Evidence map›Paper›PMID 29560257›Full record

ReviewF1000Research2018

Homeostatic synaptic scaling: molecular regulators of synaptic AMPA-type glutamate receptors.

Dhrubajyoti Chowdhury, Johannes W Hell

Open access · goldAbstract readReview
In one paragraph

Review in F1000Research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

25 citing papers in PubMed, 52 citations in OpenAlex.

  1. Article
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  14. Review
  15. The auxiliary glutamate receptor subunit dSol-1 promotes presynaptic neurotransmitter release and homeostatic potentiation.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  16. Article
  17. Article
  18. Review
  19. Activity Dependent and Independent Determinants of Synaptic Size Diversity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020
    Article
  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

2 authors at 1 institution in 1 country.

Dhrubajyoti ChowdhuryDepartment of Pharmacology, University of California Davis, Davis, California, USA.
Johannes W HellDepartment of Pharmacology, University of California Davis, Davis, California, USA.ORCID https://orcid.org/0000-0001-7960-7531
University of California, Davis · US

Funding

Role of a-actinin in Cav1.2 FunctionR01AG055357 · NIA · UNIVERSITY OF CALIFORNIA AT DAVIS · PI JOHANNES W HELL · 2016 to 2026
$4.0M
Molecular Mechanisms of Postsynaptic AMPA Receptor LocalizationR01MH097887 · NIMH · UNIVERSITY OF CALIFORNIA AT DAVIS · PI HELL, JOHANNES W · 2014 to 2018
$2.5M
Signaling by cAMP within postsynaptic nano domains R01NS078792R01NS078792 · NINDS · UNIVERSITY OF CALIFORNIA AT DAVIS · PI HELL, JOHANNES W · 2012 to 2016
$2.0M
NIA NIH HHS R01 AG055357NIMH NIH HHS R01 MH097887NINDS NIH HHS R01 NS078792
6 · The paper itself

Abstract

The ability of neurons and circuits to maintain their excitability and activity levels within the appropriate dynamic range by homeostatic mechanisms is fundamental for brain function. Neuronal hyperactivity, for instance, could cause seizures.  One such homeostatic process is synaptic scaling, also known as synaptic homeostasis. It involves a negative feedback process by which neurons adjust (scale) their postsynaptic strength over their whole synapse population to compensate for increased or decreased overall input thereby preventing neuronal hyper- or hypoactivity that could otherwise result in neuronal network dysfunction. While synaptic scaling is well-established and critical, our understanding of the underlying molecular mechanisms is still in its infancy. Homeostatic adaptation of synaptic strength is achieved through upregulation (upscaling) or downregulation (downscaling) of the functional availability of AMPA-type glutamate receptors (AMPARs) at postsynaptic sites.  Understanding how synaptic AMPARs are modulated in response to alterations in overall neuronal activity is essential to gain valuable insights into how neuronal networks adapt to changes in their environment, as well as the genesis of an array of neurological disorders. Here we discuss the key molecular mechanisms that have been implicated in tuning the synaptic abundance of postsynaptic AMPARs in order to maintain synaptic homeostasis.

Indexed as

AMPARsglutamate receptorshomeostatic plasticitysynapse

Identifiers

PMID29560257
PMCPMC5832907
OpenAlexW2788212424

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.