Evidence map›Paper›PMID 23926271›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2013

How to scale down postsynaptic strength.

Vedakumar Tatavarty, Qian Sun, Gina G Turrigiano

Abstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing 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

35 citing papers in PubMed.

  1. Article
  2. Article
  3. Activity Deprivation Modulates the Shank3/Homer1/mGluR5 Signaling Pathway to Enable Synaptic Upscaling.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025
    Article
  4. Article
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  8. Article
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  12. The Role of Amyloid-Beta and Tau in the Early Pathogenesis of Alzheimer's Disease.Medical science monitor : international medical journal of experimental and clinical research · 2021
    Review
  13. Article
  14. Cortical Seizures inInternational journal of molecular sciences · 2019
    Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Review
  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

3 authors.

Vedakumar TatavartyDepartment of Biology and Center for Behavioral Genomics, Brandeis University, Waltham, Massachusetts 02453, USA.
Qian Sun
Gina G Turrigiano

Funding

SYNAPTIC HOMEOSTASIS IN NEOCORTICAL NEURONSR01NS036853 · NINDS · BRANDEIS UNIVERSITY · PI TURRIGIANO, GINA G · 1997 to 2013
$4.4M
Synaptic homeostasis in neocortical neuronsR56NS036853 · NINDS · BRANDEIS UNIVERSITY · PI TURRIGIANO, GINA G · 2014 to 2014
$403k
NINDS NIH HHS NS036853NINDS NIH HHS R01 NS036853NINDS NIH HHS R56 NS036853
6 · The paper itself

Abstract

Synaptic scaling is a form of synaptic plasticity that contributes to the homeostatic regulation of neuronal activity both in vitro and in vivo, by bidirectionally and proportionally adjusting postsynaptic AMPA receptor (AMPAR) abundance to compensate for chronic perturbations in activity. This proportional regulation of synaptic strength allows synaptic scaling to normalize activity without disrupting the synapse-specific differences in strength thought to underlie memory storage, but how such proportional scaling of synaptic strength is accomplished at the biophysical level is unknown. Here we addressed this question in cultured rat visual cortical pyramidal neurons. We used photoactivation and fluorescence recovery after photobleaching of fluorescently tagged AMPAR to show that scaling down, but not up, decreases the steady-state accumulation of synaptic AMPAR by increasing the rate at which they unbind from and exit the postsynaptic density (Koff). This increase in Koff was not diffusion limited, was independent of AMPAR endocytosis, and was prevented by a scaffold manipulation that specifically blocks scaling down, suggesting that it is accomplished through enhanced dissociation of AMPAR from synaptic scaffold tethers. Finally, simulations show that increasing Koff decreases synaptic strength multiplicatively, by reducing the fractional occupancy of available scaffold "slots." These data demonstrate that scaling down is accomplished through a regulated increase in Koff, which in turn reduces the fractional occupancy of synaptic scaffolds to proportionally reduce synaptic strength.

Indexed as

Models, NeurologicalAnesthetics, LocalAnimalsAnimals, NewbornCells, CulturedCentral Nervous System StimulantsComputer SimulationEndocytosisExcitatory Amino Acid AgonistsExcitatory Postsynaptic PotentialsFluorescence Recovery After PhotobleachingN-MethylaspartatePhotobleachingPicrotoxinPolymersPyramidal CellsAnesthetics, LocalCentral Nervous System StimulantsExcitatory Amino Acid Agonistsglutamate receptor ionotropic, AMPA 2N-MethylaspartatePicrotoxinPolymersReceptors, AMPARecombinant Proteinssynthetic erythropoiesis proteinTetrodotoxin

Identifiers

PMID23926271
PMCPMC3735890

What OpenQuestion holds

Textmetadata
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.