ArticleISRN neurology2011
Ca/Calmodulin and presynaptic short-term plasticity.
Article in ISRN neurology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed, 10 citations in OpenAlex.
- Melatonin and the Brain-Heart Crosstalk in Neurocritically Ill Patients-From Molecular Action to Clinical Practice.International journal of molecular sciences · 2022Review
- Astrocyte Intracellular CaNeurotoxicity research · 2021Article
- Metabotropic glutamate receptor trafficking.Molecular and cellular neurosciences · 2018Review
- Millisecond CaProceedings of the Japan Academy. Series B, Physical and biological sciences · 2017Review
- Altered short-term plasticity in the prefrontal cortex after early life seizures.Neurobiology of disease · 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
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Synaptic efficacy is remodeled by neuronal firing activity at the presynaptic terminal. Presynaptic activity-dependent changes in transmitter release induce postsynaptic plasticity, including morphological change in spine, gene transcription, and protein synthesis and trafficking. The presynaptic transmitter release is triggered and regulated by Ca(2+), which enters through voltage-gated Ca(2+) (Ca(V)) channels and diffuses into the presynaptic terminal accompanying action potential firings. Residual Ca(2+) is sensed by Ca(2+)-binding proteins, among other potential actions, it mediates time- and space-dependent synaptic facilitation and depression via effects on Ca(V)2 channel gating and vesicle replenishment in the readily releasable pool (RRP). Calmodulin, a Ca(2+)-sensor protein with an EF-hand motif that binds Ca(2+), interacts with Ca(V)2 channels and autoreceptors in modulation of SNARE-mediated exocytosis.
Identifiers
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.