ReviewJournal of anatomy2007
Use-dependent control of presynaptic calcium signalling at central synapses.
Review in Journal of anatomy, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
6 citing papers in PubMed.
- Use-dependent potentiation of voltage-gated calcium channels rescues neurotransmission in nerve terminals intoxicated by botulinum neurotoxin serotype A.Scientific reports · 2017Article
- Multiple Sources of Ca2+ Contribute to Methylmercury-Induced Increased Frequency of Spontaneous Inhibitory Synaptic Responses in Cerebellar Slices of Rat.Toxicological sciences : an official journal of the Society of Toxicology · 2016Article
- Mitochondrial Calcium Uptake Modulates Synaptic Vesicle Endocytosis in Central Nerve Terminals.The Journal of biological chemistry · 2016Article
- Activity-dependent regulation of release probability at excitatory hippocampal synapses: a crucial role of fragile X mental retardation protein in neurotransmission.The European journal of neuroscience · 2014Article
- Abnormal presynaptic short-term plasticity and information processing in a mouse model of fragile X syndrome.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011Article
- Ionic conditions modulate stimulus-induced capacitance changes in isolated neurohypophysial terminals of the rat.The Journal of physiology · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Voltage-gated Ca(2+) channels activated by action potentials evoke Ca(2+) entry into presynaptic terminals thus briefly distorting the resting Ca(2+) concentration. When this happens, a number of processes are initiated to re-establish the Ca(2+) equilibrium. During the post-spike period, the increased Ca(2+) concentration could enhance the presynaptic Ca(2+) signalling. Some of the mechanisms contributing to presynaptic Ca(2+) dynamics involve endogenous Ca(2+) buffers, Ca(2+) stores, mitochondria, the sodium-calcium exchanger, extraterminal Ca(2+) depletion and presynaptic receptors. Additionally, subthreshold presynaptic depolarization has been proposed to have an effect on release of neurotransmitters through a mechanism involving changes in resting Ca(2+). Direct evidence for the role of any of these participants in shaping the presynaptic Ca(2+) dynamics comes from direct recordings of giant presynaptic terminals and from fluorescent Ca(2+) imaging of axonal boutons. Here, some of this evidence is presented and discussed.
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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.