ReviewThe Journal of physiology2013
Transients in global Ca2+ concentration induced by electrical activity in a giant nerve terminal.
Review in The Journal of physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
9 citing papers in PubMed, 14 citations in OpenAlex.
- Complexin has a dual synaptic function as checkpoint protein in vesicle priming and as a promoter of vesicle fusion.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- EGTA Can Inhibit Vesicular Release in the Nanodomain of Single CaFrontiers in synaptic neuroscience · 2019Article
- Variations in CaThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- Dynamics of volume-averaged intracellular CaThe Journal of physiology · 2017Article
- Molecular Machines Regulating the Release Probability of Synaptic Vesicles at the Active Zone.Frontiers in synaptic neuroscience · 2016Review
- Location matters: somatic and dendritic SK channels answer to distinct calcium signals.Journal of neurophysiology · 2015Article
- Reduced endogenous Ca2+ buffering speeds active zone Ca2+ signaling.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Calcium-buffering effects of gluconate and nucleotides, as determined by a novel fluorimetric titration method.The Journal of physiology · 2014Article
- Size matters: formation and function of giant synapses.The Journal of physiology · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Giant nerve terminals offer a unique opportunity to learn about dynamic changes in intracellular global Ca(2+) concentration ([Ca(2+)]i) because this quantity can be measured precisely with indicator dyes and the composition of the intra-terminal ionic milieu can be controlled. We review here recent literature on [Ca(2+)]i signalling in the calyx of Held and discuss what these measurements can tell us about endogenous Ca(2+) buffers and Ca(2+) extrusion mechanisms. We conclude that in spite of the favourable experimental conditions, some unresolved questions still remain regarding absolute values for the Ca(2+)-binding ratio, the affinity of the basic fixed buffer and the Ca(2+) affinities of the major endogenous Ca(2+) binding proteins. Uncertainties about some of these presynaptic properties, including the roles of Mg(2+) and ATP (as a Mg(2+) buffer), however, extend to the point that mechanisms controlling the decay of [Ca(2+)]i signals in unperturbed terminals may have to be reconsidered.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.