ArticlePloS one2011
An inhibitory effect of extracellular Ca2+ on Ca2+-dependent exocytosis.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed, 5 citations in OpenAlex.
- Pharmacological implications of the Ca(2+)/cAMP signaling interaction: from risk for antihypertensive therapy to potential beneficial for neurological and psychiatric disorders.Pharmacology research & perspectives · 2015Review
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Authors and funding
12 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimNeurotransmitter 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.
resultsUsing 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 µM). 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.
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