Evidence map›Paper›PMID 38395613›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2024

Astrocytes Are the Source of TNF Mediating Homeostatic Synaptic Plasticity.

Renu Heir, Zahra Abbasi, Pragya Komal, Haider F Altimimi, Marie Franquin, Dionysia Moschou, Julien Chambon, David Stellwagen

Open access · greenAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
9.4field-weighted citation impact, top 1% 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

26 citing papers in PubMed, 40 citations in OpenAlex.

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  8. Astrocyte Regulation of Spinal Circuit Function.Journal of neurochemistry · 2026
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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

8 authors at 1 institution in 1 country.

Renu HeirDepartment of Neurology and Neurosurgery, Centre for Research in Neuroscience, Research Institute of the McGill University Health Center, Montréal, Quebec H3G 1A4, Canada.
Zahra AbbasiDepartment of Neurology and Neurosurgery, Centre for Research in Neuroscience, Research Institute of the McGill University Health Center, Montréal, Quebec H3G 1A4, Canada.
Pragya KomalDepartment of Neurology and Neurosurgery, Centre for Research in Neuroscience, Research Institute of the McGill University Health Center, Montréal, Quebec H3G 1A4, Canada.
Haider F AltimimiDepartment of Neurology and Neurosurgery, Centre for Research in Neuroscience, Research Institute of the McGill University Health Center, Montréal, Quebec H3G 1A4, Canada.
Marie FranquinDepartment of Neurology and Neurosurgery, Centre for Research in Neuroscience, Research Institute of the McGill University Health Center, Montréal, Quebec H3G 1A4, Canada.
Dionysia MoschouDepartment of Neurology and Neurosurgery, Centre for Research in Neuroscience, Research Institute of the McGill University Health Center, Montréal, Quebec H3G 1A4, Canada.ORCID 0009-0003-5099-1711
Julien ChambonDepartment of Neurology and Neurosurgery, Centre for Research in Neuroscience, Research Institute of the McGill University Health Center, Montréal, Quebec H3G 1A4, Canada.ORCID 0000-0001-8031-156X
David StellwagenDepartment of Neurology and Neurosurgery, Centre for Research in Neuroscience, Research Institute of the McGill University Health Center, Montréal, Quebec H3G 1A4, Canada david.stellwagen@mcgill.ca.
McGill University Health Centre · CA

Funding

CIHR
6 · The paper itself

Abstract

Tumor necrosis factor α (TNF) mediates homeostatic synaptic plasticity (HSP) in response to chronic activity blockade, and prior work has established that it is released from glia. Here we demonstrate that astrocytes are the necessary source of TNF during HSP. Hippocampal cultures from rats of both sexes depleted of microglia still will increase TNF levels following activity deprivation and still express TTX-driven HSP. Slice cultures from mice of either sex with a conditional deletion of TNF from microglia also express HSP, but critically, slice cultures with a conditional deletion of TNF from astrocytes do not. In astrocytes, glutamate signaling is sufficient to reduce NFκB signaling and TNF mRNA levels. Further, chronic TTX treatment increases TNF in an NFκB-dependent manner, although NFκB signaling is dispensable for the neuronal response to TTX-driven HSP. Thus, astrocytes can sense neuronal activity through glutamate spillover and increase TNF production when activity falls, to drive HSP through the production of TNF.

Indexed as

AstrocytesTumor Necrosis Factor-alphaAnimalsGlutamatesMiceNeuronal PlasticityRatsSignal TransductionGlutamatesTumor Necrosis Factor-alphaastrocytecytokinehomeostatic plasticitymGluRmicrogliaTNF

Identifiers

PMID38395613
PMCPMC10993029
OpenAlexW4392094182

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.