Evidence map›Paper›PMID 21104309›Full record

ArticleJournal of computational neuroscience2011

The impacts of geometry and binding on CaMKII diffusion and retention in dendritic spines.

Michael J Byrne, M Neal Waxham, Yoshihisa Kubota

Open access · greenAbstract read
In one paragraph

Article in Journal of computational neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.4field-weighted citation impact, top 21% 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

23 citing papers in PubMed, 44 citations in OpenAlex.

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  12. Multiple spatial and kinetic subpopulations of CaMKII in spines and dendrites as resolved by single-molecule tracking PALM.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014
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  14. Review
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  17. Spatiotemporal maps of CaMKII in dendritic spines.Journal of computational neuroscience · 2012
    Article
  18. Article
  19. Measuring CaMKII concentration in dendritic spines.Journal of neuroscience methods · 2012
    Article
  20. Ca(2+) sensor proteins in dendritic spines: a race for Ca(2+).Frontiers in molecular neuroscience · 2012
    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

3 authors.

Michael J ByrneDepartment of Neurobiology and Anatomy, University of Texas Medical School, 6431 Fannin, Houston, TX 77030, USA.
M Neal Waxham
Yoshihisa Kubota

Funding

Neural Models of Plasticity: Molecules to NetworksP01NS038310 · NINDS · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI BYRNE, JOHN H · 1999 to 2009
$9.3M
NINDS NIH HHS NS038310NINDS NIH HHS P01 NS038310
6 · The paper itself

Abstract

We used a particle-based Monte Carlo simulation to dissect the regulatory mechanism of molecular translocation of CaMKII, a key regulator of neuronal synaptic function. Geometry was based upon measurements from EM reconstructions of dendrites in CA1 hippocampal pyramidal neurons. Three types of simulations were performed to investigate the effects of geometry and other mechanisms that control CaMKII translocation in and out of dendritic spines. First, the diffusional escape rate of CaMKII from model spines of varied morphologies was examined. Second, a postsynaptic density (PSD) was added to study the impact of binding sites on this escape rate. Third, translocation of CaMKII from dendrites and trapping in spines was investigated using a simulated dendrite. Based on diffusion alone, a spine of average dimensions had the ability to retain CaMKII for duration of ~4 s. However, binding sites mimicking those in the PSD controlled the residence time of CaMKII in a highly nonlinear manner. In addition, we observed that F-actin at the spine head/neck junction had a significant impact on CaMKII trapping in dendritic spines. We discuss these results in the context of possible mechanisms that may explain the experimental results that have shown extended accumulation of CaMKII in dendritic spines during synaptic plasticity and LTP induction.

Indexed as

Models, NeurologicalCalcium-Calmodulin-Dependent Protein Kinase Type 2Computer SimulationDendritic SpinesDiffusionHippocampusHumansMonte Carlo MethodNeuronsCalcium-Calmodulin-Dependent Protein Kinase Type 2

Identifiers

PMID21104309
PMCPMC3617044
OpenAlexW2032123789

What OpenQuestion holds

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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.