Chakrabarti, Rituparna

[["dc.bibliographiccitation.journal","eLife"],["dc.bibliographiccitation.volume","7"],["dc.contributor.author","Jean, Philippe"],["dc.contributor.author","Lopez de la Morena, David"],["dc.contributor.author","Michanski, Susann"],["dc.contributor.author","Jaime Tobón, Lina María"],["dc.contributor.author","Gültas, Mehmet"],["dc.contributor.author","Maxeiner, Stephan"],["dc.contributor.author","Strenzke, Nicola"],["dc.contributor.author","Chakrabarti, Rituparna"],["dc.contributor.author","Picher, Maria Magdalena"],["dc.contributor.author","Neef, Jakob"],["dc.contributor.author","Jung, SangYong"],["dc.contributor.author","Neef, Andreas"],["dc.contributor.author","Wichmann, Carolin"],["dc.contributor.author","Grabner, Chad"],["dc.contributor.author","Moser, Tobias"],["dc.date.accessioned","2020-11-24T10:41:13Z"],["dc.date.available","2020-11-24T10:41:13Z"],["dc.date.issued","2018"],["dc.description.abstract","We studied the role of the synaptic ribbon for sound encoding at the synapses between inner hair cells (IHCs) and spiral ganglion neurons (SGNs) in mice lacking RIBEYE (RBEKO/KO). Electron and immunofluorescence microscopy revealed a lack of synaptic ribbons and an assembly of several small active zones (AZs) at each synaptic contact. Spontaneous and sound-evoked firing rates of SGNs and their compound action potential were reduced, indicating impaired transmission at ribbonless IHC-SGN synapses. The temporal precision of sound encoding was impaired and the recovery of SGN-firing from adaptation indicated slowed synaptic vesicle (SV) replenishment. Activation of Ca2+-channels was shifted to more depolarized potentials and exocytosis was reduced for weak depolarizations. Presynaptic Ca2+-signals showed a broader spread, compatible with the altered Ca2+-channel clustering observed by super-resolution immunofluorescence microscopy. We postulate that RIBEYE disruption is partially compensated by multi-AZ organization. The remaining synaptic deficit indicates ribbon function in SV-replenishment and Ca2+-channel regulation."],["dc.identifier.doi","10.7554/eLife.29275"],["dc.identifier.eissn","2050-084X"],["dc.identifier.pmid","29328020"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/69157"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.relation.issn","2050-084X"],["dc.title","The synaptic ribbon is critical for sound encoding at high rates and with temporal precision"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2519"],["dc.bibliographiccitation.issue","23"],["dc.bibliographiccitation.journal","EMBO Journal"],["dc.bibliographiccitation.lastpage","2535"],["dc.bibliographiccitation.volume","35"],["dc.contributor.author","Strenzke, Nicola"],["dc.contributor.author","Chakrabarti, Rituparna"],["dc.contributor.author","Al‐Moyed, Hanan"],["dc.contributor.author","Müller, Alexandra"],["dc.contributor.author","Hoch, Gerhard"],["dc.contributor.author","Pangrsic, Tina"],["dc.contributor.author","Yamanbaeva, Gulnara"],["dc.contributor.author","Lenz, Christof"],["dc.contributor.author","Pan, Kuan‐Ting"],["dc.contributor.author","Auge, Elisabeth"],["dc.contributor.author","Geiss‐Friedlander, Ruth"],["dc.contributor.author","Urlaub, Henning"],["dc.contributor.author","Brose, Nils"],["dc.contributor.author","Wichmann, Carolin"],["dc.contributor.author","Reisinger, Ellen"],["dc.date.accessioned","2017-09-07T11:52:19Z"],["dc.date.available","2017-09-07T11:52:19Z"],["dc.date.issued","2016"],["dc.identifier.doi","10.15252/embj.201694564"],["dc.identifier.gro","3144895"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/2570"],["dc.language.iso","en"],["dc.notes.intern","Crossref Import"],["dc.notes.status","final"],["dc.relation.issn","0261-4189"],["dc.title","Hair cell synaptic dysfunction, auditory fatigue and thermal sensitivity in otoferlin Ile515Thr mutants"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","E3141"],["dc.bibliographiccitation.issue","24"],["dc.bibliographiccitation.journal","Proceedings of the National Academy of Sciences"],["dc.bibliographiccitation.lastpage","E3149"],["dc.bibliographiccitation.volume","112"],["dc.contributor.author","Jung, Sangyong"],["dc.contributor.author","Oshima-Takago, Tomoko"],["dc.contributor.author","Chakrabarti, Rituparna"],["dc.contributor.author","Wong, Aaron B."],["dc.contributor.author","Jing, Zhizi"],["dc.contributor.author","Yamanbaeva, Gulnara"],["dc.contributor.author","Picher, Maria Magdalena"],["dc.contributor.author","Wojcik, Sonja M."],["dc.contributor.author","Göttfert, Fabian"],["dc.contributor.author","Predoehl, Friederike"],["dc.contributor.author","Michel, Katrin"],["dc.contributor.author","Hell, Stefan"],["dc.contributor.author","Schoch, Susanne"],["dc.contributor.author","Strenzke, Nicola"],["dc.contributor.author","Wichmann, Carolin"],["dc.contributor.author","Moser, Tobias"],["dc.date.accessioned","2017-09-07T11:43:46Z"],["dc.date.available","2017-09-07T11:43:46Z"],["dc.date.issued","2015"],["dc.description.abstract","Ca2+ influx triggers the fusion of synaptic vesicles at the presynaptic active zone (AZ). Here we demonstrate a role of Ras-related in brain 3 (Rab3)-interacting molecules 2 alpha and beta (RIM2 alpha and RIM2 beta) in clustering voltage-gated Ca(V)1.3 Ca2+ channels at the AZs of sensory inner hair cells (IHCs). We show that IHCs of hearing mice express mainly RIM2 alpha, but also RIM2 beta and RIM3., which all localize to the AZs, as shown by immunofluorescence microscopy. Immunohistochemistry, patch-clamp, fluctuation analysis, and confocal Ca2+ imaging demonstrate that AZs of RIM2 alpha-deficient IHCs cluster fewer synaptic Ca(V)1.3 Ca2+ channels, resulting in reduced synaptic Ca2+ influx. Using superresolution microscopy, we found that Ca2+ channels remained clustered in stripes underneath anchored ribbons. Electron tomography of high-pressure frozen synapses revealed a reduced fraction of membrane-tethered vesicles, whereas the total number of membrane-proximal vesicles was unaltered. Membrane capacitance measurements revealed a reduction of exocytosis largely in proportion with the Ca2+ current, whereas the apparent Ca2+ dependence of exocytosis was unchanged. Hair cell-specific deletion of all RIM2 isoforms caused a stronger reduction of Ca2+ influx and exocytosis and significantly impaired the encoding of sound onset in the postsynaptic spiral ganglion neurons. Auditory brainstem responses indicated a mild hearing impairment on hair cell-specific deletion of all RIM2 isoforms or global inactivation of RIM2 alpha. We conclude that RIM2 alpha and RIM2 beta promote a large complement of synaptic Ca2+ channels at IHC AZs and are required for normal hearing."],["dc.identifier.doi","10.1073/pnas.1417207112"],["dc.identifier.gro","3141887"],["dc.identifier.isi","000356251800010"],["dc.identifier.pmid","26034270"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/2178"],["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","0027-8424"],["dc.title","Rab3-interacting molecules 2α and 2β promote the abundance of voltage-gated CaV1.3 Ca2+ channels at hair cell active zones"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]