Bharat, Vinita

[["dc.bibliographiccitation.artnumber","27"],["dc.bibliographiccitation.journal","Frontiers in synaptic neuroscience"],["dc.bibliographiccitation.volume","6"],["dc.contributor.author","Shinoda, Yo"],["dc.contributor.author","Ahmed, Saheeb"],["dc.contributor.author","Ramachandran, Binu"],["dc.contributor.author","Bharat, Vinita"],["dc.contributor.author","Brockelt, David"],["dc.contributor.author","Altas, Bekir"],["dc.contributor.author","Dean, Camin"],["dc.date.accessioned","2019-07-09T11:41:08Z"],["dc.date.available","2019-07-09T11:41:08Z"],["dc.date.issued","2014"],["dc.description.abstract","Brain-derived neurotrophic factor (BDNF) is widely reported to enhance synaptic vesicle (SV) exocytosis and neurotransmitter release. But it is still unclear whether BDNF enhances SV recycling at excitatory terminals only, or at both excitatory and inhibitory terminals. In the present study, in a direct comparison using cultured rat hippocampal neurons, we demonstrate that BDNF enhances both spontaneous and activity-dependent neurotransmitter release from excitatory terminals, but not from inhibitory terminals. BDNF treatment for 5 min or 48 h increased both spontaneous and activity-induced anti-synaptotagmin1 (SYT1) antibody uptake at excitatory terminals marked with vGluT1. Conversely, BDNF treatment did not enhance spontaneous or activity-induced uptake of anti-SYT1 antibodies in inhibitory terminals marked with vGAT. Time-lapse imaging of FM1-43 dye destaining in excitatory and inhibitory terminals visualized by post-hoc immunostaining of vGluT1 and vGAT also showed the same result: The rate of spontaneous and activity-induced destaining was increased by BDNF at excitatory synapses, but not at inhibitory synapses. These data demonstrate that BDNF enhances SV exocytosis in excitatory but not inhibitory terminals. Moreover, BDNF enhanced evoked SV exocytosis, even if vesicles were loaded under spontaneous vesicle recycling conditions. Thus, BDNF enhances both spontaneous and activity-dependent neurotransmitter release on both short and long time-scales, by the same mechanism."],["dc.identifier.doi","10.3389/fnsyn.2014.00027"],["dc.identifier.fs","607146"],["dc.identifier.pmid","25426063"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/11694"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/58356"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation","info:eu-repo/grantAgreement/EC/FP7/260916/EU//SYT"],["dc.relation.euproject","SytActivity"],["dc.relation.issn","1663-3563"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","BDNF enhances spontaneous and activity-dependent neurotransmitter release at excitatory terminals but not at inhibitory terminals in hippocampal neurons."],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2118"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","Cell reports"],["dc.bibliographiccitation.lastpage","2133"],["dc.bibliographiccitation.volume","21"],["dc.contributor.author","Bharat, Vinita"],["dc.contributor.author","Siebrecht, Michael"],["dc.contributor.author","Burk, Katja"],["dc.contributor.author","Ahmed, Saheeb"],["dc.contributor.author","Reissner, Carsten"],["dc.contributor.author","Kohansal-Nodehi, Mahdokht"],["dc.contributor.author","Steubler, Vicky"],["dc.contributor.author","Zweckstetter, Markus"],["dc.contributor.author","Ting, Jonathan T"],["dc.contributor.author","Dean, Camin"],["dc.date.accessioned","2019-07-09T11:44:43Z"],["dc.date.available","2019-07-09T11:44:43Z"],["dc.date.issued","2017-11-21"],["dc.description.abstract","Delivery of neurotrophins and neuropeptides via long-range trafficking of dense core vesicles (DCVs) from the cell soma to nerve terminals is essential for synapse modulation and circuit function. But the mechanism by which transiting DCVs are captured at specific sites is unknown. Here, we discovered that Synaptotagmin-4 (Syt4) regulates the capture and spatial distribution of DCVs in hippocampal neurons. We found that DCVs are highly mobile and undergo long-range translocation but switch directions only at the distal ends of axons, revealing a circular trafficking pattern. Phosphorylation of serine 135 of Syt4 by JNK steers DCV trafficking by destabilizing Syt4-Kif1A interaction, leading to a transition from microtubule-dependent DCV trafficking to capture at en passant presynaptic boutons by actin. Furthermore, neuronal activity increased DCV capture via JNK-dependent phosphorylation of the S135 site of Syt4. Our data reveal a mechanism that ensures rapid, site-specific delivery of DCVs to synapses."],["dc.identifier.doi","10.1016/j.celrep.2017.10.084"],["dc.identifier.pmid","29166604"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14878"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59077"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation","info:eu-repo/grantAgreement/EC/FP7/260916/EU//SYT ACTIVITY"],["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","612"],["dc.title","Capture of Dense Core Vesicles at Synapses by JNK-Dependent Phosphorylation of Synaptotagmin-4."],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","2149"],["dc.bibliographiccitation.firstpage","1"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Scientific reports"],["dc.bibliographiccitation.lastpage","19"],["dc.bibliographiccitation.volume","7"],["dc.contributor.author","Burk, Katja"],["dc.contributor.author","Fischer, André"],["dc.contributor.author","Murdoch, John D"],["dc.contributor.author","Koenig, Melanie"],["dc.contributor.author","Bharat, Vinita"],["dc.contributor.author","Markworth, Ronja"],["dc.contributor.author","Burkhardt, Susanne"],["dc.contributor.author","Dean, Camin"],["dc.date.accessioned","2018-01-09T14:36:50Z"],["dc.date.available","2018-01-09T14:36:50Z"],["dc.date.issued","2017-05-19"],["dc.description.abstract","The sorting of activated receptors into distinct endosomal compartments is essential to activate specific signaling cascades and cellular events including growth and survival. However, the proteins involved in this sorting are not well understood. We discovered a novel role of EndophilinAs in sorting of activated BDNF-TrkB receptors into late endosomal compartments. Mice lacking all three EndophilinAs accumulate Rab7-positive late endosomes. Moreover, EndophilinAs are differentially localized to, co-traffic with, and tubulate, distinct endosomal compartments: In response to BDNF, EndophilinA2 is recruited to both early and late endosomes, EndophilinA3 is recruited to Lamp1-positive late endosomes, and co-trafficks with Rab5 and Rab7 in both the presence and absence of BDNF, while EndophilinA1 colocalizes at lower levels with endosomes. The absence of all three EndophilinAs caused TrkB to accumulate in EEA1 and Rab7-positive endosomes, and impaired BDNF-TrkB-dependent survival signaling cascades. In addition, EndophilinA triple knockout neurons exhibited increased cell death which could not be rescued by exogenous BDNF, in a neurotrophin-dependent survival assay. Thus, EndophilinAs differentially regulate activated receptor sorting via distinct endosomal compartments to promote BDNF-dependent cell survival."],["dc.identifier.doi","10.1038/s41598-017-02202-4"],["dc.identifier.pmid","28526875"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14709"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/11603"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.relation.eissn","2045-2322"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","EndophilinAs regulate endosomal sorting of BDNF-TrkB to mediate survival signaling in hippocampal neurons"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]