Now showing 1 - 2 of 2
  • 2015Journal Article
    [["dc.bibliographiccitation.firstpage","3449"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Brain Structure and Function"],["dc.bibliographiccitation.lastpage","3467"],["dc.bibliographiccitation.volume","220"],["dc.contributor.author","Pielecka-Fortuna, Justyna"],["dc.contributor.author","Wagener, Robin Jan"],["dc.contributor.author","Martens, Ann-Kristin"],["dc.contributor.author","Goetze, Bianka"],["dc.contributor.author","Schmidt, Karl-Friedrich"],["dc.contributor.author","Staiger, Jochen F."],["dc.contributor.author","Loewel, Siegrid"],["dc.date.accessioned","2018-11-07T09:49:57Z"],["dc.date.available","2018-11-07T09:49:57Z"],["dc.date.issued","2015"],["dc.description.abstract","A hallmark of neocortical circuits is the segregation of processing streams into six distinct layers. The importance of this layered organization for cortical processing and plasticity is little understood. We investigated the structure, function and plasticity of primary visual cortex (V1) of adult mice deficient for the glycoprotein reelin and their wild-type littermates. In V1 of rl-/- mice, cells with different laminar fates are present at all cortical depths. Surprisingly, the (vertically) disorganized cortex maintains a precise retinotopic (horizontal) organization. Rl-/- mice have normal basic visual capabilities, but are compromised in more challenging perceptual tasks, such as orientation discrimination. Additionally, rl-/- animals learn and memorize a visual task as well as their wild-type littermates. Interestingly, reelin deficiency enhances visual cortical plasticity: juvenile-like ocular dominance plasticity is preserved into late adulthood. The present data offer an important insight into the capabilities of a disorganized cortical system to maintain basic functional properties."],["dc.identifier.doi","10.1007/s00429-014-0866-x"],["dc.identifier.isi","000361566000023"],["dc.identifier.pmid","25119525"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/10852"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/35606"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","Heidelberg"],["dc.relation.issn","1863-2661"],["dc.relation.issn","1863-2653"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","The disorganized visual cortex in reelin-deficient mice is functional and allows for enhanced plasticity"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]
    Details DOI PMID PMC WOS
  • 2016Journal Article
    [["dc.bibliographiccitation.artnumber","e0149771"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","PLoS One"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Greifzu, Franziska"],["dc.contributor.author","Parthier, Daniel"],["dc.contributor.author","Goetze, Bianka"],["dc.contributor.author","Schlueter, Oliver M."],["dc.contributor.author","Loewel, Siegrid"],["dc.date.accessioned","2018-11-07T10:17:47Z"],["dc.date.available","2018-11-07T10:17:47Z"],["dc.date.issued","2016"],["dc.description.abstract","Neuronal plasticity is essential to enable rehabilitation when the brain suffers from injury, such as following a stroke. One of the most established models to study cortical plasticity is ocular dominance (OD) plasticity in the primary visual cortex (V1) of the mammalian brain induced by monocular deprivation (MD). We have previously shown that OD-plasticity in adult mouse V1 is absent after a photothrombotic (PT) stroke lesion in the adjacent primary somatosensory cortex (S1). Exposing lesioned mice to conditions which reduce the inhibitory tone in V1, such as raising animals in an enriched environment or short-term dark exposure, preserved OD-plasticity after an S1-lesion. Here we tested whether modification of excitatory circuits can also be beneficial for preserving V1-plasticity after stroke. Mice lacking postsynaptic density protein-95 (PSD-95), a signaling scaffold present at mature excitatory synapses, have lifelong juvenile-like OD-plasticity caused by an increased number of AMPA (alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid) -silent synapses in V1 but unaltered inhibitory tone. In fact, using intrinsic signal optical imaging, we show here that OD-plasticity was preserved in V1 of adult PSD-95 KO mice after an S1-lesion but not in PSD-95 wildtype (WT)-mice. In addition, experience-enabled enhancement of the optomotor reflex of the open eye after MD was compromised in both lesioned PSD-95 KO and PSD-95 WT mice. Basic V1-activation and retinotopic map quality were, however, not different between lesioned PSD-95 KO mice and their WT littermates. The preserved OD-plasticity in the PSD-95 KO mice indicates that V1-plasticity after a distant stroke can be promoted by either changes in excitatory circuitry or by lowering the inhibitory tone in V1 as previously shown. Furthermore, the present data indicate that an increased number of AMPA-silent synapses preserves OD-plasticity not only in the healthy brain, but also in another experimental paradigm of cortical plasticity, namely the long-range influence on V1-plasticity after an S1-lesion."],["dc.description.sponsorship","Open-Access Publikationsfonds 2016"],["dc.identifier.doi","10.1371/journal.pone.0149771"],["dc.identifier.isi","000371434500054"],["dc.identifier.pmid","26930616"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/13131"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/41293"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Public Library Science"],["dc.relation.issn","1932-6203"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Ocular Dominance Plasticity after Stroke Was Preserved in PSD-95 Knockout Mice"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]
    Details DOI PMID PMC WOS