<?xml version="1.0" encoding="UTF-8" standalone="yes"?><add><doc><field name="objectKind">mycoreobject</field><field name="id">rosdok_disshab_0000001133</field><field name="returnId">rosdok_disshab_0000001133</field><field name="objectProject">rosdok</field><field name="objectType">disshab</field><field name="link">rosdok_derivate_0000005265</field><field name="modified">2023-08-08T10:04:44.831Z</field><field name="created">2014-03-24T12:02:16.665Z</field><field name="modifiedby">administrator</field><field name="state">published</field><field name="derCount">1</field><field name="derivates">rosdok_derivate_0000005265</field><field name="worldReadable">true</field><field name="worldReadableComplete">true</field><field name="category">derivate_types:fulltext</field><field name="allMeta">Volltext</field><field name="allMeta">fulltext</field><field name="allMeta">wf_edit_epub wf_register_epub</field><field name="category">state:published</field><field name="category.top">state:published</field><field name="allMeta">veröffentlicht</field><field name="allMeta">published</field><field name="allMeta">rosdok/id00001312</field><field name="allMeta">782236049</field><field name="allMeta">MODS updated during RosDok migration in June 2021</field><field name="allMeta">Dissertation</field><field name="allMeta">Hochschulschrift</field><field name="allMeta">1048733793</field><field name="allMeta">Gulshat</field><field name="allMeta">Badel</field><field name="allMeta">1985-</field><field name="allMeta">VerfasserIn</field><field name="allMeta">aut</field><field name="allMeta">Role of HCN Channels in Regulation of Synaptic Plasticity at Early Postnatal Medial Perforant Path</field><field name="allMeta">Die Rolle der HCN-Kanäle bei der Regulation der synaptischen Plastizität des postnatalen medialen Tractus perforans</field><field name="allMeta">en</field><field name="allMeta">1016004257</field><field name="allMeta">Prof. Dr.</field><field name="allMeta">Oliver</field><field name="allMeta">Schmitt</field><field name="allMeta">Universität Rostock, Institut für Anatomie</field><field name="allMeta">AkademischeR BetreuerIn</field><field name="allMeta">dgs</field><field name="allMeta">Prof. Dr.</field><field name="allMeta">Andreas</field><field name="allMeta">Draguhn</field><field name="allMeta">Universität Heidelberg, Institut für Physiologie und Pathophysiologie</field><field name="allMeta">AkademischeR BetreuerIn</field><field name="allMeta">dgs</field><field name="allMeta">Prof. Dr.</field><field name="allMeta">Jens-Karl</field><field name="allMeta">Eilers</field><field name="allMeta">Universität Leipzig, Carl-Ludwig-Institut für Physiologie</field><field name="allMeta">AkademischeR BetreuerIn</field><field name="allMeta">dgs</field><field name="allMeta">1029510660</field><field name="allMeta">Universität Rostock</field><field name="allMeta">Universitätsmedizin</field><field name="allMeta">Grad-verleihende Institution</field><field name="allMeta">dgg</field><field name="allMeta">10.18453/rosdok_id00001312</field><field name="allMeta">http://purl.uni-rostock.de/rosdok/id00001312</field><field name="allMeta">urn:nbn:de:gbv:28-diss2014-0064-2</field><field name="allMeta">610 Medizin, Gesundheit</field><field name="allMeta">Universitätsmedizin</field><field name="allMeta">frei zugänglich (Open Access)</field><field name="allMeta">Lizenz Metadaten: CC0</field><field name="allMeta">Nutzungsrechte erteilt</field><field name="allMeta">alle Rechte vorbehalten</field><field name="allMeta">Universität Rostock</field><field name="allMeta">Rostock</field><field name="allMeta">2014</field><field name="allMeta">monographic</field><field name="allMeta">2013</field><field name="allMeta">2014</field><field name="allMeta">Universitätsbibliothek Rostock</field><field name="allMeta">Rostock</field><field name="allMeta">2014</field><field name="allMeta">2014</field><field name="allMeta">HCN channel blocker ZD7288 depressed synaptic transmission at medial perforant path (MPP) synapses. Low-frequency stimulation (LFS) delivered to these fibers resulted in enhanced LTD after ZD7288 in P9-15 rats, but not in P30-60 rats. Hence, HCN channel activation during neuronal activity may compromise the propensity of LTD at these synapses. Results obtained with L-NAME iterated the effect of HCN channel inhibition on LTD, suggesting that retrograde signaling with NO might play a major role in the linkage between postsynaptic NMDAR activation and presynaptic HCN channel function.</field><field name="allMeta">Der HCN-Kanal-Blocker ZD7288 reduziert die synaptische Übertragung an den Synapsen des medialen Tractus perforans. Niederfrequente Stimulation dieses Traktes führt zu einer Langzeitdepression (LTD), welche durch Vorbehandlung mit ZD7288 bei frühpostnatalen Ratten (P9-15) gesteigert werden kann. Bei älteren Tieren (P30-60) fand sich keine Veränderung der LTD durch ZD7288. 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Universitätsmedizin</field><field name="allMeta">Universitätsmedizin</field><field name="allMeta">Uni.Rostock.Fakultaet.MED</field><field name="allMeta">http://d-nb.info/gnd/1029510660</field><field name="category">accesscondition:openaccess</field><field name="category.top">accesscondition:openaccess</field><field name="allMeta">frei zugänglich (Open Access)</field><field name="allMeta">open access</field><field name="allMeta">http://purl.org/coar/access_right/c_abf2</field><field name="allMeta">OA</field><field name="allMeta">free</field><field name="allMeta">info:eu-repo/semantics/openAccess</field><field name="allMeta">[DE-28]Open Access$gControlled Vocabulary for Access Rights$uhttp://purl.org/coar/access_right/c_abf2</field><field name="category">licenseinfo:metadata</field><field name="category.top">licenseinfo:metadata</field><field name="allMeta">Lizenzen für Metadaten</field><field name="category">licenseinfo:metadata.cc0</field><field 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name="category.top">licenseinfo:work.rightsreserved</field><field name="allMeta">alle Rechte vorbehalten</field><field name="allMeta">all rights reserved</field><field name="allMeta">/creativecommons/r/reserved/0.9/88x31.png</field><field name="allMeta">[DE-28]Urheberrechtsschutz 1.0$gRights Statements$uhttp://rightsstatements.org/vocab/InC/1.0/</field><field name="allMeta">http://rightsstatements.org/vocab/InC/1.0/</field><field name="allMeta">http://rightsstatements.org/vocab/InC/1.0/</field><field name="mods.title">Role of HCN Channels in Regulation of Synaptic Plasticity at Early Postnatal Medial Perforant Path</field><field name="mods.title">Die Rolle der HCN-Kanäle bei der Regulation der synaptischen Plastizität des postnatalen medialen Tractus perforans</field><field name="mods.title.main">Role of HCN Channels in Regulation of Synaptic Plasticity at Early Postnatal Medial Perforant Path</field><field name="mods.title.subtitle"></field><field name="mods.nameIdentifier">gnd:1048733793</field><field name="mods.nameIdentifier">gnd:1016004257</field><field name="mods.nameIdentifier">gnd:1029510660</field><field name="mods.nameIdentifier.top">gnd:1048733793</field><field name="mods.nameIdentifier.top">gnd:1016004257</field><field name="mods.nameIdentifier.top">gnd:1029510660</field><doc><field name="id">rosdok_disshab_0000001133-d40241e39</field><field name="mods.nameIdentifier">gnd:1048733793</field><field name="mods.name">Gulshat Badel</field><field name="mods.name.top">Gulshat Badel</field></doc><doc><field name="id">rosdok_disshab_0000001133-d40241e62</field><field name="mods.nameIdentifier">gnd:1016004257</field><field name="mods.name">Prof. Dr. Oliver Schmitt</field><field name="mods.name.top">Prof. Dr. Oliver Schmitt</field></doc><doc><field name="id">rosdok_disshab_0000001133-d40241e77</field><field name="mods.name">Prof. Dr. Andreas Draguhn</field><field name="mods.name.top">Prof. Dr. Andreas Draguhn</field></doc><doc><field name="id">rosdok_disshab_0000001133-d40241e91</field><field name="mods.name">Prof. Dr. Jens-Karl Eilers</field><field name="mods.name.top">Prof. Dr. Jens-Karl Eilers</field></doc><doc><field name="id">rosdok_disshab_0000001133-d40241e104</field><field name="mods.nameIdentifier">gnd:1029510660</field><field name="mods.name">Universität Rostock Universitätsmedizin</field><field name="mods.name.top">Universität Rostock Universitätsmedizin</field></doc><field name="mods.name">Gulshat Badel</field><field name="mods.name">Prof. Dr. Oliver Schmitt</field><field name="mods.name">Prof. Dr. Andreas Draguhn</field><field name="mods.name">Prof. Dr. Jens-Karl Eilers</field><field name="mods.name">Universität Rostock Universitätsmedizin</field><field name="mods.name.top">Gulshat Badel</field><field name="mods.name.top">Prof. Dr. Oliver Schmitt</field><field name="mods.name.top">Prof. Dr. Andreas Draguhn</field><field name="mods.name.top">Prof. Dr. Jens-Karl Eilers</field><field name="mods.name.top">Universität Rostock Universitätsmedizin</field><field name="mods.author">Gulshat Badel</field><field name="mods.place">Rostock</field><field name="mods.publisher">Universität Rostock</field><field name="mods.genre">epub.dissertation</field><field name="mods.identifier">10.18453/rosdok_id00001312</field><field name="mods.identifier">http://purl.uni-rostock.de/rosdok/id00001312</field><field name="mods.identifier">urn:nbn:de:gbv:28-diss2014-0064-2</field><field name="mods.subject">hippocampus</field><field name="mods.subject">dentate gyrus</field><field name="mods.subject">long-term depression</field><field name="mods.subject">nitric oxide</field><field name="mods.abstract">HCN channel blocker ZD7288 depressed synaptic transmission at medial perforant path (MPP) synapses. Low-frequency stimulation (LFS) delivered to these fibers resulted in enhanced LTD after ZD7288 in P9-15 rats, but not in P30-60 rats. Hence, HCN channel activation during neuronal activity may compromise the propensity of LTD at these synapses. Results obtained with L-NAME iterated the effect of HCN channel inhibition on LTD, suggesting that retrograde signaling with NO might play a major role in the linkage between postsynaptic NMDAR activation and presynaptic HCN channel function.</field><field name="mods.abstract">Der HCN-Kanal-Blocker ZD7288 reduziert die synaptische Übertragung an den Synapsen des medialen Tractus perforans. Niederfrequente Stimulation dieses Traktes führt zu einer Langzeitdepression (LTD), welche durch Vorbehandlung mit ZD7288 bei frühpostnatalen Ratten (P9-15) gesteigert werden kann.  Bei älteren Tieren (P30-60) fand sich keine Veränderung der LTD durch ZD7288. Experimente mit L-NAME, einem Inhibitor der NO-Synthase, zeigten ähnliche Ergebnisse, sodass ein retrograder Signalweg mit NO eine wichtige Rolle bei der Modulation synaptischer Plastizität durch HCN-Kanäle spielen könnte.</field><field name="mods.dateIssued">2014</field><field name="mods.yearIssued">2014</field><field name="mods.type">epub.dissertation</field><field name="search_result_link_text">1
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        rosdok/id00001312782236049MODS updated during RosDok migration in June 2021DissertationHochschulschrift1048733793GulshatBadel1985-VerfasserInautRole of HCN Channels in Regulation of Synaptic Plasticity at Early Postnatal Medial Perforant PathDie Rolle der HCN-Kanäle bei der Regulation der synaptischen Plastizität des postnatalen medialen Tractus perforansen1016004257Prof. Dr.OliverSchmittUniversität Rostock, Institut für AnatomieAkademischeR BetreuerIndgsProf. Dr.AndreasDraguhnUniversität Heidelberg, Institut für Physiologie und PathophysiologieAkademischeR BetreuerIndgsProf. Dr.Jens-KarlEilersUniversität Leipzig, Carl-Ludwig-Institut für PhysiologieAkademischeR BetreuerIndgs1029510660Universität RostockUniversitätsmedizinGrad-verleihende Institutiondgg10.18453/rosdok_id00001312http://purl.uni-rostock.de/rosdok/id00001312urn:nbn:de:gbv:28-diss2014-0064-2610 Medizin, GesundheitUniversitätsmedizinfrei zugänglich (Open Access)Lizenz Metadaten: CC0Nutzungsrechte erteiltalle Rechte vorbehaltenUniversität RostockRostock2014monographic20132014Universitätsbibliothek RostockRostock20142014HCN channel blocker ZD7288 depressed synaptic transmission at medial perforant path (MPP) synapses. Low-frequency stimulation (LFS) delivered to these fibers resulted in enhanced LTD after ZD7288 in P9-15 rats, but not in P30-60 rats. Hence, HCN channel activation during neuronal activity may compromise the propensity of LTD at these synapses. Results obtained with L-NAME iterated the effect of HCN channel inhibition on LTD, suggesting that retrograde signaling with NO might play a major role in the linkage between postsynaptic NMDAR activation and presynaptic HCN channel function.Der HCN-Kanal-Blocker ZD7288 reduziert die synaptische Übertragung an den Synapsen des medialen Tractus perforans. Niederfrequente Stimulation dieses Traktes führt zu einer Langzeitdepression (LTD), welche durch Vorbehandlung mit ZD7288 bei frühpostnatalen Ratten (P9-15) gesteigert werden kann.  Bei älteren Tieren (P30-60) fand sich keine Veränderung der LTD durch ZD7288. Experimente mit L-NAME, einem Inhibitor der NO-Synthase, zeigten ähnliche Ergebnisse, sodass ein retrograder Signalweg mit NO eine wichtige Rolle bei der Modulation synaptischer Plastizität durch HCN-Kanäle spielen könnte.hippocampusdentate gyruslong-term depressionnitric oxideUniversitätsbibliothek Rostockhttp://purl.uni-rostock.de/rosdok/id00001312
      
    
  
  
    
      2014-03-24T12:02:16.665Z
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      administrator</field><field name="derivateLabel">fulltext</field><field name="ir.pdffulltext_url">file/rosdok_disshab_0000001133/rosdok_derivate_0000005265/Dissertation_Badel_2014.pdf</field><field name="mods.title">Role of HCN Channels in Regulation of Synaptic Plasticity at Early Postnatal Medial Perforant Path</field><field name="mods.title">Die Rolle der HCN-Kanäle bei der Regulation der synaptischen Plastizität des postnatalen medialen Tractus perforans</field><field name="mods.title.main">Role of HCN Channels in Regulation of Synaptic Plasticity at Early Postnatal Medial Perforant Path</field><field name="mods.title.subtitle"></field><field name="mods.nameIdentifier">gnd:1048733793</field><field name="mods.nameIdentifier">gnd:1016004257</field><field name="mods.nameIdentifier">gnd:1029510660</field><field name="mods.nameIdentifier.top">gnd:1048733793</field><field name="mods.nameIdentifier.top">gnd:1016004257</field><field name="mods.nameIdentifier.top">gnd:1029510660</field><doc><field name="id">rosdok_disshab_0000001133-d40241e39</field><field name="mods.nameIdentifier">gnd:1048733793</field><field name="mods.name">Gulshat Badel</field><field name="mods.name.top">Gulshat Badel</field></doc><doc><field name="id">rosdok_disshab_0000001133-d40241e62</field><field name="mods.nameIdentifier">gnd:1016004257</field><field name="mods.name">Prof. Dr. Oliver Schmitt</field><field name="mods.name.top">Prof. Dr. Oliver Schmitt</field></doc><doc><field name="id">rosdok_disshab_0000001133-d40241e77</field><field name="mods.name">Prof. Dr. Andreas Draguhn</field><field name="mods.name.top">Prof. Dr. Andreas Draguhn</field></doc><doc><field name="id">rosdok_disshab_0000001133-d40241e91</field><field name="mods.name">Prof. Dr. Jens-Karl Eilers</field><field name="mods.name.top">Prof. Dr. Jens-Karl Eilers</field></doc><doc><field name="id">rosdok_disshab_0000001133-d40241e104</field><field name="mods.nameIdentifier">gnd:1029510660</field><field name="mods.name">Universität Rostock Universitätsmedizin</field><field name="mods.name.top">Universität Rostock Universitätsmedizin</field></doc><field name="mods.name">Gulshat Badel</field><field name="mods.name">Prof. Dr. Oliver Schmitt</field><field name="mods.name">Prof. Dr. Andreas Draguhn</field><field name="mods.name">Prof. Dr. Jens-Karl Eilers</field><field name="mods.name">Universität Rostock Universitätsmedizin</field><field name="mods.name.top">Gulshat Badel</field><field name="mods.name.top">Prof. Dr. Oliver Schmitt</field><field name="mods.name.top">Prof. Dr. Andreas Draguhn</field><field name="mods.name.top">Prof. Dr. Jens-Karl Eilers</field><field name="mods.name.top">Universität Rostock Universitätsmedizin</field><field name="mods.author">Gulshat Badel</field><field name="mods.place">Rostock</field><field name="mods.publisher">Universität Rostock</field><field name="mods.genre">epub.dissertation</field><field name="mods.identifier">10.18453/rosdok_id00001312</field><field name="mods.identifier">http://purl.uni-rostock.de/rosdok/id00001312</field><field name="mods.identifier">urn:nbn:de:gbv:28-diss2014-0064-2</field><field name="mods.subject">hippocampus</field><field name="mods.subject">dentate gyrus</field><field name="mods.subject">long-term depression</field><field name="mods.subject">nitric oxide</field><field name="mods.abstract">HCN channel blocker ZD7288 depressed synaptic transmission at medial perforant path (MPP) synapses. Low-frequency stimulation (LFS) delivered to these fibers resulted in enhanced LTD after ZD7288 in P9-15 rats, but not in P30-60 rats. Hence, HCN channel activation during neuronal activity may compromise the propensity of LTD at these synapses. Results obtained with L-NAME iterated the effect of HCN channel inhibition on LTD, suggesting that retrograde signaling with NO might play a major role in the linkage between postsynaptic NMDAR activation and presynaptic HCN channel function.</field><field name="mods.abstract">Der HCN-Kanal-Blocker ZD7288 reduziert die synaptische Übertragung an den Synapsen des medialen Tractus perforans. Niederfrequente Stimulation dieses Traktes führt zu einer Langzeitdepression (LTD), welche durch Vorbehandlung mit ZD7288 bei frühpostnatalen Ratten (P9-15) gesteigert werden kann.  Bei älteren Tieren (P30-60) fand sich keine Veränderung der LTD durch ZD7288. Experimente mit L-NAME, einem Inhibitor der NO-Synthase, zeigten ähnliche Ergebnisse, sodass ein retrograder Signalweg mit NO eine wichtige Rolle bei der Modulation synaptischer Plastizität durch HCN-Kanäle spielen könnte.</field><field name="mods.dateIssued">2014</field><field name="mods.yearIssued">2014</field><field name="ir.identifier">[xslt]Saxon</field><field name="recordIdentifier">rosdok/id00001312</field><field name="purl">https://purl.uni-rostock.de/rosdok/id00001312</field><field name="ppn">782236049</field><field name="doi">10.18453/rosdok_id00001312</field><field name="urn">urn:nbn:de:gbv:28-diss2014-0064-2</field><field name="ir.creator.result">Gulshat Badel</field><field name="ir.creator.sort">Badel Gulshat</field><field name="ir.title.result">Role of HCN Channels in Regulation of Synaptic Plasticity at Early Postnatal Medial Perforant Path</field><field name="ir.doctype.result">Dissertation</field><field name="ir.doctype_en.result">doctoral thesis</field><field name="ir.originInfo.result">Universität Rostock, 2014</field><field name="ir.abstract300.result">HCN channel blocker ZD7288 depressed synaptic transmission at medial perforant path (MPP) synapses. Low-frequency stimulation (LFS) delivered to these fibers resulted in enhanced LTD after ZD7288 in P9-15 rats, but not in P30-60 rats. Hence, HCN channel activation during neuronal activity may…</field><field name="ir.creator_all">Gulshat Badel</field><field name="ir.title_all">Role of HCN Channels in Regulation of Synaptic Plasticity at Early Postnatal Medial Perforant Path</field><field name="ir.title_all">Die Rolle der HCN-Kanäle bei der Regulation der synaptischen Plastizität des postnatalen medialen Tractus perforans</field><field name="ir.location_all">Universitätsbibliothek Rostock</field><field name="ir.location_all">http://purl.uni-rostock.de/rosdok/id00001312</field><field name="ir.creator_all">1048733793</field><field name="ir.creator_all">Gulshat</field><field name="ir.creator_all">Badel</field><field name="ir.creator_all">1985-</field><field name="ir.creator_all"></field><field name="ir.creator_all">VerfasserIn</field><field name="ir.creator_all">aut</field><field name="ir.creator_all">1016004257</field><field name="ir.creator_all">Prof. Dr.</field><field name="ir.creator_all">Oliver</field><field name="ir.creator_all">Schmitt</field><field name="ir.creator_all">Universität Rostock, Institut für Anatomie</field><field name="ir.creator_all"></field><field name="ir.creator_all">AkademischeR BetreuerIn</field><field name="ir.creator_all">dgs</field><field name="ir.creator_all">Prof. Dr.</field><field name="ir.creator_all">Andreas</field><field name="ir.creator_all">Draguhn</field><field name="ir.creator_all">Universität Heidelberg, Institut für Physiologie und Pathophysiologie</field><field name="ir.creator_all"></field><field name="ir.creator_all">AkademischeR BetreuerIn</field><field name="ir.creator_all">dgs</field><field name="ir.creator_all">Prof. Dr.</field><field name="ir.creator_all">Jens-Karl</field><field name="ir.creator_all">Eilers</field><field name="ir.creator_all">Universität Leipzig, Carl-Ludwig-Institut für Physiologie</field><field name="ir.creator_all"></field><field name="ir.creator_all">AkademischeR BetreuerIn</field><field name="ir.creator_all">dgs</field><field name="ir.creator_all">1029510660</field><field name="ir.creator_all">Universität Rostock</field><field name="ir.creator_all">Universitätsmedizin</field><field name="ir.creator_all"></field><field name="ir.creator_all">Grad-verleihende Institution</field><field name="ir.creator_all">dgg</field><field name="ir.identifier">[doi]10.18453/rosdok_id00001312</field><field name="ir.identifier">[purl]http://purl.uni-rostock.de/rosdok/id00001312</field><field name="ir.identifier">[urn]urn:nbn:de:gbv:28-diss2014-0064-2</field><field name="ir.oai.setspec.open_access">open_access</field><field name="ir.pubyear_start">2014</field><field name="ir.pubyear_end">2014</field><field name="ir.epoch_class.facet">epoch:21th_century</field><field name="ir.language_class.facet">rfc5646:en</field><field name="ir.doctype_class.facet">doctype:epub.dissertation</field><field name="ir.accesscondition_class.facet">accesscondition:openaccess</field><field name="ir.sdnb_class.facet">SDNB:610</field><field name="ir.institution_class.facet">institution:unirostock.umr</field><field name="ir.state_class.facet">state:published</field></doc></add>