Evidence map›Paper›PMID 24312013›Full record

ReviewFrontiers in cellular neuroscience2013

Emerging links between homeostatic synaptic plasticity and neurological disease.

Joyce Wondolowski, Dion Dickman

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in cellular neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
86citing papers in PubMed, 1 pooled it
8.8field-weighted citation impact, top 2% 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

86 citing papers in PubMed, 1 synthesis or guideline pooled it, 139 citations in OpenAlex.

  1. Pooled it
  2. Temporal and Cell-Specific Regulation of Synaptic Homeostasis by the Chromatin Remodeler Chd1.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  3. Review
  4. Nonionic signaling rapidly remodels postsynaptic DLG to induce retrograde homeostatic plasticity.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  5. Article
  6. Review
  7. Article
  8. Genetic implication of GABAFrontiers in pharmacology · 2025
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Glial Sphingosine-Mediated Epigenetic Regulation Stabilizes Synaptic Function inThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2023
    Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article

26 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.

Joyce WondolowskiDepartment of Biology, University of Southern California Los Angeles, CA, USA.
Dion Dickman
University of Southern California · US

Funding

Dysbindin and the Mechanisms Controlling Homeostatic Synaptic PlasticityR00MH092351 · NIMH · UNIVERSITY OF SOUTHERN CALIFORNIA · PI DICKMAN, DION KAI · 2012 to 2014
$696k
Dysbindin and the Mechanisms Controlling Homeostatic Synaptic PlasticityK99MH092351 · NIMH · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI DICKMAN, DION KAI · 2010 to 2011
$175k
NIMH NIH HHS K99 MH092351NIMH NIH HHS R00 MH092351
6 · The paper itself

Abstract

Homeostatic signaling systems are ubiquitous forms of biological regulation, having been studied for hundreds of years in the context of diverse physiological processes including body temperature and osmotic balance. However, only recently has this concept been brought to the study of excitatory and inhibitory electrical activity that the nervous system uses to establish and maintain stable communication. Synapses are a primary target of neuronal regulation with a variety of studies over the past 15 years demonstrating that these cellular junctions are under bidirectional homeostatic control. Recent work from an array of diverse systems and approaches has revealed exciting new links between homeostatic synaptic plasticity and a variety of seemingly disparate neurological and psychiatric diseases. These include autism spectrum disorders, intellectual disabilities, schizophrenia, and Fragile X Syndrome. Although the molecular mechanisms through which defective homeostatic signaling may lead to disease pathogenesis remain unclear, rapid progress is likely to be made in the coming years using a powerful combination of genetic, imaging, electrophysiological, and next generation sequencing approaches. Importantly, understanding homeostatic synaptic plasticity at a cellular and molecular level may lead to developments in new therapeutic innovations to treat these diseases. In this review we will examine recent studies that demonstrate homeostatic control of postsynaptic protein translation, retrograde signaling, and presynaptic function that may contribute to the etiology of complex neurological and psychiatric diseases.

Indexed as

homeostasisneurological diseasepresynaptic plasticityretrograde signalingsynaptic plasticity

Identifiers

PMID24312013
PMCPMC3836049
OpenAlexW2061312413

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.