Gollisch, Tim

[["dc.bibliographiccitation.firstpage","183"],["dc.bibliographiccitation.lastpage","189"],["dc.bibliographiccitation.seriesnr","723"],["dc.bibliographiccitation.volume","723"],["dc.contributor.author","Michalakis, Stylianos"],["dc.contributor.author","Mühlfriedel, Regine"],["dc.contributor.author","Tanimoto, Naoyuki"],["dc.contributor.author","Krishnamoorthy, Vidhyasankar"],["dc.contributor.author","Koch, Susanne"],["dc.contributor.author","Fischer, M. Dominik"],["dc.contributor.author","Becirovic, Elvir"],["dc.contributor.author","Bai, Lin"],["dc.contributor.author","Huber, Gesine"],["dc.contributor.author","Beck, Susanne C."],["dc.contributor.author","Fahl, Edda"],["dc.contributor.author","Büning, Hildegard"],["dc.contributor.author","Schmidt, Jennifer"],["dc.contributor.author","Zong, Xiangang"],["dc.contributor.author","Gollisch, Tim"],["dc.contributor.author","Biel, Martin"],["dc.contributor.author","Seeliger, Mathias W."],["dc.contributor.editor","LaVail, Matthew M."],["dc.contributor.editor","Ash, John D."],["dc.contributor.editor","Anderson, Robert E."],["dc.contributor.editor","Hollyfield, Joe G."],["dc.contributor.editor","Grimm, Christian"],["dc.date.accessioned","2021-03-05T08:58:54Z"],["dc.date.available","2021-03-05T08:58:54Z"],["dc.date.issued","2012"],["dc.identifier.doi","10.1007/978-1-4614-0631-0_25"],["dc.identifier.eisbn","978-1-4614-0631-0"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/80293"],["dc.notes.intern","DOI Import GROB-393"],["dc.publisher","Springer US"],["dc.publisher.place","Boston, MA"],["dc.relation.crisseries","Advances in Experimental Medicine and Biology"],["dc.relation.eisbn","978-1-4614-0631-0"],["dc.relation.isbn","978-1-4614-0630-3"],["dc.relation.ispartof","Retinal Degenerative Diseases"],["dc.relation.issn","0065-2598"],["dc.title","Gene Therapy Restores Missing Cone-Mediated Vision in the CNGA3−/− Mouse Model of Achromatopsia"],["dc.type","book_chapter"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2057"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","Molecular Therapy"],["dc.bibliographiccitation.lastpage","2063"],["dc.bibliographiccitation.volume","18"],["dc.contributor.author","Michalakis, Stylianos"],["dc.contributor.author","Mühlfriedel, Regine"],["dc.contributor.author","Tanimoto, Naoyuki"],["dc.contributor.author","Krishnamoorthy, Vidhyasankar"],["dc.contributor.author","Koch, Susanne"],["dc.contributor.author","Fischer, M. Dominik"],["dc.contributor.author","Becirovic, Elvir"],["dc.contributor.author","Bai, Lin"],["dc.contributor.author","Huber, Gesine"],["dc.contributor.author","Beck, Susanne C."],["dc.contributor.author","Fahl, Edda"],["dc.contributor.author","Büning, Hildegard"],["dc.contributor.author","Paquet-Durand, François"],["dc.contributor.author","Zong, Xiangang"],["dc.contributor.author","Gollisch, Tim"],["dc.contributor.author","Biel, Martin"],["dc.contributor.author","Seeliger, Mathias W."],["dc.date.accessioned","2021-03-05T08:58:27Z"],["dc.date.available","2021-03-05T08:58:27Z"],["dc.date.issued","2010"],["dc.identifier.doi","10.1038/mt.2010.149"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/80140"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-393"],["dc.relation.issn","1525-0016"],["dc.title","Restoration of Cone Vision in the CNGA3−/− Mouse Model of Congenital Complete Lack of Cone Photoreceptor Function"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","149"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Nature Communications"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Liu, Jian K."],["dc.contributor.author","Schreyer, Helene M."],["dc.contributor.author","Onken, Arno"],["dc.contributor.author","Rozenblit, Fernando"],["dc.contributor.author","Khani, Mohammad H."],["dc.contributor.author","Krishnamoorthy, Vidhyasankar"],["dc.contributor.author","Panzeri, Stefano"],["dc.contributor.author","Gollisch, Tim"],["dc.date.accessioned","2019-02-27T09:39:23Z"],["dc.date.available","2019-02-27T09:39:23Z"],["dc.date.issued","2017"],["dc.description.abstract","Neurons in sensory systems often pool inputs over arrays of presynaptic cells, giving rise to functional subunits inside a neuron's receptive field. The organization of these subunits provides a signature of the neuron's presynaptic functional connectivity and determines how the neuron integrates sensory stimuli. Here we introduce the method of spike-triggered non-negative matrix factorization for detecting the layout of subunits within a neuron's receptive field. The method only requires the neuron's spiking responses under finely structured sensory stimulation and is therefore applicable to large populations of simultaneously recorded neurons. Applied to recordings from ganglion cells in the salamander retina, the method retrieves the receptive fields of presynaptic bipolar cells, as verified by simultaneous bipolar and ganglion cell recordings. The identified subunit layouts allow improved predictions of ganglion cell responses to natural stimuli and reveal shared bipolar cell input into distinct types of ganglion cells.How a neuron integrates sensory information requires knowledge about its functional presynaptic connections. Here the authors report a new method using non-negative matrix factorization to identify the layout of presynaptic bipolar cell inputs onto retinal ganglion cells and predict their responses to natural stimuli."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2017"],["dc.identifier.doi","10.1038/s41467-017-00156-9"],["dc.identifier.eissn","2041-1723"],["dc.identifier.pmid","28747662"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14543"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/57634"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Inference of neuronal functional circuitry with spike-triggered non-negative matrix factorization"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e22431"],["dc.bibliographiccitation.journal","eLife"],["dc.bibliographiccitation.volume","6"],["dc.contributor.author","Krishnamoorthy, Vidhyasankar"],["dc.contributor.author","Weick, Michael"],["dc.contributor.author","Gollisch, Tim"],["dc.date.accessioned","2020-12-10T18:48:05Z"],["dc.date.available","2020-12-10T18:48:05Z"],["dc.date.issued","2017"],["dc.description.abstract","Standard models of stimulus encoding in the retina postulate that image presentations activate neurons according to the increase of preferred contrast inside the receptive field. During natural vision, however, images do not arrive in isolation, but follow each other rapidly, separated by sudden gaze shifts. We here report that, contrary to standard models, specific ganglion cells in mouse retina are suppressed after a rapid image transition by changes in visual patterns across the transition, but respond with a distinct spike burst when the same pattern reappears. This sensitivity to image recurrence depends on opposing effects of glycinergic and GABAergic inhibition and can be explained by a circuit of local serial inhibition. Rapid image transitions thus trigger a mode of operation that differs from the processing of simpler stimuli and allows the retina to tag particular image parts or to detect transition types that lead to recurring stimulus patterns."],["dc.identifier.doi","10.7554/eLife.22431"],["dc.identifier.eissn","2050-084X"],["dc.identifier.isi","000396096500001"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/79010"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","2050-084X"],["dc.title","Sensitivity to image recurrence across eye-movement-like image transitions through local serial inhibition in the retina"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e0181011"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","PloS one"],["dc.bibliographiccitation.volume","12"],["dc.contributor.author","Hoon, Mrinalini"],["dc.contributor.author","Krishnamoorthy, Vidhyasankar"],["dc.contributor.author","Gollisch, Tim"],["dc.contributor.author","Falkenburger, Bjoern"],["dc.contributor.author","Varoqueaux, Frederique"],["dc.date.accessioned","2019-07-09T11:43:30Z"],["dc.date.available","2019-07-09T11:43:30Z"],["dc.date.issued","2017"],["dc.description.abstract","The postsynaptic adhesion proteins Neuroligins (NLs) are essential for proper synapse function, and their alterations are associated with a variety of neurodevelopmental disorders. It is increasingly clear that each NL isoform occupies specific subsets of synapses and is able to regulate the function of discrete networks. Studies of NL2 and NL4 in the retina in particular have contributed towards uncovering their role in inhibitory synapse function. In this study we show that NL3 is also predominantly expressed at inhibitory postsynapses in the retinal inner plexiform layer (IPL), where it colocalizes with both GABAA- and glycinergic receptor clusters in a 3:2 ratio. In the NL3 deletion-mutant (knockout or KO) mouse, we uncovered a dramatic reduction of the number of GABAAα2-subunit containing GABAA receptor clusters at the IPL. Retinal activity was thereafter assessed in KO and wild-type (WT) littermates by multi-electrode-array recordings of the output cells of retina, the retinal ganglion cells (RGCs). RGCs in the NL3 KO showed reduced spontaneous activity and an altered response to white noise stimulation. Moreover, upon application of light flashes, the proportion of cells firing at light offset (OFF RGCs) was significantly lower in the NL3 KO compared to WT littermates, whereas the relative number of cells firing at light onset (ON RGCs) increased. Interestingly, although GABAAα2-bearing receptors have been related to direction-selective circuits of the retina, features of direction selective-retinal ganglion cells recorded remained unperturbed in the NL3 KO. Together our data underscore the importance of NL3 for the integrity of specific GABAAergic retinal circuits and identifies NL3 as an important regulator of retinal activity."],["dc.identifier.doi","10.1371/journal.pone.0181011"],["dc.identifier.pmid","28708891"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14546"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/58897"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","1932-6203"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.subject.ddc","610"],["dc.title","Loss of Neuroligin3 specifically downregulates retinal GABAAα2 receptors without abolishing direction selectivity."],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.contributor.author","de Montigny, Jean"],["dc.contributor.author","Krishnamoorthy, Vidhyasankar"],["dc.contributor.author","Rozenblit, Fernando"],["dc.contributor.author","Gollisch, Tim"],["dc.contributor.author","Sernagor, Evelyne"],["dc.date.accessioned","2021-03-05T08:58:52Z"],["dc.date.available","2021-03-05T08:58:52Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1101/2019.12.27.888792"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/80279"],["dc.notes.intern","DOI Import GROB-393"],["dc.title","Evidence for novel transient clusters of cholinergic ganglion cells in the neonatal mouse retina"],["dc.type","preprint"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","12192"],["dc.bibliographiccitation.issue","35"],["dc.bibliographiccitation.journal","The Journal of Neuroscience"],["dc.bibliographiccitation.lastpage","12203"],["dc.bibliographiccitation.volume","32"],["dc.contributor.author","Dieck, Susanne Tom"],["dc.contributor.author","Specht, Dana"],["dc.contributor.author","Strenzke, Nicola"],["dc.contributor.author","Hida, Yamato"],["dc.contributor.author","Krishnamoorthy, Vidhyasankar"],["dc.contributor.author","Schmidt, Karl-Friedrich"],["dc.contributor.author","Inoue, Eiji"],["dc.contributor.author","Ishizaki, Hiroyoshi"],["dc.contributor.author","Tanaka-Okamoto, Miki"],["dc.contributor.author","Miyoshi, Jun"],["dc.contributor.author","Hagiwara, Akari"],["dc.contributor.author","Brandstaetter, Johann Helmut"],["dc.contributor.author","Löwel, Siegrid"],["dc.contributor.author","Gollisch, Tim"],["dc.contributor.author","Ohtsuka, Toshihisa"],["dc.contributor.author","Moser, Tobias"],["dc.date.accessioned","2017-09-07T11:48:27Z"],["dc.date.available","2017-09-07T11:48:27Z"],["dc.date.issued","2012"],["dc.description.abstract","How size and shape of presynaptic active zones are regulated at the molecular level has remained elusive. Here we provide insight from studying rod photoreceptor ribbon-type active zones after disruption of CAST/ERC2, one of the cytomatrix of the active zone (CAZ) proteins. Rod photoreceptors were present in normal numbers, and the a-wave of the electroretinogram (ERG)-reflecting their physiological population response-was unchanged in CAST knock-out (CAST(-/-)) mice. Using immunofluorescence and electron microscopy, we found that the size of the rod presynaptic active zones, their Ca2+ channel complement, and the extension of the outer plexiform layer were diminished. Moreover, we observed sprouting of horizontal and bipolar cells toward the outer nuclear layer indicating impaired rod transmitter release. However, rod synapses of CAST(-/-) mice, unlike in mouse mutants for the CAZ protein Bassoon, displayed anchored ribbons, normal vesicle densities, clustered Ca2+ channels, and essentially normal molecular organization. The reduction of the rod active zone size went along with diminished amplitudes of the b-wave in scotopic ERGs. Assuming, based on the otherwise intact synaptic structure, an unaltered function of the remaining release apparatus, we take our finding to suggest a scaling of release rate with the size of the active zone. Multielectrode-array recordings of retinal ganglion cells showed decreased contrast sensitivity. This was also observed by optometry, which, moreover, revealed reduced visual acuity. We conclude that CAST supports large active zone size and high rates of transmission at rod ribbon synapses, which are required for normal vision."],["dc.identifier.doi","10.1523/JNEUROSCI.0752-12.2012"],["dc.identifier.gro","3142475"],["dc.identifier.isi","000308213900025"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/8696"],["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","1529-2401"],["dc.relation.issn","0270-6474"],["dc.title","Deletion of the Presynaptic Scaffold CAST Reduces Active Zone Size in Rod Photoreceptors and Impairs Visual Processing"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]