Evidence map›Paper›PMID 30355624›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2018

Retinoic Acid Receptor RARα-Dependent Synaptic Signaling Mediates Homeostatic Synaptic Plasticity at the Inhibitory Synapses of Mouse Visual Cortex.

Lei R Zhong, Xin Chen, Esther Park, Thomas C Südhof, Lu Chen

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2018. 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
2.1field-weighted citation impact, top 13% 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

35 citing papers in PubMed, 58 citations in OpenAlex.

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  9. Blockade of GluN2B-Containing NMDA Receptors Prevents Potentiation and Depression of Responses during Ocular Dominance Plasticity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024
    Article
  10. Article
  11. Beneficial Effects ofNutrients · 2024
    Review
  12. Article
  13. Review
  14. Mouse models of fragile X-related disorders.Disease models & mechanisms · 2023
    Review
  15. Article
  16. Article
  17. Article
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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

5 authors at 2 institutions in 2 countries.

Lei R ZhongDepartment of Neurosurgery, Department of Psychiatry and Behavioral Sciences, and.ORCID 0000-0002-5035-7919
Xin ChenDepartment of Neurosurgery, Department of Psychiatry and Behavioral Sciences, and.
Esther ParkDepartment of Neurosurgery, Department of Psychiatry and Behavioral Sciences, and.ORCID 0000-0002-1594-7753
Thomas C SüdhofHoward Hughes Medical Institute, Department of Molecular and Cellular Physiology, Stanford University School of Medicine, Stanford, California 94305-5453.
Lu ChenDepartment of Neurosurgery, Department of Psychiatry and Behavioral Sciences, and luchen1@stanford.edu.ORCID 0000-0002-8097-2699
Institute of Behavioral Sciences · JPHoward Hughes Medical Institute · US

Funding

Induced neuronal cells: A novel tool to study neuropsychiatric diseasesR01MH092931 · NIMH · STANFORD UNIVERSITY · PI Thomas C. Sudhof, Marius Wernig · 2010 to 2026
$9.7M
Developmental Pathophysiology of Synapses in a Mouse Model of Fragile X SyndromeR01HD084215 · NICHD · STANFORD UNIVERSITY · PI CHEN, LU · 2014 to 2018
$3.3M
Regulation of synaptic transmission by retinoic acid signalingR01MH091193 · NIMH · STANFORD UNIVERSITY · PI CHEN, LU · 2011 to 2015
$2.3M
Dynamics and molecular mechanism of synaptic connectivity change during learningR01MH104227 · NIMH · UNIVERSITY OF CALIFORNIA SANTA CRUZ · PI ZUO, YI · 2014 to 2018
$2.1M
Contribution of astrocytes to the Fragile X SyndromeR01MH109475 · NIMH · UNIVERSITY OF CALIFORNIA SANTA CRUZ · PI ZUO, YI · 2016 to 2020
$2.0M
NICHD NIH HHS R01 HD084215NIMH NIH HHS R01 MH091193NIMH NIH HHS R01 MH092931NIMH NIH HHS R01 MH104227NIMH NIH HHS R01 MH109475
6 · The paper itself

Abstract

Homeostatic synaptic plasticity is a synaptic mechanism through which the nervous system adjusts synaptic excitation and inhibition to maintain network stability. Retinoic acid (RA) and its receptor RARα have been established as critical mediators of homeostatic synaptic plasticity.

Indexed as

AnimalsFemaleHomeostasisMaleMiceMice, Inbred C57BLMice, KnockoutMice, TransgenicNeural InhibitionNeuronal PlasticityReceptors, Retinoic AcidSynapsesVisual CortexReceptors, Retinoic Acidbinocular enucleationhomeostatic plasticityinhibitory synapsesparvalbumin-positive neuronretinoic acid receptor

Identifiers

PMID30355624
PMCPMC6284108
OpenAlexW2898515321

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.