Evidence map›Paper›PMID 20485563›Full record

ArticlePLoS computational biology2010

Quantifying the effects of elastic collisions and non-covalent binding on glutamate receptor trafficking in the post-synaptic density.

Fidel Santamaria, Jossina Gonzalez, George J Augustine, Sridhar Raghavachari

Abstract read
In one paragraph

Article in PLoS computational biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
–field-weighted citation impact
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

29 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Physicochemical Principles of Adhesion Mechanisms in the Brain.International journal of molecular sciences · 2023
    Review
  5. Article
  6. Functional organization of postsynaptic glutamate receptors.Molecular and cellular neurosciences · 2018
    Review
  7. Review
  8. Article
  9. Article
  10. Review
  11. Protein Crowding within the Postsynaptic Density Can Impede the Escape of Membrane Proteins.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Review
  18. Review
  19. LTD expression is independent of glutamate receptor subtype.Frontiers in synaptic neuroscience · 2014
    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.

Fidel SantamariaBiology Department, The University of Texas at San Antonio, San Antonio, Texas, United States of America. fidel.santamaria@utsa.edu
Jossina Gonzalez
George J Augustine
Sridhar Raghavachari

Funding

RCMI Center for Interdiscplinary Health Research CIHRG12MD007591 · NIMHD · UNIVERSITY OF TEXAS SAN ANTONIO · PI PERRY, GEORGE · 2012 to 2016
$10.4M
CRCNS: Quantitative description of initial biochemical steps in LTPR01DA027807 · NIDA · BRANDEIS UNIVERSITY · PI LISMAN, JOHN E · 2009 to 2013
$1.6M
NIDA NIH HHS R01 DA027807NIMHD NIH HHS G12 MD007591
6 · The paper itself

Abstract

One mechanism of information storage in neurons is believed to be determined by the strength of synaptic contacts. The strength of an excitatory synapse is partially due to the concentration of a particular type of ionotropic glutamate receptor (AMPAR) in the post-synaptic density (PSD). AMPAR concentration in the PSD has to be plastic, to allow the storage of new memories; but it also has to be stable to preserve important information. Although much is known about the molecular identity of synapses, the biophysical mechanisms by which AMPAR can enter, leave and remain in the synapse are unclear. We used Monte Carlo simulations to determine the influence of PSD structure and activity in maintaining homeostatic concentrations of AMPARs in the synapse. We found that, the high concentration and excluded volume caused by PSD molecules result in molecular crowding. Diffusion of AMPAR in the PSD under such conditions is anomalous. Anomalous diffusion of AMPAR results in retention of these receptors inside the PSD for periods ranging from minutes to several hours in the absence of strong binding of receptors to PSD molecules. Trapping of receptors in the PSD by crowding effects was very sensitive to the concentration of PSD molecules, showing a switch-like behavior for retention of receptors. Non-covalent binding of AMPAR to anchored PSD molecules allowed the synapse to become well-mixed, resulting in normal diffusion of AMPAR. Binding also allowed the exchange of receptors in and out of the PSD. We propose that molecular crowding is an important biophysical mechanism to maintain homeostatic synaptic concentrations of AMPARs in the PSD without the need of energetically expensive biochemical reactions. In this context, binding of AMPAR with PSD molecules could collaborate with crowding to maintain synaptic homeostasis but could also allow synaptic plasticity by increasing the exchange of these receptors with the surrounding extra-synaptic membrane.

Indexed as

Models, NeurologicalComputer SimulationMonte Carlo MethodProtein BindingProtein TransportReceptors, GlutamateSynaptic MembranesReceptors, Glutamate

Identifiers

PMID20485563
PMCPMC2869312

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Registered trials

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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.