Evidence map›Paper›PMID 28709913›Full record

ArticleBrain, behavior, and immunity2017

Upregulation of neuronal kynurenine 3-monooxygenase mediates depression-like behavior in a mouse model of neuropathic pain.

Geoffroy Laumet, Wenjun Zhou, Robert Dantzer, Jules D Edralin, XiaoJiao Huo, David P Budac, Jason C O'Connor, Anna W Lee, Cobi J Heijnen, Annemieke Kavelaars

Abstract read
In one paragraph

Article in Brain, behavior, and immunity, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

52 citing papers in PubMed, 77 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
  5. Review
  6. [Mechanisms by which the gut microbiota regulates depressive disorder via the tryptophan metabolic pathway].Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2025
    Review
  7. Article
  8. Review
  9. Review
  10. Article
  11. Review
  12. Review
  13. Article
  14. Review
  15. Article
  16. Review
  17. Article
  18. Review
  19. Potential Role of Yoga Intervention in the Management of Chronic Non-malignant Pain.Evidence-based complementary and alternative medicine : eCAM · 2022
    Review
  20. Article
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

10 authors at 4 institutions in 2 countries.

Geoffroy LaumetLaboratory of Neuroimmunology, Department of Symptom Research, The University of Texas MD Anderson Cancer Center, Houston, TX, USA. Electronic address: GOLaumet@mdanderson.org.
Wenjun ZhouLaboratory of Neuroimmunology, Department of Symptom Research, The University of Texas MD Anderson Cancer Center, Houston, TX, USA. Electronic address: Wenjun.Zhou@bcm.edu.
Robert DantzerLaboratory of Neuroimmunology, Department of Symptom Research, The University of Texas MD Anderson Cancer Center, Houston, TX, USA. Electronic address: RDantzer@mdanderson.org.
Jules D EdralinLaboratory of Neuroimmunology, Department of Symptom Research, The University of Texas MD Anderson Cancer Center, Houston, TX, USA. Electronic address: JDEdralin@mdanderson.org.
XiaoJiao HuoLaboratory of Neuroimmunology, Department of Symptom Research, The University of Texas MD Anderson Cancer Center, Houston, TX, USA. Electronic address: XHuo@mdanderson.org.
David P BudacBioanalysis and Physiology, Lundbeck Research, Paramus, NJ, USA. Electronic address: dbudac@yahoo.com.
Jason C O'ConnorDepartment of Pharmacology, The University of Texas Health Science Center and Audie L. Murphy VA Hospital, South Texas Veteran's Heath Care System, San Antonio, TX, USA. Electronic address: oconnorj@uthscsa.edu.
Anna W LeeNeuroinflammation Disease Biology Unit, Lundbeck Research USA, Paramus, NJ, USA(3). Electronic address: anna.newyork@gmail.com.
Cobi J HeijnenLaboratory of Neuroimmunology, Department of Symptom Research, The University of Texas MD Anderson Cancer Center, Houston, TX, USA. Electronic address: CJHeijnen@mdanderson.org.
Annemieke KavelaarsLaboratory of Neuroimmunology, Department of Symptom Research, The University of Texas MD Anderson Cancer Center, Houston, TX, USA. Electronic address: AKavelaars@mdanderson.org.
The University of Texas MD Anderson Cancer Center · USThe University of Texas Health Science Center at San Antonio · USTKL Research · USYahoo (United Kingdom) · GB

Funding

Neuroimmune Mechanisms of Recovery from Comorbid Depression and Chronic PainR01NS073939 · NINDS · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI DANTZER, ROBERT, HEIJNEN, COBI J · 2011 to 2020
$4.0M
Biobehavioral Role of Brain Kynurenine Metabolism in Mental IllnessR01MH090127 · NIMH · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI O'CONNOR, JASON C · 2010 to 2014
$1.8M
A novel molecular switch regulating transition from acute to chronic pain.R01NS074999 · NINDS · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI KAVELAARS, ANNEMIEKE · 2011 to 2015
$1.7M
Role of Brain-Derived Neurotrophic Factor in Regulating Neuroinflammation in Mental HealthI01BX003195 · VA · SOUTH TEXAS VETERANS HEALTH CARE SYSTEM · PI Jason C O'Connor · 2017 to 2026
–
BLRD VA I01 BX003195NIMH NIH HHS R01 MH090127NINDS NIH HHS R01 NS073939NINDS NIH HHS R01 NS074999
6 · The paper itself

Abstract

Pain and depression often co-occur, but the underlying mechanisms have not been elucidated. Here, we used the spared nerve injury (SNI) model in mice to induce both neuropathic pain and depression-like behavior. We investigated whether brain interleukin (IL)-1 signaling and activity of kynurenine 3-monoxygenase (KMO), a key enzyme for metabolism of kynurenine into the neurotoxic NMDA receptor agonist quinolinic acid, are necessary for comorbid neuropathic pain and depression-like behavior. SNI mice showed increased expression levels of Il1b and Kmo mRNA in the contralateral side of the brain. The SNI-induced increase of Kmo mRNA was associated with increased KMO protein and elevated quinolinic acid and reduced kynurenic acid in the contralateral hippocampus. The increase in KMO-protein in response to SNI mostly took place in hippocampal NeuN-positive neurons rather than microglia. Inhibition of brain IL-1 signaling by intracerebroventricular administration of IL-1 receptor antagonist after SNI prevented the increase in Kmo mRNA and depression-like behavior measured by forced swim test. However, inhibition of brain IL-1 signaling has no effect on mechanical allodynia. In addition, intracerebroventricular administration of the KMO inhibitor Ro 61-8048 abrogated depression-like behavior without affecting mechanical allodynia after SNI. We show for the first time that the development of depression-like behavior in the SNI model requires brain IL-1 signaling and activation of neuronal KMO, while pain is independent of this pathway. Inhibition of KMO may represent a promising target for treating depression.

Indexed as

AnimalsDepressionDisease Models, AnimalHippocampusHyperalgesiaInterleukin-1Kynurenine 3-MonooxygenaseMaleMice, Inbred C57BLMicrogliaNeuralgiaNeuronsPeripheral Nerve InjuriesRNA, MessengerSignal TransductionUp-RegulationInterleukin-1Kynurenine 3-MonooxygenaseRNA, MessengerComorbidityDepressionHippocampusInterleukin-1Kynurenine 3-monooxygenaseKynurenine pathwayPainPsychoneuroimmunologyQuinolinic acid

Identifiers

PMID28709913
PMCPMC5650931
OpenAlexW2736208466

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.