ArticlePLoS computational biology2010
Quantifying the effects of elastic collisions and non-covalent binding on glutamate receptor trafficking in the post-synaptic density.
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.
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Who cites it
29 citing papers in PubMed.
- Extracellular space diffusion modelling identifies distinct functional advantages of glutamatergic and GABAergic synapse geometries.Fluids and barriers of the CNS · 2026Article
- Extracellular space diffusion modelling identifies distinct functional advantages of archetypical glutamatergic and GABAergic synapse geometries.bioRxiv : the preprint server for biology · 2025Article
- Fractional order memcapacitive neuromorphic elements reproduce and predict neuronal function.Scientific reports · 2024Article
- Physicochemical Principles of Adhesion Mechanisms in the Brain.International journal of molecular sciences · 2023Review
- Molecular Crowding and Diffusion-Capture in Synapses.iScience · 2020Article
- Functional organization of postsynaptic glutamate receptors.Molecular and cellular neurosciences · 2018Review
- Subsynaptic spatial organization as a regulator of synaptic strength and plasticity.Current opinion in neurobiology · 2018Review
- AMPA receptor trafficking and its role in heterosynaptic plasticity.Scientific reports · 2018Article
- Self-crowding of AMPA receptors in the excitatory postsynaptic density can effectuate anomalous receptor sub-diffusion.PLoS computational biology · 2018Article
- Transcellular Nanoalignment of Synaptic Function.Neuron · 2017Review
- 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 · 2016Article
- Control of Transmembrane Protein Diffusion within the Postsynaptic Density Assessed by Simultaneous Single-Molecule Tracking and Localization Microscopy.Frontiers in synaptic neuroscience · 2016Article
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- Neuronal spike timing adaptation described with a fractional leaky integrate-and-fire model.PLoS computational biology · 2014Article
- Plasticity of dendritic spines: subcompartmentalization of signaling.Annual review of physiology · 2014Review
- Simulation tools for particle-based reaction-diffusion dynamics in continuous space.BMC biophysics · 2014Review
- Barriers in the brain: resolving dendritic spine morphology and compartmentalization.Frontiers in neuroanatomy · 2014Review
- LTD expression is independent of glutamate receptor subtype.Frontiers in synaptic neuroscience · 2014Article
- AMPARs and synaptic plasticity: the last 25 years.Neuron · 2013Article
Corrections and comments
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Authors and funding
4 authors.
Funding
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.
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Registered trials
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