Evidence map›Paper›PMID 24983627›Full record

ArticlePLoS biology2014

Calcineurin mediates synaptic scaling via synaptic trafficking of Ca2+-permeable AMPA receptors.

Seonil Kim, Edward B Ziff

Open access · goldAbstract read
In one paragraph

Article in PLoS biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
83citing papers in PubMed, 1 pooled it
4.3field-weighted citation impact, top 5% 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

83 citing papers in PubMed, 1 synthesis or guideline pooled it, 120 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Review
  5. Review
  6. Review
  7. Ketamine Reverses Chronic Stress-Induced Behavioral Changes via the Expression of CaFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article
  8. Article
  9. AMPAR Regulation in Synaptic Plasticity: The Roles of Calcineurin, CK2, and α2δ-1.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025
    Article
  10. Article
  11. Review
  12. Calcineurin regulates synaptic CaThe Journal of physiology · 2024
    Article
  13. Article
  14. Article
  15. Diverging from the Norm: Reevaluating What Miniature Excitatory Postsynaptic Currents Tell Us about Homeostatic Synaptic Plasticity.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2024
    Review
  16. Article
  17. Article
  18. Article
  19. The autism-associated loss of δ-catenin functions disrupts social behavior.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  20. Article

23 more citing papers are in PubMed but not listed here.

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

2 authors at 1 institution in 1 country.

Seonil KimDepartment of Biochemistry and Molecular Pharmacology, New York University Langone Medical Center, New York, New York, United States of America.
Edward B ZiffDepartment of Biochemistry and Molecular Pharmacology, New York University Langone Medical Center, New York, New York, United States of America.
NYU Langone Health · US

Funding

Calcium Permeable AMPA Receptors: Signaling, Toxicity and ControlR01NS061920 · NINDS · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI ZIFF, EDWARD B · 2009 to 2013
$1.9M
NINDS NIH HHS R01 NS061920NINDS NIH HHS R01NS061920
6 · The paper itself

Abstract

Homeostatic synaptic plasticity is a negative-feedback mechanism for compensating excessive excitation or inhibition of neuronal activity. When neuronal activity is chronically suppressed, neurons increase synaptic strength across all affected synapses via synaptic scaling. One mechanism for this change is alteration of synaptic AMPA receptor (AMPAR) accumulation. Although decreased intracellular Ca2+ levels caused by chronic inhibition of neuronal activity are believed to be an important trigger of synaptic scaling, the mechanism of Ca2+-mediated AMPAR-dependent synaptic scaling is not yet understood. Here, we use dissociated mouse cortical neurons and employ Ca2+ imaging, electrophysiological, cell biological, and biochemical approaches to describe a novel mechanism in which homeostasis of Ca2+ signaling modulates activity deprivation-induced synaptic scaling by three steps: (1) suppression of neuronal activity decreases somatic Ca2+ signals; (2) reduced activity of calcineurin, a Ca2+-dependent serine/threonine phosphatase, increases synaptic expression of Ca2+-permeable AMPARs (CPARs) by stabilizing GluA1 phosphorylation; and (3) Ca2+ influx via CPARs restores CREB phosphorylation as a homeostatic response by Ca2+-induced Ca2+ release from the ER. Therefore, we suggest that synaptic scaling not only maintains neuronal stability by increasing postsynaptic strength but also maintains nuclear Ca2+ signaling by synaptic expression of CPARs and ER Ca2+ propagation.

Indexed as

AnimalsCalcineurinCalcium SignalingEndoplasmic ReticulumHomeostasisMiceNeuronal PlasticityProtein TransportReceptors, AMPATetrodotoxinCalcineurinReceptors, AMPATetrodotoxin

Identifiers

PMID24983627
PMCPMC4077568
OpenAlexW2049294722

What OpenQuestion holds

Textmetadata
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.