Brose, Nils

[["dc.bibliographiccitation.artnumber","2530.e5"],["dc.bibliographiccitation.firstpage","2521"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","Cell Reports"],["dc.bibliographiccitation.volume","26"],["dc.contributor.author","López-Murcia, Francisco José"],["dc.contributor.author","Reim, Kerstin"],["dc.contributor.author","Jahn, Olaf"],["dc.contributor.author","Taschenberger, Holger"],["dc.contributor.author","Brose, Nils"],["dc.date.accessioned","2019-07-09T11:50:32Z"],["dc.date.available","2019-07-09T11:50:32Z"],["dc.date.issued","2019"],["dc.description.abstract","SNARE-mediated synaptic vesicle (SV) fusion is controlled by multiple regulatory proteins that determine neurotransmitter release efficiency. Complexins are essential SNARE regulators whose mode of action is unclear, as available evidence indicates positive SV fusion facilitation and negative \"fusion clamp\"-like activities, with the latter occurring only in certain contexts. Because these contradictory findings likely originate in part from different experimental perturbation strategies, we attempted to resolve them by examining a conditional complexin-knockout mouse line as the most stringent genetic perturbation model available. We found that acute complexin loss after synaptogenesis in autaptic and mass-cultured hippocampal neurons reduces SV fusion probability and thus abates the rates of spontaneous, synchronous, asynchronous, and delayed transmitter release but does not affect SV priming or cause \"unclamping\" of spontaneous SV fusion. Thus, complexins act as facilitators of SV fusion but are dispensable for \"fusion clamping\" in mammalian forebrain neurons."],["dc.identifier.doi","10.1016/j.celrep.2019.02.030"],["dc.identifier.pmid","30840877"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/15955"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59788"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation","info:eu-repo/grantAgreement/EC/H2020/670283/EU//SYNPRIME"],["dc.relation.issn","2211-1247"],["dc.rights","CC BY-NC-ND 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc-nd/4.0"],["dc.subject.ddc","573"],["dc.subject.ddc","612"],["dc.title","Acute Complexin Knockout Abates Spontaneous and Evoked Transmitter Release"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","5400"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Nature Communications"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Babaev, Olga"],["dc.contributor.author","Cruces-Solis, Hugo"],["dc.contributor.author","Piletti Chatain, Carolina"],["dc.contributor.author","Hammer, Matthieu"],["dc.contributor.author","Wenger, Sally"],["dc.contributor.author","Ali, Heba"],["dc.contributor.author","Karalis, Nikolaos"],["dc.contributor.author","de Hoz, Livia"],["dc.contributor.author","Schlüter, Oliver M."],["dc.contributor.author","Yanagawa, Yuchio"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.contributor.author","Taschenberger, Holger"],["dc.contributor.author","Brose, Nils"],["dc.contributor.author","Krueger-Burg, Dilja"],["dc.date.accessioned","2019-07-09T11:50:16Z"],["dc.date.available","2019-07-09T11:50:16Z"],["dc.date.issued","2018"],["dc.description.abstract","Abnormalities in synaptic inhibition play a critical role in psychiatric disorders, and accordingly, it is essential to understand the molecular mechanisms linking components of the inhibitory postsynapse to psychiatrically relevant neural circuits and behaviors. Here we study the role of IgSF9b, an adhesion protein that has been associated with affective disorders, in the amygdala anxiety circuitry. We show that deletion of IgSF9b normalizes anxiety-related behaviors and neural processing in mice lacking the synapse organizer Neuroligin-2 (Nlgn2), which was proposed to complex with IgSF9b. This normalization occurs through differential effects of Nlgn2 and IgSF9b at inhibitory synapses in the basal and centromedial amygdala (CeM), respectively. Moreover, deletion of IgSF9b in the CeM of adult Nlgn2 knockout mice has a prominent anxiolytic effect. Our data place IgSF9b as a key regulator of inhibition in the amygdala and indicate that IgSF9b-expressing synapses in the CeM may represent a target for anxiolytic therapies."],["dc.identifier.doi","10.1038/s41467-018-07762-1"],["dc.identifier.pmid","30573727"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/15897"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59736"],["dc.identifier.url","https://sfb1190.med.uni-goettingen.de/production/literature/publications/49"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation","info:eu-repo/grantAgreement/EC/FP7/213342/EU//AIMS"],["dc.relation","SFB 1190: Transportmaschinen und Kontaktstellen zellulärer Kompartimente"],["dc.relation","SFB 1190 | P10: Rekrutierung und Verankerung von Neurotransmitterrezeptoren an GABAergen Synapsen - Zellbiologie und molekulare Mechanismen"],["dc.relation.issn","2041-1723"],["dc.relation.workinggroup","RG Brose"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.subject.ddc","612"],["dc.subject.mesh","Amygdala"],["dc.subject.mesh","Animals"],["dc.subject.mesh","Anxiety Disorders"],["dc.subject.mesh","Cell Adhesion Molecules, Neuronal"],["dc.subject.mesh","Membrane Proteins"],["dc.subject.mesh","Mice"],["dc.subject.mesh","Mice, Knockout"],["dc.subject.mesh","Nerve Tissue Proteins"],["dc.subject.mesh","RNA Interference"],["dc.subject.mesh","Synapses"],["dc.subject.mesh","Synaptic Transmission"],["dc.title","IgSF9b regulates anxiety behaviors through effects on centromedial amygdala inhibitory synapses"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","3980"],["dc.bibliographiccitation.issue","24"],["dc.bibliographiccitation.journal","Neuron"],["dc.bibliographiccitation.lastpage","4000.e7"],["dc.bibliographiccitation.volume","109"],["dc.contributor.author","Lipstein, Noa"],["dc.contributor.author","Chang, Shuwen"],["dc.contributor.author","Lin, Kun-Han"],["dc.contributor.author","López-Murcia, Francisco José"],["dc.contributor.author","Neher, Erwin"],["dc.contributor.author","Taschenberger, Holger"],["dc.contributor.author","Brose, Nils"],["dc.date.accessioned","2022-01-11T14:05:37Z"],["dc.date.available","2022-01-11T14:05:37Z"],["dc.date.issued","2021"],["dc.identifier.doi","10.1016/j.neuron.2021.09.054"],["dc.identifier.pii","S0896627321007273"],["dc.identifier.pmid","34706220"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/97705"],["dc.identifier.url","https://mbexc.uni-goettingen.de/literature/publications/401"],["dc.identifier.url","https://sfb1286.uni-goettingen.de/literature/publications/139"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-507"],["dc.relation","EXC 2067: Multiscale Bioimaging"],["dc.relation","SFB 1286: Quantitative Synaptologie"],["dc.relation.issn","0896-6273"],["dc.relation.workinggroup","RG Brose"],["dc.relation.workinggroup","RG Neher (Membrane Biophysics)"],["dc.rights","CC BY-NC-ND 4.0"],["dc.title","Munc13-1 is a Ca2+-phospholipid-dependent vesicle priming hub that shapes synaptic short-term plasticity and enables sustained neurotransmission"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","843"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Neuron"],["dc.bibliographiccitation.lastpage","860.e8"],["dc.bibliographiccitation.volume","108"],["dc.contributor.author","Imig, Cordelia"],["dc.contributor.author","López-Murcia, Francisco José"],["dc.contributor.author","Maus, Lydia"],["dc.contributor.author","García-Plaza, Inés Hojas"],["dc.contributor.author","Mortensen, Lena Sünke"],["dc.contributor.author","Schwark, Manuela"],["dc.contributor.author","Schwarze, Valentin"],["dc.contributor.author","Angibaud, Julie"],["dc.contributor.author","Nägerl, U. Valentin"],["dc.contributor.author","Taschenberger, Holger"],["dc.contributor.author","Brose, Nils"],["dc.contributor.author","Cooper, Benjamin H."],["dc.date.accessioned","2021-04-14T08:28:49Z"],["dc.date.available","2021-04-14T08:28:49Z"],["dc.date.issued","2020"],["dc.description.abstract","Electron microscopy can resolve synapse ultrastructure with nanometer precision, but the capture of time-resolved, activity-dependent synaptic membrane-trafficking events has remained challenging, particularly in functionally distinct synapses in a tissue context. We present a method that combines optogenetic stimulation-coupled cryofixation (“flash-and-freeze”) and electron microscopy to visualize membrane trafficking events and synapse-state-specific changes in presynaptic vesicle organization with high spatiotemporal resolution in synapses of cultured mouse brain tissue. With our experimental workflow, electrophysiological and “flash-and-freeze” electron microscopy experiments can be performed under identical conditions in artificial cerebrospinal fluid alone, without the addition of external cryoprotectants, which are otherwise needed to allow adequate tissue preservation upon freezing. Using this approach, we reveal depletion of docked vesicles and resolve compensatory membrane recycling events at individual presynaptic active zones at hippocampal mossy fiber synapses upon sustained stimulation."],["dc.identifier.doi","10.1016/j.neuron.2020.09.004"],["dc.identifier.pmid","32991831"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/82716"],["dc.identifier.url","https://mbexc.uni-goettingen.de/literature/publications/72"],["dc.identifier.url","https://sfb1286.uni-goettingen.de/literature/publications/58"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation","EXC 2067: Multiscale Bioimaging"],["dc.relation","SFB 1286: Quantitative Synaptologie"],["dc.relation","SFB 1286 | A01: Die Ultrastruktur der Synapse in Aktion"],["dc.relation.issn","0896-6273"],["dc.relation.workinggroup","RG Brose"],["dc.relation.workinggroup","RG Cooper"],["dc.rights","CC BY 4.0"],["dc.title","Ultrastructural Imaging of Activity-Dependent Synaptic Membrane-Trafficking Events in Cultured Brain Slices"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]