Evidence map›Paper›PMID 26147001›Full record

ArticlePloS one2015

A Model of Post-Infection Fatigue Is Associated with Increased TNF and 5-HT2A Receptor Expression in Mice.

Yvonne Couch, Qin Xie, Louise Lundberg, Trevor Sharp, Daniel C Anthony

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
0.9field-weighted citation impact, top 32% 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

23 citing papers in PubMed, 1 synthesis or guideline pooled it, 37 citations in OpenAlex.

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  10. Rebound activation of 5-HT neurons following SSRI discontinuation.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2024
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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 1 institution in 1 country.

Yvonne CouchDepartment of Pharmacology, Mansfield Road, Oxford, OX1 3QT, United Kingdom.
Qin XieDepartment of Pharmacology, Mansfield Road, Oxford, OX1 3QT, United Kingdom.
Louise LundbergDepartment of Pharmacology, Mansfield Road, Oxford, OX1 3QT, United Kingdom; Public Health England, Centre for Radiation, Chemical and Environmental Hazards, Chilton, Didcot, Oxford OX11 0RQ, United Kingdom.
Trevor SharpDepartment of Pharmacology, Mansfield Road, Oxford, OX1 3QT, United Kingdom.
Daniel C AnthonyDepartment of Pharmacology, Mansfield Road, Oxford, OX1 3QT, United Kingdom.
Public Health England · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

It is well documented that serotonin (5-HT) plays an important role in psychiatric illness. For example, myalgic encephalomyelitis (ME/CFS), which is often provoked by infection, is a disabling illness with an unknown aetiology and diagnosis is based on symptom-specific criteria. However, 5-HT2A receptor expression and peripheral cytokines are known to be upregulated in ME. We sought to examine the relationship between the 5-HT system and cytokine expression following systemic bacterial endotoxin challenge (LPS, 0.5 mg/kg i.p.), at a time when the acute sickness behaviours have largely resolved. At 24 hours post-injection mice exhibit no overt changes in locomotor behaviour, but do show increased immobility in a forced swim test, as well as decreased sucrose preference and reduced marble burying activity, indicating a depressive-like state. While peripheral IDO activity was increased after LPS challenge, central activity levels remained stable and there was no change in total brain 5-HT levels or 5-HIAA/5-HT. However, within the brain, levels of TNF and 5-HT2A receptor mRNA within various regions increased significantly. This increase in receptor expression is reflected by an increase in the functional response of the 5-HT2A receptor to agonist, DOI. These data suggest that regulation of fatigue and depressive-like moods after episodes of systemic inflammation may be regulated by changes in 5-HT receptor expression, rather than by levels of enzyme activity or cytokine expression in the CNS.

Indexed as

Disease Models, AnimalAnimalsFatigueInfectionsLipopolysaccharidesMaleMiceReceptor, Serotonin, 5-HT2ATumor Necrosis Factor-alphaLipopolysaccharidesReceptor, Serotonin, 5-HT2ATumor Necrosis Factor-alpha

Identifiers

PMID26147001
PMCPMC4493081
OpenAlexW807567824

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.