Nouvian, Régis

[["dc.bibliographiccitation.firstpage","411"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Nature Neuroscience"],["dc.bibliographiccitation.lastpage","413"],["dc.bibliographiccitation.volume","14"],["dc.contributor.author","Nouvian, Régis"],["dc.contributor.author","Neef, Jakob"],["dc.contributor.author","Bulankina, Anna V"],["dc.contributor.author","Reisinger, Ellen"],["dc.contributor.author","Pangršič, Tina"],["dc.contributor.author","Frank, Thomas"],["dc.contributor.author","Sikorra, Stefan"],["dc.contributor.author","Brose, Nils"],["dc.contributor.author","Binz, Thomas"],["dc.contributor.author","Moser, Tobias"],["dc.date.accessioned","2017-09-07T11:44:19Z"],["dc.date.available","2017-09-07T11:44:19Z"],["dc.date.issued","2011"],["dc.description.abstract","SNARE proteins mediate membrane fusion. Neurosecretion depends on neuronal soluble NSF attachment protein receptors ( SNAREs; SNAP-25, syntaxin-1, and synaptobrevin-1 or synaptobrevin-2) and is blocked by neurotoxin-mediated cleavage or genetic ablation. We found that exocytosis in mouse inner hair cells (IHCs) was insensitive to neurotoxins and genetic ablation of neuronal SNAREs. mRNA, but no synaptically localized protein, of neuronal SNAREs was present in IHCs. Thus, IHC exocytosis is unconventional and may operate independently of neuronal SNAREs."],["dc.identifier.doi","10.1038/nn.2774"],["dc.identifier.gro","3142757"],["dc.identifier.isi","000288849400007"],["dc.identifier.pmid","21378973"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/196"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","1097-6256"],["dc.title","Exocytosis at the hair cell ribbon synapse apparently operates without neuronal SNARE proteins"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","4886"],["dc.bibliographiccitation.issue","13"],["dc.bibliographiccitation.journal","The Journal of Neuroscience"],["dc.bibliographiccitation.lastpage","4895"],["dc.bibliographiccitation.volume","31"],["dc.contributor.author","Reisinger, Ellen"],["dc.contributor.author","Bresee, Chris"],["dc.contributor.author","Neef, Jakob"],["dc.contributor.author","Nair, Ramya"],["dc.contributor.author","Reuter, Kirsten"],["dc.contributor.author","Bulankina, Anna"],["dc.contributor.author","Nouvian, Régis"],["dc.contributor.author","Koch, Manuel"],["dc.contributor.author","Bückers, Johanna"],["dc.contributor.author","Kastrup, Lars"],["dc.contributor.author","Roux, Isabelle"],["dc.contributor.author","Petit, Christine"],["dc.contributor.author","Hell, Stefan W."],["dc.contributor.author","Brose, Nils"],["dc.contributor.author","Rhee, Jeong-Seop"],["dc.contributor.author","Kügler, Sebastian"],["dc.contributor.author","Brigande, John V."],["dc.contributor.author","Moser, Tobias"],["dc.date.accessioned","2017-09-07T11:44:21Z"],["dc.date.available","2017-09-07T11:44:21Z"],["dc.date.issued","2011"],["dc.description.abstract","Cochlear inner hair cells (IHCs) use Ca(2+)-dependent exocytosis of glutamate to signal sound information. Otoferlin (Otof), a C(2) domain protein essential for IHC exocytosis and hearing, may serve as a Ca(2+) sensor in vesicle fusion in IHCs that seem to lack the classical neuronal Ca(2+) sensors synaptotagmin 1 (Syt1) and Syt2. Support for the Ca(2+) sensor of fusion hypothesis for otoferlin function comes from biochemical experiments, but additional roles in late exocytosis upstream of fusion have been indicated by physiological studies. Here, we tested the functional equivalence of otoferlin and Syt1 in three neurosecretory model systems: auditory IHCs, adrenal chromaffin cells, and hippocampal neurons. Long- term and short- term ectopic expression of Syt1 in IHCs of Otof(-/-) mice by viral gene transfer in the embryonic inner ear and organotypic culture failed to rescue their Ca(2+) influx- triggered exocytosis. Conversely, virally mediated overexpression of otoferlin did not restore phasic exocytosis in Syt1- deficient chromaffin cells or neurons but enhanced asynchronous release in the latter. We further tested exocytosis in Otof(-/-) hippocampal neurons and in Syt1(-/-) IHCs but found no deficits in vesicle fusion. Expression analysis of different synaptotagminisoforms indicated that Syt1andSyt2 are absentfrommatureIHCs. Ourdata argue againstasimple functional equivalence of the two C(2) domain proteins in exocytosis of IHC ribbon synapses, chromaffin cells, and hippocampal synapses."],["dc.identifier.doi","10.1523/JNEUROSCI.5122-10.2011"],["dc.identifier.gro","3142759"],["dc.identifier.isi","000288938200015"],["dc.identifier.pmid","21451027"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/198"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10 / Funder: NIDCD NIH HHS [P30 DC005983, R01 DC008595, R01DC8595]"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","0270-6474"],["dc.title","Probing the Functional Equivalence of Otoferlin and Synaptotagmin 1 in Exocytosis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","705"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","The Journal of neuroscience"],["dc.bibliographiccitation.lastpage","716"],["dc.bibliographiccitation.volume","34"],["dc.contributor.author","Neef, Jakob"],["dc.contributor.author","Jung, SangYong"],["dc.contributor.author","Wong, Aaron B."],["dc.contributor.author","Reuter, Kirsten"],["dc.contributor.author","Pangršič, Tina"],["dc.contributor.author","Chakrabarti, Rituparna"],["dc.contributor.author","Kügler, Sebastian"],["dc.contributor.author","Lenz, Christine"],["dc.contributor.author","Nouvian, Regis"],["dc.contributor.author","Boumil, Rebecca M."],["dc.contributor.author","Frankel, Wayne N."],["dc.contributor.author","Wichmann, Carolin"],["dc.contributor.author","Moser, Tobias"],["dc.date.accessioned","2017-09-07T11:46:53Z"],["dc.date.available","2017-09-07T11:46:53Z"],["dc.date.issued","2014"],["dc.description.abstract","Synaptic vesicle recycling sustains high rates of neurotransmission at the ribbon-type active zones (AZs) of mouse auditory inner hair cells (IHCs), but its modes and molecular regulation are poorly understood. Electron microscopy indicated the presence of clathrin-mediated endocytosis (CME) and bulk endocytosis. The endocytic proteins dynamin, clathrin, and amphiphysin are expressed and broadly distributed in IHCs. We used confocal vglut1-pHluorin imaging and membrane capacitance (C-m) measurements to study the spatial organization and dynamics of IHC exocytosis and endocytosis. Viral gene transfer expressed vglut1-pHluorin in IHCs and targeted it to synaptic vesicles. The intravesicular pH was similar to 6.5, supporting only a modest increase of vglut1-pHluorin fluorescence during exocytosis and pH neutralization. Ca2+ influx triggered an exocytic increase of vglut1-pHluorin fluorescence at the AZs, around which it remained for several seconds. The endocytic C-m decline proceeded with constant rate (linear component) after exocytosis of the readily releasable pool (RRP). When exocytosis exceeded three to four RRP equivalents, IHCs additionally recruited a faster C-m decline (exponential component) that increased with the amount of preceding exocytosis and likely reflects bulk endocytosis. The dynamin inhibitor Dyngo-4a and the clathrin blocker pitstop 2 selectively impaired the linear component of endocytic C-m decline. A missense mutation of dynamin 1 (fitful) inhibited endocytosis to a similar extent as Dyngo-4a. We propose that IHCs use dynamin-dependent endocytosis via CME to support vesicle cycling during mild stimulation but recruit bulk endocytosis to balance massive exocytosis."],["dc.identifier.doi","10.1523/JNEUROSCI.3313-13.2014"],["dc.identifier.gro","3142198"],["dc.identifier.isi","000329916600004"],["dc.identifier.pmid","24431429"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/5621"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Soc Neuroscience"],["dc.relation.issn","0270-6474"],["dc.title","Modes and Regulation of Endocytic Membrane Retrieval in Mouse Auditory Hair Cells"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]