Evidence map›Paper›PMID 36104437›Full record

ArticleMolecular psychiatry2022

Sustained TNF signaling is required for the synaptic and anxiety-like behavioral response to acute stress.

Gina M Kemp, Haider F Altimimi, Yoonmi Nho, Renu Heir, Adam Klyczek, David Stellwagen

Open access · hybridAbstract read
In one paragraph

Article in Molecular psychiatry, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
3.5field-weighted citation impact, top 6% 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

36 citing papers in PubMed, 44 citations in OpenAlex.

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  14. TNF-α Inhibition Modulates CX3CR1, Pyroptosis-related Genes, and BDNF to Alleviate Anxiety-like Behavior in Type 2 Diabetic Rats.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2025
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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

6 authors at 1 institution in 1 country.

Gina M KempDepartment of Neurology and Neurosurgery, Centre for Research in Neuroscience, Research Institute of the McGill University Health Center, Montréal, QC, Canada.ORCID http://orcid.org/0000-0001-5804-1858
Haider F AltimimiDepartment of Neurology and Neurosurgery, Centre for Research in Neuroscience, Research Institute of the McGill University Health Center, Montréal, QC, Canada.
Yoonmi NhoDepartment of Neurology and Neurosurgery, Centre for Research in Neuroscience, Research Institute of the McGill University Health Center, Montréal, QC, Canada.
Renu HeirDepartment of Neurology and Neurosurgery, Centre for Research in Neuroscience, Research Institute of the McGill University Health Center, Montréal, QC, Canada.
Adam KlyczekDepartment of Neurology and Neurosurgery, Centre for Research in Neuroscience, Research Institute of the McGill University Health Center, Montréal, QC, Canada.
David StellwagenDepartment of Neurology and Neurosurgery, Centre for Research in Neuroscience, Research Institute of the McGill University Health Center, Montréal, QC, Canada. david.stellwagen@mcgill.ca.ORCID http://orcid.org/0000-0003-3509-103X
McGill University Health Centre · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acute stress triggers plasticity of forebrain synapses as well as behavioral changes. Here we reveal that Tumor Necrosis Factor α (TNF) is a required downstream mediator of the stress response in mice, necessary for stress-induced synaptic potentiation in the ventral hippocampus and for an increase in anxiety-like behaviour. Acute stress is sufficient to activate microglia, triggering the long-term release of TNF. Critically, on-going TNF signaling specifically in the ventral hippocampus is necessary to sustain both the stress-induced synaptic and behavioral changes, as these could be reversed hours after induction by antagonizing TNF signaling. This demonstrates that TNF maintains the synaptic and behavioral stress response in vivo, making TNF a potential novel therapeutic target for stress disorders.

Indexed as

AnxietyStress, PsychologicalTumor Necrosis Factor-alphaAnimalsHippocampusLong-Term PotentiationMiceMicrogliaNeuronal PlasticitySynapsesTumor Necrosis Factor-alpha

Identifiers

PMID36104437
PMCPMC9734040
OpenAlexW4295679029

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.