Evidence map›Paper›PMID 24385951›Full record

ArticleFrontiers in cellular neuroscience2013

Tumor necrosis factor alpha maintains denervation-induced homeostatic synaptic plasticity of mouse dentate granule cells.

Denise Becker, Nadine Zahn, Thomas Deller, Andreas Vlachos

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Frontiers in cellular neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
1.8field-weighted citation impact, top 17% 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

27 citing papers in PubMed, 45 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Astrocytes Are the Source of TNF Mediating Homeostatic Synaptic Plasticity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024
    Article
  6. Article
  7. Microglial Cytokines Mediate Plasticity Induced by 10 Hz Repetitive Magnetic Stimulation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
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  14. TNF-Mediated Homeostatic Synaptic Plasticity: FromFrontiers in cellular neuroscience · 2020
    Review
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4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Denise BeckerInstitute of Clinical Neuroanatomy, Neuroscience Center, Goethe-University Frankfurt Frankfurt, Germany.
Nadine ZahnInstitute of Clinical Neuroanatomy, Neuroscience Center, Goethe-University Frankfurt Frankfurt, Germany.
Thomas DellerInstitute of Clinical Neuroanatomy, Neuroscience Center, Goethe-University Frankfurt Frankfurt, Germany.
Andreas VlachosInstitute of Clinical Neuroanatomy, Neuroscience Center, Goethe-University Frankfurt Frankfurt, Germany.
Goethe University Frankfurt · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neurons which lose part of their input respond with a compensatory increase in excitatory synaptic strength. This observation is of particular interest in the context of neurological diseases, which are accompanied by the loss of neurons and subsequent denervation of connected brain regions. However, while the cellular and molecular mechanisms of pharmacologically induced homeostatic synaptic plasticity have been identified to a certain degree, denervation-induced homeostatic synaptic plasticity remains not well understood. Here, we employed the entorhinal denervation in vitro model to study the role of tumor necrosis factor alpha (TNFα) on changes in excitatory synaptic strength of mouse dentate granule cells following partial deafferentation. Our experiments disclose that TNFα is required for the maintenance of a compensatory increase in excitatory synaptic strength at 3-4 days post lesion (dpl), but not for the induction of synaptic scaling at 1-2 dpl. Furthermore, laser capture microdissection combined with quantitative PCR demonstrates an increase in TNFα-mRNA levels in the denervated zone, which is consistent with our previous finding on a local, i.e., layer-specific increase in excitatory synaptic strength at 3-4 dpl. Immunostainings for the glial fibrillary acidic protein and TNFα suggest that astrocytes are a source of TNFα in our experimental setting. We conclude that TNFα-signaling is a major regulatory system that aims at maintaining the homeostatic synaptic response of denervated neurons.

Indexed as

astrocytesbrain injuryentorhinal cortex lesionhomeostatic synaptic scalingorganotypic slice cultures

Identifiers

PMID24385951
PMCPMC3866521
OpenAlexW2003756337

What OpenQuestion holds

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LicenceCC BY
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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.