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dc.contributor.authorMorton, Andrew
dc.contributor.authorMarland, Jamie R K
dc.contributor.authorCousin, Michael A
dc.date.accessioned2015-12-02T11:40:07Z
dc.date.available2015-12-02T11:40:07Z
dc.date.issued2015-08
dc.identifier.citationMorton , A , Marland , J R K & Cousin , M A 2015 , ' Synaptic vesicle exocytosis and increased cytosolic calcium are both necessary but not sufficient for activity-dependent bulk endocytosis ' , Journal of Neurochemistry , vol. 134 , no. 3 , pp. 405-415 . https://doi.org/10.1111/jnc.13132en
dc.identifier.issn0022-3042
dc.identifier.otherPURE: 184104423
dc.identifier.otherPURE UUID: f0d88c65-ae65-4f28-8813-3a8e6dd9754a
dc.identifier.otherPubMed: 25913068
dc.identifier.otherScopus: 84935418154
dc.identifier.urihttps://hdl.handle.net/10023/7879
dc.descriptionThis work was supported by the Medical Research Council [Grant number: G1002117] and a PhD studentship from the Biotechnology and Biological Sciences Research Council.en
dc.description.abstractActivity-dependent bulk endocytosis (ADBE) is the dominant synaptic vesicle (SV) endocytosis mode in central nerve terminals during intense neuronal activity. By definition, this mode is triggered by neuronal activity; however, key questions regarding its mechanism of activation remain unaddressed. To determine the basic requirements for ADBE triggering in central nerve terminals, we decoupled SV fusion events from activity-dependent calcium influx using either clostridial neurotoxins or buffering of intracellular calcium. ADBE was monitored both optically and morphologically by observing uptake of the fluid phase markers tetramethylrhodamine-dextran and horse radish peroxidase respectively. Ablation of SV fusion with tetanus toxin resulted in the arrest of ADBE, but had no effect on other calcium-dependent events such as activity-dependent dynamin I dephosphorylation, indicating that SV exocytosis is necessary for triggering. Furthermore, the calcium chelator EGTA abolished ADBE while leaving SV exocytosis intact, demonstrating that ADBE is triggered by intracellular free calcium increases outside the active zone. Activity-dependent dynamin I dephosphorylation was also arrested in EGTA-treated neurons, consistent with its proposed role in triggering ADBE. Thus SV fusion and increased cytoplasmic free calcium are both necessary but not sufficient individually to trigger ADBE. This article is protected by copyright. All rights reserved.
dc.format.extent11
dc.language.isoeng
dc.relation.ispartofJournal of Neurochemistryen
dc.rights© 2015 The Authors. Journal of Neurochemistry published by John Wiley & Sons Ltd on behalf of International Society for Neurochemistry. This is an open access article under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/), which permits use, distribution and reproduction in any medium, provided the original work is properly cited.en
dc.subjectCalciumen
dc.subjectDynaminen
dc.subjectEndocytosisen
dc.subjectExocytosisen
dc.subjectPresynapseen
dc.subjectVesicleen
dc.subjectRC0321 Neuroscience. Biological psychiatry. Neuropsychiatryen
dc.subjectQD Chemistryen
dc.subjectNDASen
dc.subject.lccRC0321en
dc.subject.lccQDen
dc.titleSynaptic vesicle exocytosis and increased cytosolic calcium are both necessary but not sufficient for activity-dependent bulk endocytosisen
dc.typeJournal articleen
dc.description.versionPublisher PDFen
dc.contributor.institutionUniversity of St Andrews. School of Physics and Astronomyen
dc.identifier.doihttps://doi.org/10.1111/jnc.13132
dc.description.statusPeer revieweden


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