derived migrating interneurons and upregulated while they invade the developing cortex. Functional investigations using calcium imaging, electrophysiological recordings and migration assays indicate that CGE-derived INs increase their response to 5-HT
3A
R activation during the late phase of cortical plate invasion. Using genetic loss-of-function approaches and
in vivo
grafts, we further demonstrate that the 5-HT
3A
R is cell autonomously required for the migration and proper positioning of reelin-expressing CGE-derived INs in the neocortex. Our findings reveal a requirement for a serotonin receptor in controlling the migration and laminar positioning of a specific subtype of cortical IN.
During brain development, neuronal excitability controls the laminar migration of cortical interneurons from the caudal ganglionic eminences (CGEs). Here the authors identify the 5-HT
3A
receptor as a specific marker of CGE-derived cortical interneurons (cINs), and as a stimulator of cIN migration.</description><subject>14/1</subject><subject>14/19</subject><subject>14/63</subject><subject>38/61</subject><subject>631/378/2571</subject><subject>631/80/84</subject><subject>631/80/86</subject><subject>64/110</subject><subject>Animals</subject><subject>Cell Adhesion Molecules, Neuronal - metabolism</subject><subject>Cell Movement - genetics</subject><subject>Extracellular Matrix Proteins - metabolism</subject><subject>Gene expression</subject><subject>Gene Expression Regulation, Developmental - genetics</subject><subject>Humanities and Social Sciences</subject><subject>Interneurons - metabolism</subject><subject>Mice</subject><subject>multidisciplinary</subject><subject>Neocortex - embryology</subject><subject>Neocortex - metabolism</subject><subject>Nerve Tissue Proteins - metabolism</subject><subject>Receptors, Serotonin, 5-HT3 - genetics</subject><subject>Science</subject><subject>Science (multidisciplinary)</subject><subject>Serine Endopeptidases - metabolism</subject><subject>Serotonin</subject><subject>Transcription factors</subject><issn>2041-1723</issn><issn>2041-1723</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</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>eNplkc1KAzEUhYMottRufAAZcCNKNX-TzGyEUrQKBRfqOqRp0k6ZSWqSEX17U1pr1SySS-7HuedyADhF8BpBUtxY5ZomsBzTA9DFkKIB4pgc7tUd0A9hCdMhJSooPQYdnFNYcl50wfhZexedrWzmtdKr6HxGhplyNnpXh6yyUXurW-9s1lRzL2OVqvTrsrjQmdVOOR_1xwk4MrIOur99e-D1_u5l9DCYPI0fR8PJQFGK46AwOS7zWY6ZRMywnJaIcIIVNLJkJidGzjSnuMDSMERKgxnD6eaSz6bFtECkB243uqt22uiZ0smnrMXKV430n8LJSvzu2Goh5u5dUMwIokUSuNgKePfW6hBFUwWl61qmXdogEMMccsg4Tej5H3TpWm_TemuKIc4hKhN1uaGUdyF4bXZmEBTriMRPRAk-27e_Q78DScDVBgipZefa7838L_cF5qucTg</recordid><startdate>20141120</startdate><enddate>20141120</enddate><creator>Murthy, Sahana</creator><creator>Niquille, Mathieu</creator><creator>Hurni, Nicolas</creator><creator>Limoni, Greta</creator><creator>Frazer, Sarah</creator><creator>Chameau, Pascal</creator><creator>van Hooft, Johannes A.</creator><creator>Vitalis, Tania</creator><creator>Dayer, Alexandre</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</general><general>Nature Pub. 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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>Murthy, Sahana</au><au>Niquille, Mathieu</au><au>Hurni, Nicolas</au><au>Limoni, Greta</au><au>Frazer, Sarah</au><au>Chameau, Pascal</au><au>van Hooft, Johannes A.</au><au>Vitalis, Tania</au><au>Dayer, Alexandre</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Serotonin receptor 3A controls interneuron migration into the neocortex</atitle><jtitle>Nature communications</jtitle><stitle>Nat Commun</stitle><addtitle>Nat Commun</addtitle><date>2014-11-20</date><risdate>2014</risdate><volume>5</volume><issue>1</issue><spage>5524</spage><epage>5524</epage><pages>5524-5524</pages><artnum>5524</artnum><issn>2041-1723</issn><eissn>2041-1723</eissn><abstract>Neuronal excitability has been shown to control the migration and cortical integration of reelin-expressing cortical interneurons (INs) arising from the caudal ganglionic eminence (CGE), supporting the possibility that neurotransmitters could regulate this process. Here we show that the ionotropic serotonin receptor 3A (5-HT
3A
R) is specifically expressed in CGE-derived migrating interneurons and upregulated while they invade the developing cortex. Functional investigations using calcium imaging, electrophysiological recordings and migration assays indicate that CGE-derived INs increase their response to 5-HT
3A
R activation during the late phase of cortical plate invasion. Using genetic loss-of-function approaches and
in vivo
grafts, we further demonstrate that the 5-HT
3A
R is cell autonomously required for the migration and proper positioning of reelin-expressing CGE-derived INs in the neocortex. Our findings reveal a requirement for a serotonin receptor in controlling the migration and laminar positioning of a specific subtype of cortical IN.
During brain development, neuronal excitability controls the laminar migration of cortical interneurons from the caudal ganglionic eminences (CGEs). Here the authors identify the 5-HT
3A
receptor as a specific marker of CGE-derived cortical interneurons (cINs), and as a stimulator of cIN migration.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>25409778</pmid><doi>10.1038/ncomms6524</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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subjects | 14/1 14/19 14/63 38/61 631/378/2571 631/80/84 631/80/86 64/110 Animals Cell Adhesion Molecules, Neuronal - metabolism Cell Movement - genetics Extracellular Matrix Proteins - metabolism Gene expression Gene Expression Regulation, Developmental - genetics Humanities and Social Sciences Interneurons - metabolism Mice multidisciplinary Neocortex - embryology Neocortex - metabolism Nerve Tissue Proteins - metabolism Receptors, Serotonin, 5-HT3 - genetics Science Science (multidisciplinary) Serine Endopeptidases - metabolism Serotonin Transcription factors |
title | Serotonin receptor 3A controls interneuron migration into the neocortex |
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