ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2011
Correlated variations in the parameters that regulate dendritic calcium signaling in mouse retinal ganglion cells.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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.
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Who cites it
3 citing papers in PubMed, 6 citations in OpenAlex.
- Purification of retinal ganglion cells using low-pressure flow cytometry.Frontiers in molecular neuroscience · 2023Article
- Endogenous calcium buffering at photoreceptor synaptic terminals in salamander retina.Synapse (New York, N.Y.) · 2014Article
- Spatial distribution of excitatory synapses on the dendrites of ganglion cells in the mouse retina.PloS one · 2014Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The amplitude and time course of stimulus-evoked second messenger signals carried by intracellular changes in free calcium ([Ca](free)) depend on the total influx of Ca(2+), the fraction bound to endogenous buffer and the rate of extrusion. Estimates of the values of these three parameters in proximal dendrites of 15 mouse α retinal ganglion cells were made using the "added buffer" method and found to vary greatly from one experiment to the next. The variations in the measured parameters were strongly correlated across the sample of cells. This reduced the variability in the amplitude and time course of the dendritic Ca(2+) signal and suggests that the expression of Ca(2+) channels, binding proteins and extrusion mechanisms is homeostatically coordinated to maintain the amplitude and kinetics of the Ca(2+) signal within a physiologically appropriate range.
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Registered trials
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