Please use this identifier to cite or link to this item: https://doi.org/10.1371/journal.pone.0024573
DC FieldValue
dc.titleAn inhibitory effect of extracellular Ca 2+ on Ca 2+-dependent exocytosis
dc.contributor.authorXiong W.
dc.contributor.authorLiu T.
dc.contributor.authorWang Y.
dc.contributor.authorChen X.
dc.contributor.authorSun L.
dc.contributor.authorGuo N.
dc.contributor.authorZheng H.
dc.contributor.authorZheng L.
dc.contributor.authorRuat M.
dc.contributor.authorHan W.
dc.contributor.authorZhang C.X.
dc.contributor.authorZhou Z.
dc.date.accessioned2019-11-11T08:37:17Z
dc.date.available2019-11-11T08:37:17Z
dc.date.issued2011
dc.identifier.citationXiong W., Liu T., Wang Y., Chen X., Sun L., Guo N., Zheng H., Zheng L., Ruat M., Han W., Zhang C.X., Zhou Z. (2011). An inhibitory effect of extracellular Ca 2+ on Ca 2+-dependent exocytosis. PLoS ONE 6 (10) : e24573. ScholarBank@NUS Repository. https://doi.org/10.1371/journal.pone.0024573
dc.identifier.issn19326203
dc.identifier.urihttps://scholarbank.nus.edu.sg/handle/10635/162028
dc.description.abstractAim: Neurotransmitter release is elicited by an elevation of intracellular Ca 2+ concentration ([Ca 2+] i). The action potential triggers Ca 2+ influx through Ca 2+ channels which causes local changes of [Ca 2+] i for vesicle release. However, any direct role of extracellular Ca 2+ (besides Ca 2+ influx) on Ca 2+-dependent exocytosis remains elusive. Here we set out to investigate this possibility on rat dorsal root ganglion (DRG) neurons and chromaffin cells, widely used models for studying vesicle exocytosis. Results: Using photolysis of caged Ca 2+ and caffeine-induced release of stored Ca 2+, we found that extracellular Ca 2+ inhibited exocytosis following moderate [Ca 2+] i rises (2-3 ?M). The IC 50 for extracellular Ca 2+ inhibition of exocytosis (ECIE) was 1.38 mM and a physiological reduction (~30%) of extracellular Ca 2+ concentration ([Ca 2+] o) significantly increased the evoked exocytosis. At the single vesicle level, quantal size and release frequency were also altered by physiological [Ca 2+] o. The calcimimetics Mg 2+, Cd 2+, G418, and neomycin all inhibited exocytosis. The extracellular Ca 2+-sensing receptor (CaSR) was not involved because specific drugs and knockdown of CaSR in DRG neurons did not affect ECIE. Conclusion/Significance: As an extension of the classic Ca 2+ hypothesis of synaptic release, physiological levels of extracellular Ca 2+ play dual roles in evoked exocytosis by providing a source of Ca 2+ influx, and by directly regulating quantal size and release probability in neuronal cells. © 2011 Xiong et al.
dc.rightsAttribution 4.0 International
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/
dc.sourceUnpaywall 20191101
dc.subjectantibiotic g 418
dc.subjectcadmium
dc.subjectcaffeine
dc.subjectcalcium ion
dc.subjectcalcium sensing receptor
dc.subjectmagnesium ion
dc.subjectneomycin
dc.subjectcaffeine
dc.subjectcalcimimetic agent
dc.subjectcalcium
dc.subjectanimal cell
dc.subjectanimal tissue
dc.subjectarticle
dc.subjectcalcium transport
dc.subjectcell vacuole
dc.subjectchromaffin cell
dc.subjectconcentration (parameters)
dc.subjectexocytosis
dc.subjectextracellular calcium
dc.subjectinhibition kinetics
dc.subjectnerve cell
dc.subjectnonhuman
dc.subjectphotolysis
dc.subjectrat
dc.subjectspinal ganglion
dc.subjectanimal
dc.subjectcell membrane
dc.subjectcytology
dc.subjectdrug effect
dc.subjectextracellular space
dc.subjectmetabolism
dc.subjectWistar rat
dc.subjectRattus
dc.subjectAnimals
dc.subjectCaffeine
dc.subjectCalcimimetic Agents
dc.subjectCalcium
dc.subjectCell Membrane
dc.subjectChromaffin Cells
dc.subjectExocytosis
dc.subjectExtracellular Space
dc.subjectGanglia, Spinal
dc.subjectNeurons
dc.subjectPhotolysis
dc.subjectRats
dc.subjectRats, Wistar
dc.typeArticle
dc.contributor.departmentDEAN'S OFFICE (DUKE-NUS MEDICAL SCHOOL)
dc.contributor.departmentDUKE-NUS MEDICAL SCHOOL
dc.description.doi10.1371/journal.pone.0024573
dc.description.sourcetitlePLoS ONE
dc.description.volume6
dc.description.issue10
dc.description.pagee24573
dc.published.statePublished
Appears in Collections:Elements
Staff Publications

Show simple item record
Files in This Item:
File Description SizeFormatAccess SettingsVersion 
10_1371_journal_pone_0024573.pdf625.76 kBAdobe PDF

OPEN

NoneView/Download

Google ScholarTM

Check

Altmetric


This item is licensed under a Creative Commons License Creative Commons