Goetze, Bianka

[["dc.bibliographiccitation.firstpage","E3131"],["dc.bibliographiccitation.issue","24"],["dc.bibliographiccitation.journal","Proceedings of the National Academy of Sciences of the United States of America"],["dc.bibliographiccitation.lastpage","E3140"],["dc.bibliographiccitation.volume","112"],["dc.contributor.author","Huang, Xiaojie"],["dc.contributor.author","Stodieck, Sophia Katharina"],["dc.contributor.author","Goetze, Bianka"],["dc.contributor.author","Cui, Lei"],["dc.contributor.author","Wong, Man Ho"],["dc.contributor.author","Wenzel, Colin"],["dc.contributor.author","Hosang, Leon"],["dc.contributor.author","Dong, Yan"],["dc.contributor.author","Loewel, Siegrid"],["dc.contributor.author","Schlueter, Oliver M."],["dc.date.accessioned","2018-11-07T09:55:51Z"],["dc.date.available","2018-11-07T09:55:51Z"],["dc.date.issued","2015"],["dc.description.abstract","During critical periods, all cortical neural circuits are refined to optimize their functional properties. The prevailing notion is that the balance between excitation and inhibition determines the onset and closure of critical periods. In contrast, we show that maturation of silent glutamatergic synapses onto principal neurons was sufficient to govern the duration of the critical period for ocular dominance plasticity in the visual cortex of mice. Specifically, postsynaptic density protein-95 (PSD-95) was absolutely required for experience-dependent maturation of silent synapses, and its absence before the onset of critical periods resulted in lifelong juvenile ocular dominance plasticity. Loss of PSD-95 in the visual cortex after the closure of the critical period reinstated silent synapses, resulting in reopening of juvenile-like ocular dominance plasticity. Additionally, silent synapse-based ocular dominance plasticity was largely independent of the inhibitory tone, whose developmental maturation was independent of PSD-95. Moreover, glutamatergic synaptic transmission onto parvalbumin-positive interneurons was unaltered in PSD-95 KO mice. These findings reveal not only that PSD-95-dependent silent synapse maturation in visual cortical principal neurons terminates the critical period for ocular dominance plasticity but also indicate that, in general, once silent synapses are consolidated in any neural circuit, initial experience-dependent functional optimization and critical periods end."],["dc.identifier.doi","10.1073/pnas.1506488112"],["dc.identifier.isi","000356251800009"],["dc.identifier.pmid","26015564"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/36839"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Natl Acad Sciences"],["dc.relation.issn","0027-8424"],["dc.title","Progressive maturation of silent synapses governs the duration of a critical period"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","119"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Neuron"],["dc.bibliographiccitation.lastpage","132"],["dc.bibliographiccitation.volume","91"],["dc.contributor.author","Saab, Aiman S."],["dc.contributor.author","Tzvetavona, Iva D."],["dc.contributor.author","Trevisiol, Andrea"],["dc.contributor.author","Baltan, Selva"],["dc.contributor.author","Dibaj, Payam"],["dc.contributor.author","Kusch, Kathrin"],["dc.contributor.author","Möbius, Wiebke"],["dc.contributor.author","Goetze, Bianka"],["dc.contributor.author","Jahn, Hannah M."],["dc.contributor.author","Huang, Wenhui"],["dc.contributor.author","Steffens, Heinz"],["dc.contributor.author","Schomburg, Eike D."],["dc.contributor.author","Pérez-Samartín, Alberto"],["dc.contributor.author","Pérez-Cerdá, Fernando"],["dc.contributor.author","Bakhtiari, Davood"],["dc.contributor.author","Matute, Carlos"],["dc.contributor.author","Löwel, Siegrid"],["dc.contributor.author","Griesinger, Christian"],["dc.contributor.author","Hirrlinger, Johannes"],["dc.contributor.author","Kirchhoff, Frank"],["dc.contributor.author","Nave, Klaus-Armin"],["dc.date.accessioned","2017-09-07T11:44:48Z"],["dc.date.available","2017-09-07T11:44:48Z"],["dc.date.issued","2016"],["dc.description.abstract","Oligodendrocytes make myelin and support axons metabolically with lactate. However, it is unknown how glucose utilization and glycolysis are adapted to the different axonal energy demands. Spiking axons release glutamate and oligodendrocytes express NMDA receptors of unknown function. Here we show that the stimulation of oligodendroglial NMDA receptors mobilizes glucose transporter GLUT1, leading to its incorporation into the myelin compartment in vivo. When myelinated optic nerves from conditional NMDA receptor mutants are challenged with transient oxygen-glucose deprivation, they show a reduced functional recovery when returned to oxygen-glucose but are indistinguishable from wild-type when provided with oxygen-lactate. Moreover, the functional integrity of isolated optic nerves, which are electrically silent, is extended by preincubation with NMDA, mimicking axonal activity, and shortened by NMDA receptor blockers. This reveals a novel aspect of neuronal energy metabolismin which activity-dependent glutamate release enhances oligodendroglial glucose uptake and glycolytic support of fast spiking axons."],["dc.identifier.doi","10.1016/j.neuron.2016.05.016"],["dc.identifier.gro","3141651"],["dc.identifier.isi","000382394300016"],["dc.identifier.pmid","27292539"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/5454"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.eissn","1097-4199"],["dc.relation.issn","0896-6273"],["dc.title","Oligodendroglial NMDA Receptors Regulate Glucose Import and Axonal Energy Metabolism"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1"],["dc.bibliographiccitation.journal","Experimental Gerontology"],["dc.bibliographiccitation.lastpage","11"],["dc.bibliographiccitation.volume","60"],["dc.contributor.author","Stodieck, Sophia Katharina"],["dc.contributor.author","Greifzu, Franziska"],["dc.contributor.author","Goetze, Bianka"],["dc.contributor.author","Schmidt, Karl-Friedrich"],["dc.contributor.author","Loewel, Siegrid"],["dc.date.accessioned","2018-11-07T09:32:06Z"],["dc.date.available","2018-11-07T09:32:06Z"],["dc.date.issued","2014"],["dc.description.abstract","In the primary visual cortex (V1), monocular deprivation (MD) induces a shift in the ocular dominance (OD) of binocular neurons towards the open eye (Wiesel and Hubel, 1963; Gordon and Stryker, 1996). In V1 of C57Bl/6J mice, this OD-plasticity is maximal in juveniles, declines in adults and is absent beyond postnatal day (PD) 110 (Lehmann and Lowel, 2008) if mice are raised in standard cages. Since it was recently shown that brief dark exposure (DE) restored OD-plasticity in young adult rats (PD70-100) (He et al., 2006), we wondered whether DE would restore OD-plasticity also in adult and old mice and after a cortical stroke. To this end, we raised mice in standard cages until adulthood and transferred them to a dark room for 10-14 days. Using intrinsic signal optical imaging we demonstrate that short-term DE can restore OD-plasticity after MD in both adult (PD138) and old mice (PD535), and that OD-shifts were mediated by an increase of open eye responses in V1. Interestingly, restored OD-plasticity after DE was accompanied by a reduction of both parvalbumin expressing cells and perineuronal nets and was prevented by increasing intracortical inhibition with diazepam. DE also maintained OD-plasticity in adult mice (PD150) after a stroke in the primary somatosensory cortex. In contrast, short-term DE did not affect basic visual parameters as measured by optomotry. In conclusion, short-termDEwas able to restore OD-plasticity in both adult and aging mice and even preserved plasticity after a cortical stroke, most likely mediated by reducing intracortical inhibition. (C) 2014 The Authors. Published by Elsevier Inc."],["dc.identifier.doi","10.1016/j.exger.2014.09.007"],["dc.identifier.isi","000346068300001"],["dc.identifier.pmid","25220148"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/31673"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Pergamon-elsevier Science Ltd"],["dc.relation.issn","1873-6815"],["dc.relation.issn","0531-5565"],["dc.title","Brief dark exposure restored ocular dominance plasticity in aging mice and after a cortical stroke"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["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"]]

[["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"]]