Dresbach, Thomas

[["dc.bibliographiccitation.firstpage","521"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Neuron"],["dc.bibliographiccitation.lastpage","533"],["dc.bibliographiccitation.volume","87"],["dc.contributor.author","Körber, Christoph"],["dc.contributor.author","Horstmann, Heinz"],["dc.contributor.author","Venkataramani, Varun"],["dc.contributor.author","Herrmannsdörfer, Frank"],["dc.contributor.author","Kremer, Thomas"],["dc.contributor.author","Kaiser, Michaela"],["dc.contributor.author","Schwenger, Darius B."],["dc.contributor.author","Ahmed, Saheeb"],["dc.contributor.author","Dean, Camin"],["dc.contributor.author","Dresbach, Thomas"],["dc.contributor.author","Kuner, Thomas"],["dc.date.accessioned","2018-09-28T09:27:35Z"],["dc.date.available","2018-09-28T09:27:35Z"],["dc.date.issued","2015"],["dc.description.abstract","Mover, a member of the exquisitely small group of vertebrate-specific presynaptic proteins, has been discovered as an interaction partner of the scaffolding protein Bassoon, yet its function has not been elucidated. We used adeno-associated virus (AAV)-mediated shRNA expression to knock down Mover in the calyx of Held in vivo. Although spontaneous synaptic transmission remained unaffected, we found a strong increase of the evoked EPSC amplitude. The size of the readily releasable pool was unaltered, but short-term depression was accelerated and enhanced, consistent with an increase in release probability after Mover knockdown. This increase in release probability was not caused by alterations in Ca(2+) influx but rather by a higher Ca(2+) sensitivity of the release machinery, as demonstrated by presynaptic Ca(2+) uncaging. We therefore conclude that Mover expression in certain subsets of synapses negatively regulates synaptic release probability, constituting a novel mechanism to tune synaptic transmission."],["dc.identifier.doi","10.1016/j.neuron.2015.07.001"],["dc.identifier.pmid","26212709"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/15842"],["dc.language.iso","en"],["dc.notes.status","zu prüfen"],["dc.relation.eissn","1097-4199"],["dc.title","Modulation of Presynaptic Release Probability by the Vertebrate-Specific Protein Mover"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","13564"],["dc.bibliographiccitation.issue","32"],["dc.bibliographiccitation.journal","Proceedings of the National Academy of Sciences"],["dc.bibliographiccitation.lastpage","13569"],["dc.bibliographiccitation.volume","106"],["dc.contributor.author","Wittenmayer, Nina"],["dc.contributor.author","Koerber, Christoph"],["dc.contributor.author","Liu, Huisheng"],["dc.contributor.author","Kremer, Thomas"],["dc.contributor.author","Varoqueaux, Frederique"],["dc.contributor.author","Chapman, Edwin R."],["dc.contributor.author","Brose, Nils"],["dc.contributor.author","Kuner, Thomas"],["dc.contributor.author","Dresbach, Thomas"],["dc.date.accessioned","2017-09-07T11:46:51Z"],["dc.date.available","2017-09-07T11:46:51Z"],["dc.date.issued","2009"],["dc.description.abstract","Presynaptic nerve terminals pass through distinct stages of maturation after their initial assembly. Here we show that the postsynaptic cell adhesion molecule Neuroligin1 regulates key steps of presynaptic maturation. Presynaptic terminals from Neuroligin1-knockout mice remain structurally and functionally immature with respect to active zone stability and synaptic vesicle pool size, as analyzed in cultured hippocampal neurons. Conversely, overexpression of Neuroligin1 in immature neurons, that is within the first 5 days after plating, induced the formation of presynaptic boutons that had hallmarks of mature boutons. In particular, Neuroligin1 enhanced the size of the pool of recycling synaptic vesicles, the rate of synaptic vesicle exocytosis, the fraction of boutons responding to depolarization, as well as the responsiveness of the presynaptic release machinery to phorbol ester stimulation. Moreover, Neuroligin1 induced the formation of active zones that remained stable in the absence of F-actin, another hallmark of advanced maturation. Acquisition of F-actin independence of the active zone marker Bassoon during culture development or induced via overexpression of Neuroligin1 was activity-dependent. The extracellular domain of Neuroligin1 was sufficient to induce assembly of functional presynaptic terminals, while the intracellular domain was required for terminal maturation. These data show that induction of presynaptic terminal assembly and maturation involve mechanistically distinct actions of Neuroligins, and that Neuroligin1 is essential for presynaptic terminal maturation."],["dc.identifier.doi","10.1073/pnas.0905819106"],["dc.identifier.gro","3143076"],["dc.identifier.isi","000268877300075"],["dc.identifier.pmid","19628693"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/550"],["dc.notes.intern","WoS Import 2017-03-10 / Funder: Deutsche Forschungsgemeinschaft [DR 373/3-2, DR 373/3-3]"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Natl Acad Sciences"],["dc.relation.issn","0027-8424"],["dc.title","Postsynaptic Neuroligin1 regulates presynaptic maturation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]