Influence of Binocular Competition on the Expression Profiles of CRMP2, CRMP4, Dyn I, and Syt I in Developing Cat Visual Cortex
Identifieur interne : 001836 ( Istex/Corpus ); précédent : 001835; suivant : 001837Influence of Binocular Competition on the Expression Profiles of CRMP2, CRMP4, Dyn I, and Syt I in Developing Cat Visual Cortex
Auteurs : Lieselotte Cnops ; Tjing-Tjing Hu ; Kalina Burnat ; Lutgarde ArckensSource :
- Cerebral Cortex [ 1047-3211 ] ; 2007-10-19.
Abstract
The visual cortex is vulnerable to changes in visual input, especially during the critical period when numerous molecules drive the refinement of the circuitry. From a list of potential actors identified in a recent proteomics study, we selected 2 collapsin response mediator proteins (CRMP2/CRMP4) and 2 synaptic proteins, Dynamin I (Dyn I) and Synaptotagmin I (Syt I), for in-depth analysis of their developmental expression profile in cat visual cortex. CRMP2 and CRMP4 levels were high early in life and clearly declined toward adulthood. In contrast, Dyn I expression levels progressively augmented during maturation. Syt I showed low levels at eye opening and in adults, high levels around the peak of the critical period, and maximal levels at juvenile age. We further determined a role for each molecule in ocular dominance plasticity. CRMP2 and Syt I levels decreased in area 17 upon monocular deprivation, whereas CRMP4 and Dyn I levels remained unaffected. In contrast, binocular removal of pattern vision had no influence on CRMP2 and Syt I expression in kitten area 17. This study illustrates that not the loss of quality of vision through visual deprivation, but disruption of normal binocular visual experience is crucial to induce the observed molecular changes.
Url:
DOI: 10.1093/cercor/bhm157
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From a list of potential actors identified in a recent proteomics study, we selected 2 collapsin response mediator proteins (CRMP2/CRMP4) and 2 synaptic proteins, Dynamin I (Dyn I) and Synaptotagmin I (Syt I), for in-depth analysis of their developmental expression profile in cat visual cortex. CRMP2 and CRMP4 levels were high early in life and clearly declined toward adulthood. In contrast, Dyn I expression levels progressively augmented during maturation. Syt I showed low levels at eye opening and in adults, high levels around the peak of the critical period, and maximal levels at juvenile age. We further determined a role for each molecule in ocular dominance plasticity. CRMP2 and Syt I levels decreased in area 17 upon monocular deprivation, whereas CRMP4 and Dyn I levels remained unaffected. In contrast, binocular removal of pattern vision had no influence on CRMP2 and Syt I expression in kitten area 17. 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Email: <email>Lut.Arckens@bio.kuleuven.be</email>.</corresp></author-notes><pub-date pub-type="epub-ppub"><month>5</month><year>2008</year></pub-date><pub-date pub-type="epub"><day>19</day><month>10</month><year>2007</year></pub-date><volume>18</volume><issue>5</issue><fpage>1221</fpage><lpage>1231</lpage><permissions><copyright-statement>© 2007 The Authors</copyright-statement><copyright-year>2008</copyright-year><license license-type="open-access"><p>This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.0/uk/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.</p></license></permissions><abstract><p>The visual cortex is vulnerable to changes in visual input, especially during the critical period when numerous molecules drive the refinement of the circuitry. From a list of potential actors identified in a recent proteomics study, we selected 2 collapsin response mediator proteins (CRMP2/CRMP4) and 2 synaptic proteins, Dynamin I (Dyn I) and Synaptotagmin I (Syt I), for in-depth analysis of their developmental expression profile in cat visual cortex. CRMP2 and CRMP4 levels were high early in life and clearly declined toward adulthood. In contrast, Dyn I expression levels progressively augmented during maturation. Syt I showed low levels at eye opening and in adults, high levels around the peak of the critical period, and maximal levels at juvenile age. We further determined a role for each molecule in ocular dominance plasticity. CRMP2 and Syt I levels decreased in area 17 upon monocular deprivation, whereas CRMP4 and Dyn I levels remained unaffected. In contrast, binocular removal of pattern vision had no influence on CRMP2 and Syt I expression in kitten area 17. This study illustrates that not the loss of quality of vision through visual deprivation, but disruption of normal binocular visual experience is crucial to induce the observed molecular changes.</p></abstract><kwd-group><kwd>area 17</kwd><kwd>binocular deprivation</kwd><kwd>critical period</kwd><kwd>kitten</kwd><kwd>monocular deprivation</kwd><kwd>postnatal development</kwd></kwd-group></article-meta></front></article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo><title>Influence of Binocular Competition on the Expression Profiles of CRMP2, CRMP4, Dyn I, and Syt I in Developing Cat Visual Cortex</title></titleInfo><titleInfo type="alternative" contentType="CDATA"><title>Influence of Binocular Competition on the Expression Profiles of CRMP2, CRMP4, Dyn I, and Syt I in Developing Cat Visual Cortex</title></titleInfo><name type="personal"><namePart type="given">Lieselotte</namePart><namePart type="family">Cnops</namePart><affiliation>Laboratory of Neuroplasticity and Neuroproteomics, Katholieke Universiteit Leuven, Leuven, Belgium</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Tjing-Tjing</namePart><namePart type="family">Hu</namePart><affiliation>Laboratory of Neuroplasticity and Neuroproteomics, Katholieke Universiteit Leuven, Leuven, Belgium</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Kalina</namePart><namePart type="family">Burnat</namePart><affiliation>Laboratory of Neuroplasticity and Neuroproteomics, Katholieke Universiteit Leuven, Leuven, Belgium</affiliation><affiliation>Laboratory of Neuroplasticity, Nencki Institute of Experimental Biology, Warsaw, Poland</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal" displayLabel="corresp"><namePart type="given">Lutgarde</namePart><namePart type="family">Arckens</namePart><affiliation>Laboratory of Neuroplasticity and Neuroproteomics, Katholieke Universiteit Leuven, Leuven, Belgium</affiliation><affiliation>E-mail: Lut.Arckens@bio.kuleuven.be</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="research-article"></genre><subject><topic>Articles</topic></subject><originInfo><publisher>Oxford University Press</publisher><dateIssued encoding="w3cdtf">2007-10-19</dateIssued><dateCreated encoding="w3cdtf">2007-10-19</dateCreated><copyrightDate encoding="w3cdtf">2008</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType></physicalDescription><abstract>The visual cortex is vulnerable to changes in visual input, especially during the critical period when numerous molecules drive the refinement of the circuitry. From a list of potential actors identified in a recent proteomics study, we selected 2 collapsin response mediator proteins (CRMP2/CRMP4) and 2 synaptic proteins, Dynamin I (Dyn I) and Synaptotagmin I (Syt I), for in-depth analysis of their developmental expression profile in cat visual cortex. CRMP2 and CRMP4 levels were high early in life and clearly declined toward adulthood. In contrast, Dyn I expression levels progressively augmented during maturation. Syt I showed low levels at eye opening and in adults, high levels around the peak of the critical period, and maximal levels at juvenile age. We further determined a role for each molecule in ocular dominance plasticity. CRMP2 and Syt I levels decreased in area 17 upon monocular deprivation, whereas CRMP4 and Dyn I levels remained unaffected. In contrast, binocular removal of pattern vision had no influence on CRMP2 and Syt I expression in kitten area 17. This study illustrates that not the loss of quality of vision through visual deprivation, but disruption of normal binocular visual experience is crucial to induce the observed molecular changes.</abstract><subject><genre>keywords</genre><topic>area 17</topic><topic>binocular deprivation</topic><topic>critical period</topic><topic>kitten</topic><topic>monocular deprivation</topic><topic>postnatal development</topic></subject><relatedItem type="host"><titleInfo><title>Cerebral Cortex</title></titleInfo><genre type="journal">journal</genre><identifier type="ISSN">1047-3211</identifier><identifier type="eISSN">1460-2199</identifier><identifier type="PublisherID">cercor</identifier><identifier type="PublisherID-hwp">cercor</identifier><part><date>2007</date><detail type="volume"><caption>vol.</caption><number>18</number></detail><detail type="issue"><caption>no.</caption><number>5</number></detail><extent unit="pages"><start>1221</start><end>1231</end></extent></part></relatedItem><identifier type="istex">18EE68BDAF1713CB384621206C35D22CE9D648AC</identifier><identifier type="DOI">10.1093/cercor/bhm157</identifier><accessCondition type="use and reproduction" contentType="open-access">This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.0/uk/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.</accessCondition><recordInfo><recordContentSource>OUP</recordContentSource></recordInfo></mods></metadata><covers><json:item><original>true</original><mimetype>text/html</mimetype><extension>html</extension><uri>https://api.istex.fr/document/18EE68BDAF1713CB384621206C35D22CE9D648AC/covers/html</uri></json:item><json:item><original>true</original><mimetype>image/tiff</mimetype><extension>tiff</extension><uri>https://api.istex.fr/document/18EE68BDAF1713CB384621206C35D22CE9D648AC/covers/tiff</uri></json:item></covers><annexes><json:item><original>true</original><mimetype>image/jpeg</mimetype><extension>jpeg</extension><uri>https://api.istex.fr/document/18EE68BDAF1713CB384621206C35D22CE9D648AC/annexes/jpeg</uri></json:item><json:item><original>true</original><mimetype>image/gif</mimetype><extension>gif</extension><uri>https://api.istex.fr/document/18EE68BDAF1713CB384621206C35D22CE9D648AC/annexes/gif</uri></json:item><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/18EE68BDAF1713CB384621206C35D22CE9D648AC/annexes/pdf</uri></json:item></annexes><enrichments><istex:catWosTEI uri="https://api.istex.fr/document/18EE68BDAF1713CB384621206C35D22CE9D648AC/enrichments/catWos"><teiHeader><profileDesc><textClass><classCode scheme="WOS">NEUROSCIENCES</classCode></textClass></profileDesc></teiHeader></istex:catWosTEI><json:item><type>refBibs</type><uri>https://api.istex.fr/document/18EE68BDAF1713CB384621206C35D22CE9D648AC/enrichments/refBibs</uri></json:item></enrichments><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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