Characterization of the glycinergic input to bipolar cells of the mouse retina
Identifieur interne : 001268 ( Main/Corpus ); précédent : 001267; suivant : 001269Characterization of the glycinergic input to bipolar cells of the mouse retina
Auteurs : Elena Ivanova ; Ulrike Müller ; Heinz W SsleSource :
- European Journal of Neuroscience [ 0953-816X ] ; 2006-01.
English descriptors
Abstract
Glycine and γ‐aminobutyric acid (GABA) are the major inhibitory transmitters of the mammalian retina, and bipolar cells receive GABAergic and glycinergic inhibition from multiple amacrine cell types. Here we evaluated the functional properties and subunit composition of glycine receptors (GlyRs) in bipolar cells. Patch‐clamp recordings were performed from retinal slices of wild‐type, GlyRα1‐deficient (Glra1spd‐ot) and GlyRα3‐deficient (Glra3–/–) mice. Whole‐cell currents following glycine application and spontaneous inhibitory postsynaptic currents (IPSCs) were analysed. During the recordings the cells were filled with Alexa 488 and, thus, unequivocally identified. Glycine‐induced currents of bipolar cells were picrotoxinin‐insensitive and thus represent heteromeric channels composed of α and β subunits. Glycine‐induced currents and IPSCs were absent from all bipolar cells of Glra1spd‐ot mice, indicating that GlyRα1 is an essential subunit of bipolar cell GlyRs. By comparing IPSCs of bipolar cells in wild‐type and Glra3–/– mice, no statistically significant differences were found. OFF‐cone bipolar (CB) cells receive a strong glycinergic input from AII amacrine cells, that is preferentially based on the fast α1β‐containing channels (mean decay time constant τ = 5.9 ± 1.4 ms). We did not observe glycinergic IPSCs in ON‐CB cells and could elicit only small, if any, glycinergic currents. Rod bipolar cells receive a prominent glycinergic input that is mainly mediated by α1β‐containing channels (τ = 5.5 ± 1.6 ms). Slow IPSCs, the characteristic of GlyRs containing the α2 subunit, were not observed in bipolar cells. Thus, different bipolar cell types receive kinetically fast glycinergic inputs, preferentially mediated by GlyRs composed of α1 and β subunits.
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DOI: 10.1111/j.1460-9568.2005.04557.x
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Here we evaluated the functional properties and subunit composition of glycine receptors (GlyRs) in bipolar cells. Patch‐clamp recordings were performed from retinal slices of wild‐type, GlyRα1‐deficient (Glra1spd‐ot) and GlyRα3‐deficient (Glra3–/–) mice. Whole‐cell currents following glycine application and spontaneous inhibitory postsynaptic currents (IPSCs) were analysed. During the recordings the cells were filled with Alexa 488 and, thus, unequivocally identified. Glycine‐induced currents of bipolar cells were picrotoxinin‐insensitive and thus represent heteromeric channels composed of α and β subunits. Glycine‐induced currents and IPSCs were absent from all bipolar cells of Glra1spd‐ot mice, indicating that GlyRα1 is an essential subunit of bipolar cell GlyRs. By comparing IPSCs of bipolar cells in wild‐type and Glra3–/– mice, no statistically significant differences were found. OFF‐cone bipolar (CB) cells receive a strong glycinergic input from AII amacrine cells, that is preferentially based on the fast α1β‐containing channels (mean decay time constant τ = 5.9 ± 1.4 ms). We did not observe glycinergic IPSCs in ON‐CB cells and could elicit only small, if any, glycinergic currents. Rod bipolar cells receive a prominent glycinergic input that is mainly mediated by α1β‐containing channels (τ = 5.5 ± 1.6 ms). Slow IPSCs, the characteristic of GlyRs containing the α2 subunit, were not observed in bipolar cells. Thus, different bipolar cell types receive kinetically fast glycinergic inputs, preferentially mediated by GlyRs composed of α1 and β subunits.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Elena Ivanova</name><affiliations><json:string>Department Neuroanatomy, Max‐Planck‐Institute for Brain Research, Frankfurt/Main, Germany</json:string></affiliations></json:item><json:item><name>Ulrike Müller</name><affiliations><json:string>Department Neurochemistry, Max‐Planck‐Institute for Brain Research, Frankfurt/Main, Germany</json:string></affiliations></json:item><json:item><name>Heinz Wässle</name><affiliations><json:string>Department Neuroanatomy, Max‐Planck‐Institute for Brain Research, Frankfurt/Main, Germany</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Glra1 spd‐ot mouse</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Glra3–/– mouse</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>glycine receptors</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>glycinergic IPSCs</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>retina</value></json:item></subject><language><json:string>eng</json:string></language><abstract>Glycine and γ‐aminobutyric acid (GABA) are the major inhibitory transmitters of the mammalian retina, and bipolar cells receive GABAergic and glycinergic inhibition from multiple amacrine cell types. Here we evaluated the functional properties and subunit composition of glycine receptors (GlyRs) in bipolar cells. Patch‐clamp recordings were performed from retinal slices of wild‐type, GlyRα1‐deficient (Glra1spd‐ot) and GlyRα3‐deficient (Glra3–/–) mice. Whole‐cell currents following glycine application and spontaneous inhibitory postsynaptic currents (IPSCs) were analysed. During the recordings the cells were filled with Alexa 488 and, thus, unequivocally identified. Glycine‐induced currents of bipolar cells were picrotoxinin‐insensitive and thus represent heteromeric channels composed of α and β subunits. Glycine‐induced currents and IPSCs were absent from all bipolar cells of Glra1spd‐ot mice, indicating that GlyRα1 is an essential subunit of bipolar cell GlyRs. By comparing IPSCs of bipolar cells in wild‐type and Glra3–/– mice, no statistically significant differences were found. OFF‐cone bipolar (CB) cells receive a strong glycinergic input from AII amacrine cells, that is preferentially based on the fast α1β‐containing channels (mean decay time constant τ = 5.9 ± 1.4 ms). We did not observe glycinergic IPSCs in ON‐CB cells and could elicit only small, if any, glycinergic currents. Rod bipolar cells receive a prominent glycinergic input that is mainly mediated by α1β‐containing channels (τ = 5.5 ± 1.6 ms). Slow IPSCs, the characteristic of GlyRs containing the α2 subunit, were not observed in bipolar cells. 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Here we evaluated the functional properties and subunit composition of glycine receptors (GlyRs) in bipolar cells. Patch‐clamp recordings were performed from retinal slices of wild‐type, GlyRα1‐deficient (Glra1spd‐ot) and GlyRα3‐deficient (Glra3–/–) mice. Whole‐cell currents following glycine application and spontaneous inhibitory postsynaptic currents (IPSCs) were analysed. During the recordings the cells were filled with Alexa 488 and, thus, unequivocally identified. Glycine‐induced currents of bipolar cells were picrotoxinin‐insensitive and thus represent heteromeric channels composed of α and β subunits. Glycine‐induced currents and IPSCs were absent from all bipolar cells of Glra1spd‐ot mice, indicating that GlyRα1 is an essential subunit of bipolar cell GlyRs. By comparing IPSCs of bipolar cells in wild‐type and Glra3–/– mice, no statistically significant differences were found. OFF‐cone bipolar (CB) cells receive a strong glycinergic input from AII amacrine cells, that is preferentially based on the fast α1β‐containing channels (mean decay time constant τ = 5.9 ± 1.4 ms). We did not observe glycinergic IPSCs in ON‐CB cells and could elicit only small, if any, glycinergic currents. Rod bipolar cells receive a prominent glycinergic input that is mainly mediated by α1β‐containing channels (τ = 5.5 ± 1.6 ms). Slow IPSCs, the characteristic of GlyRs containing the α2 subunit, were not observed in bipolar cells. Thus, different bipolar cell types receive kinetically fast glycinergic inputs, preferentially mediated by GlyRs composed of α1 and β subunits.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>Glra1 spd‐ot mouse</term></item><item><term>Glra3–/– mouse</term></item><item><term>glycine receptors</term></item><item><term>glycinergic IPSCs</term></item><item><term>retina</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2006-01">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/C55C3672B7F62719CA6978EAB0488E5B18165E74/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component version="2.0" type="serialArticle" xml:lang="en"><header><publicationMeta level="product"><publisherInfo><publisherName>Blackwell Publishing Ltd</publisherName><publisherLoc>Oxford, UK</publisherLoc></publisherInfo><doi origin="wiley" registered="yes">10.1111/(ISSN)1460-9568</doi><issn type="print">0953-816X</issn><issn type="electronic">1460-9568</issn><idGroup><id type="product" value="EJN"></id><id type="publisherDivision" value="ST"></id></idGroup><titleGroup><title type="main" sort="EUROPEAN JOURNAL OF NEUROSCIENCE">European Journal of Neuroscience</title></titleGroup></publicationMeta><publicationMeta level="part" position="01002"><doi origin="wiley">10.1111/ejn.2006.23.issue-2</doi><numberingGroup><numbering type="journalVolume" number="23">23</numbering><numbering type="journalIssue" number="2">2</numbering></numberingGroup><coverDate startDate="2006-01">January 2006</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="6" status="forIssue"><doi origin="wiley">10.1111/j.1460-9568.2005.04557.x</doi><idGroup><id type="unit" value="EJN4557"></id></idGroup><countGroup><count type="pageTotal" number="15"></count></countGroup><titleGroup><title type="tocHeading1">Research Reports</title></titleGroup><eventGroup><event type="firstOnline" date="2006-01-18"></event><event type="publishedOnlineFinalForm" date="2006-01-18"></event><event type="xmlConverted" agent="Converter:BPG_TO_WML3G version:2.3.12 mode:FullText" date="2010-07-12"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:4.0.1" date="2014-03-12"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-10-16"></event></eventGroup><numberingGroup><numbering type="pageFirst" number="350">350</numbering><numbering type="pageLast" number="364">364</numbering></numberingGroup><correspondenceTo>Dr H. Wässle, as above.
E‐mail: <email normalForm="waessle@mpih-frankfurt.mpg.de">waessle@mpih‐frankfurt.mpg.de</email></correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:EJN.EJN4557.pdf"></link></linkGroup></publicationMeta><contentMeta><unparsedEditorialHistory>Received 26 September 2005, revised 10 November 2005, accepted 15 November 2005</unparsedEditorialHistory><countGroup><count type="figureTotal" number="7"></count><count type="tableTotal" number="0"></count><count type="formulaTotal" number="0"></count><count type="referenceTotal" number="75"></count><count type="wordTotal" number="12290"></count><count type="linksPubMed" number="0"></count><count type="linksCrossRef" number="0"></count></countGroup><titleGroup><title type="main">Characterization of the glycinergic input to bipolar cells of the mouse retina</title><title type="shortAuthors">E. Ivanova <i>et al</i>.</title><title type="short">Bipolar cell glycinergic input</title></titleGroup><creators><creator creatorRole="author" xml:id="cr1" affiliationRef="#a1"><personName><givenNames>Elena</givenNames><familyName>Ivanova</familyName></personName></creator><creator creatorRole="author" xml:id="cr2" affiliationRef="#a2"><personName><givenNames>Ulrike</givenNames><familyName>Müller</familyName></personName></creator><creator creatorRole="author" xml:id="cr3" affiliationRef="#a1"><personName><givenNames>Heinz</givenNames><familyName>Wässle</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="a1" countryCode="DE"><unparsedAffiliation>Department Neuroanatomy, Max‐Planck‐Institute for Brain Research, Frankfurt/Main, Germany</unparsedAffiliation></affiliation><affiliation xml:id="a2" countryCode="DE"><unparsedAffiliation>Department Neurochemistry, Max‐Planck‐Institute for Brain Research, Frankfurt/Main, Germany</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en"><keyword xml:id="k1"><i>Glra1</i><sup><i>spd‐ot</i></sup> mouse</keyword><keyword xml:id="k2"><i>Glra3</i><sup>–</sup>/<sup>–</sup> mouse</keyword><keyword xml:id="k3">glycine receptors</keyword><keyword xml:id="k4">glycinergic IPSCs</keyword><keyword xml:id="k5">retina</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>Glycine and γ‐aminobutyric acid (GABA) are the major inhibitory transmitters of the mammalian retina, and bipolar cells receive GABAergic and glycinergic inhibition from multiple amacrine cell types. Here we evaluated the functional properties and subunit composition of glycine receptors (GlyRs) in bipolar cells. Patch‐clamp recordings were performed from retinal slices of wild‐type, GlyRα1‐deficient (<i>Glra1</i><sup><i>spd‐ot</i></sup>) and GlyRα3‐deficient (<i>Glra3</i><sup><i>–/–</i></sup>) mice. Whole‐cell currents following glycine application and spontaneous inhibitory postsynaptic currents (IPSCs) were analysed. During the recordings the cells were filled with Alexa 488 and, thus, unequivocally identified. Glycine‐induced currents of bipolar cells were picrotoxinin‐insensitive and thus represent heteromeric channels composed of α and β subunits. Glycine‐induced currents and IPSCs were absent from all bipolar cells of <i>Glra1</i><sup><i>spd‐ot</i></sup> mice, indicating that GlyRα1 is an essential subunit of bipolar cell GlyRs. By comparing IPSCs of bipolar cells in wild‐type and <i>Glra3</i><sup><i>–/–</i></sup> mice, no statistically significant differences were found. OFF‐cone bipolar (CB) cells receive a strong glycinergic input from AII amacrine cells, that is preferentially based on the fast α1β‐containing channels (mean decay time constant τ = 5.9 ± 1.4 ms). We did not observe glycinergic IPSCs in ON‐CB cells and could elicit only small, if any, glycinergic currents. Rod bipolar cells receive a prominent glycinergic input that is mainly mediated by α1β‐containing channels (τ = 5.5 ± 1.6 ms). Slow IPSCs, the characteristic of GlyRs containing the α2 subunit, were not observed in bipolar cells. Thus, different bipolar cell types receive kinetically fast glycinergic inputs, preferentially mediated by GlyRs composed of α1 and β subunits.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Characterization of the glycinergic input to bipolar cells of the mouse retina</title></titleInfo><titleInfo type="abbreviated"><title>Bipolar cell glycinergic input</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Characterization of the glycinergic input to bipolar cells of the mouse retina</title></titleInfo><name type="personal"><namePart type="given">Elena</namePart><namePart type="family">Ivanova</namePart><affiliation>Department Neuroanatomy, Max‐Planck‐Institute for Brain Research, Frankfurt/Main, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Ulrike</namePart><namePart type="family">Müller</namePart><affiliation>Department Neurochemistry, Max‐Planck‐Institute for Brain Research, Frankfurt/Main, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Heinz</namePart><namePart type="family">Wässle</namePart><affiliation>Department Neuroanatomy, Max‐Planck‐Institute for Brain Research, Frankfurt/Main, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>Blackwell Publishing Ltd</publisher><place><placeTerm type="text">Oxford, UK</placeTerm></place><dateIssued encoding="w3cdtf">2006-01</dateIssued><edition>Received 26 September 2005, revised 10 November 2005, accepted 15 November 2005</edition><copyrightDate encoding="w3cdtf">2006</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType><extent unit="figures">7</extent><extent unit="references">75</extent><extent unit="words">12290</extent></physicalDescription><abstract lang="en">Glycine and γ‐aminobutyric acid (GABA) are the major inhibitory transmitters of the mammalian retina, and bipolar cells receive GABAergic and glycinergic inhibition from multiple amacrine cell types. Here we evaluated the functional properties and subunit composition of glycine receptors (GlyRs) in bipolar cells. Patch‐clamp recordings were performed from retinal slices of wild‐type, GlyRα1‐deficient (Glra1spd‐ot) and GlyRα3‐deficient (Glra3–/–) mice. Whole‐cell currents following glycine application and spontaneous inhibitory postsynaptic currents (IPSCs) were analysed. During the recordings the cells were filled with Alexa 488 and, thus, unequivocally identified. Glycine‐induced currents of bipolar cells were picrotoxinin‐insensitive and thus represent heteromeric channels composed of α and β subunits. Glycine‐induced currents and IPSCs were absent from all bipolar cells of Glra1spd‐ot mice, indicating that GlyRα1 is an essential subunit of bipolar cell GlyRs. By comparing IPSCs of bipolar cells in wild‐type and Glra3–/– mice, no statistically significant differences were found. OFF‐cone bipolar (CB) cells receive a strong glycinergic input from AII amacrine cells, that is preferentially based on the fast α1β‐containing channels (mean decay time constant τ = 5.9 ± 1.4 ms). We did not observe glycinergic IPSCs in ON‐CB cells and could elicit only small, if any, glycinergic currents. Rod bipolar cells receive a prominent glycinergic input that is mainly mediated by α1β‐containing channels (τ = 5.5 ± 1.6 ms). Slow IPSCs, the characteristic of GlyRs containing the α2 subunit, were not observed in bipolar cells. Thus, different bipolar cell types receive kinetically fast glycinergic inputs, preferentially mediated by GlyRs composed of α1 and β subunits.</abstract><subject lang="en"><genre>Keywords</genre><topic>Glra1 spd‐ot mouse</topic><topic>Glra3–/– mouse</topic><topic>glycine receptors</topic><topic>glycinergic IPSCs</topic><topic>retina</topic></subject><relatedItem type="host"><titleInfo><title>European Journal of Neuroscience</title></titleInfo><genre type="Journal">journal</genre><identifier type="ISSN">0953-816X</identifier><identifier type="eISSN">1460-9568</identifier><identifier type="DOI">10.1111/(ISSN)1460-9568</identifier><identifier type="PublisherID">EJN</identifier><part><date>2006</date><detail type="volume"><caption>vol.</caption><number>23</number></detail><detail type="issue"><caption>no.</caption><number>2</number></detail><extent unit="pages"><start>350</start><end>364</end><total>15</total></extent></part></relatedItem><identifier type="istex">C55C3672B7F62719CA6978EAB0488E5B18165E74</identifier><identifier type="DOI">10.1111/j.1460-9568.2005.04557.x</identifier><identifier type="ArticleID">EJN4557</identifier><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Blackwell Publishing Ltd</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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