Evidence map›Paper›PMID 19773812›Full record

ArticleMolecular psychiatry2010

Stress and IL-1beta contribute to the development of depressive-like behavior following peripheral nerve injury.

G J Norman, K Karelina, N Zhang, J C Walton, J S Morris, A C Devries

Open access · greenAbstract read
In one paragraph

Article in Molecular psychiatry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 98 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
98citing papers in PubMed, 1 pooled it
4.9field-weighted citation impact, top 5% 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

98 citing papers in PubMed, 1 synthesis or guideline pooled it, 208 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
  4. VlPAG/DRN Microglia Drive Neuropathic Pain-Induced Depression via a Defined Neuroimmune Axis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
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38 more citing papers are in PubMed but not listed here.

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 2 institutions in 1 country.

G J NormanDepartment of Psychology, The Ohio State University, Columbus, OH 43210, USA. norman.106@osu.edu
K Karelina
N Zhang
J C Walton
J S Morris
A C Devries
The Ohio State University · USInstitute for Behavioral Medicine · US

Funding

Ohio State Neuroscience Centr CoreP30NS045758 · NINDS · OHIO STATE UNIVERSITY · PI MCTIGUE, DANA M · 2004 to 2015
$7.7M
Psychosocial Influences on NociceptionR01NR010806 · NINR · OHIO STATE UNIVERSITY · PI DEVRIES, ANNE COURTNEY · 2008 to 2012
$1.8M
NINDS NIH HHS P30 NS045758NINR NIH HHS 5R01NR010806NINR NIH HHS R01 NR010806
6 · The paper itself

Abstract

The physiological link between neuropathic pain and depression remains unknown despite a high comorbidity between these two disorders. A mouse model of spared nerve injury (SNI) was used to test the hypothesis that nerve injury precipitates depression through the induction of inflammation in the brain, and that prior exposure to stress exacerbates the behavioral and neuroinflammatory consequences of nerve injury. As compared with sham surgery, SNI induced mechanical allodynia, and significantly increased depressive-like behavior. Moreover, SNI animals displayed increased interleukin-1beta (IL-1beta) gene expression within the frontal cortex and concurrent increases in the expression of glial fibrillary acidic protein (GFAP) within the periaqueductal grey (PAG). Additionally, exposure to chronic restraint stress for 2 weeks before SNI exacerbated mechanical allodynia and depressive-like behavior, and resulted in an increase in IL-1beta gene expression in the frontal cortex and brain-derived neurotrophic factor (BDNF) gene expression in PAG. Treatment with metyrapone (MET), a corticosteroid synthesis inhibitor, before stress eliminated deleterious effects of chronic stress on SNI. Finally, this study showed that interference with IL-1beta signaling, through administration of IL-1 receptor antagonist (IL-1ra), ameliorated the effects of neuropathic pain on depressive-like behavior. Taken together, these data suggest that peripheral nerve injury leads to increased cytokine expression in the brain, which in turn, contributes to the development of depressive-like behavior. Furthermore, stress can facilitate the development of depressive-like behavior after nerve injury by promoting IL-1beta expression.

Indexed as

Analysis of VarianceAnimalsCorticosteroneCytokinesDepressionDisease Models, AnimalExploratory BehaviorGene Expression RegulationHyperalgesiaInterleukin-1betaMaleMiceMice, Inbred C57BLPain ThresholdPeripheral Nervous System DiseasesRNA, MessengerCorticosteroneCytokinesInterleukin-1betaRNA, Messenger

Identifiers

PMID19773812
PMCPMC5214062
OpenAlexW1973816589

What OpenQuestion holds

Textmetadata
LicenceTDM
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.