Evidence map›Paper›PMID 18446197›Full record

ArticlePloS one2008

Calmodulin activation by calcium transients in the postsynaptic density of dendritic spines.

Daniel X Keller, Kevin M Franks, Thomas M Bartol, Terrence J Sejnowski

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
3.4field-weighted citation impact, top 7% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

51 citing papers in PubMed, 100 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. A spatial model of autophosphorylation of CabioRxiv : the preprint server for biology · 2024
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  8. Review
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  10. Stationary CaBiophysical journal · 2021
    Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Competitive Tuning Among CaCellular and molecular bioengineering · 2018
    Article
  16. Article
  17. Article
  18. Article
  19. Reproducibility in Computational Neuroscience Models and Simulations.IEEE transactions on bio-medical engineering · 2016
    Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 2 institutions in 1 country.

Daniel X KellerThe Salk Institute, Computational Neurobiology Laboratory, and Howard Hughes Medical Institute, La Jolla, California, United States of America. dkeller@salk.edu
Kevin M Franks
Thomas M Bartol
Terrence J Sejnowski
University of California, San Diego · USHoward Hughes Medical Institute · US

Funding

Simulation of Activation of CaMKII in Glutamatergic SynapsesP01NS044306 · NINDS · CALIFORNIA INSTITUTE OF TECHNOLOGY · PI SEJNOWKSI, TERRENCE I · 2003 to 2007
$4.1M
MCell/DReAMM: A Microphysiological Modeling EnvironmentR01GM068630 · NIGMS · CARNEGIE-MELLON UNIVERSITY · PI STILES, JOEL R. · 2003 to 2006
$2.0M
Howard Hughes Medical InstituteNIGMS NIH HHS GM068630NIGMS NIH HHS R01 GM068630NINDS NIH HHS P01 NS044306NINDS NIH HHS P01-NS044306
6 · The paper itself

Abstract

The entry of calcium into dendritic spines can trigger a sequence of biochemical reactions that begins with the activation of calmodulin (CaM) and ends with long-term changes to synaptic strengths. The degree of activation of CaM can depend on highly local elevations in the concentration of calcium and the duration of transient increases in calcium concentration. Accurate measurement of these local changes in calcium is difficult because the spaces are so small and the numbers of molecules are so low. We have therefore developed a Monte Carlo model of intracellular calcium dynamics within the spine that included calcium binding proteins, calcium transporters and ion channels activated by voltage and glutamate binding. The model reproduced optical recordings using calcium indicator dyes and showed that without the dye the free intracellular calcium concentration transient was much higher than predicted from the fluorescent signal. Excitatory postsynaptic potentials induced large, long-lasting calcium gradients across the postsynaptic density, which activated CaM. When glutamate was released at the synapse 10 ms before an action potential occurred, simulating activity patterns that strengthen hippocampal synapses, the calcium gradient and activation of CaM in the postsynaptic density were much greater than when the order was reversed, a condition that decreases synaptic strengths, suggesting a possible mechanism underlying the induction of long-term changes in synaptic strength. The spatial and temporal mechanisms for selectivity in CaM activation demonstrated here could be used in other signaling pathways.

Indexed as

Calcium SignalingAction PotentialsCalciumCalcium-Binding ProteinsCalcium ChannelsCalmodulinComputer SimulationDendritic SpinesDiffusionExcitatory Postsynaptic PotentialsIndicators and ReagentsIon Channel GatingMembrane MicrodomainsModels, BiologicalMutant ProteinsSynapsesCalciumCalcium-Binding ProteinsCalcium ChannelsCalmodulinIndicators and ReagentsMutant Proteins

Identifiers

PMID18446197
PMCPMC2312328
OpenAlexW2139815948

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.