Evidence map›Paper›PMID 27519154›Full record

ArticleBrain, behavior, and immunity2016

Morphine amplifies mechanical allodynia via TLR4 in a rat model of spinal cord injury.

Amanda Ellis, Peter M Grace, Julie Wieseler, Jacob Favret, Kendra Springer, Bryce Skarda, Monica Ayala, Mark R Hutchinson, Scott Falci, Kenner C Rice and 2 more

Open access · greenAbstract read
In one paragraph

Article in Brain, behavior, and immunity, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
6.6field-weighted citation impact, top 3% 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

49 citing papers in PubMed, 78 citations in OpenAlex.

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  8. Mu-Opioid Receptor (MOR) Dependence of Pain in Chemotherapy-Induced Peripheral Neuropathy.The Journal of neuroscience : the official journal of the Society for Neuroscience · 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

12 authors at 4 institutions in 2 countries.

Amanda EllisUniversity of Colorado Boulder, Department of Psychology and Neuroscience, Center for Neuroscience, Boulder, CO, USA.
Peter M GraceUniversity of Colorado Boulder, Department of Psychology and Neuroscience, Center for Neuroscience, Boulder, CO, USA; School of Medicine, University of Adelaide, Adelaide, SA, Australia.
Julie WieselerUniversity of Colorado Boulder, Department of Psychology and Neuroscience, Center for Neuroscience, Boulder, CO, USA.
Jacob FavretUniversity of Colorado Boulder, Department of Psychology and Neuroscience, Center for Neuroscience, Boulder, CO, USA.
Kendra SpringerUniversity of Colorado Boulder, Department of Psychology and Neuroscience, Center for Neuroscience, Boulder, CO, USA.
Bryce SkardaUniversity of Colorado Boulder, Department of Psychology and Neuroscience, Center for Neuroscience, Boulder, CO, USA.
Monica AyalaUniversity of Colorado Boulder, Department of Psychology and Neuroscience, Center for Neuroscience, Boulder, CO, USA.
Mark R HutchinsonSchool of Medicine, University of Adelaide, Adelaide, SA, Australia; Australian Research Council Centre of Excellence for Nanoscale BioPhotonics, Australia.
Scott FalciCraig Hospital, Englewood, CO, USA.
Kenner C RiceChemical Biology Research Branch, National Institute on Drug Abuse and National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Rockville, MD, USA.
Steven F MaierUniversity of Colorado Boulder, Department of Psychology and Neuroscience, Center for Neuroscience, Boulder, CO, USA.
Linda R WatkinsUniversity of Colorado Boulder, Department of Psychology and Neuroscience, Center for Neuroscience, Boulder, CO, USA. Electronic address: linda.watkins@colorado.edu.
University of Colorado Boulder · USARC Centre for Nanoscale BioPhotonicsCraig Hospital · USNational Institute on Alcohol Abuse and Alcoholism · US

Funding

Medicinal Chemistry of Drugs Acting on Toll-like ReceptorsZIADA000530 · NIDA · NATIONAL INSTITUTE ON DRUG ABUSE · PI RICE, KENNER · 2009 to 2020
$4.0M
Pain facilitation via neuron-to-glia signalingR01DA017670 · NIDA · UNIVERSITY OF COLORADO AT BOULDER · PI WATKINS, LINDA · 2005 to 2009
$2.0M
Preventing Transition of Acute-to-Chronic Neuropathic Pain: Models, Mechanisms &R01DE021966 · NIDCR · UNIVERSITY OF COLORADO · PI BARTH, DANIEL S., FLESHNER, MONIKA · 2011 to 2015
$2.0M
Exploring the Potential of Glia for Regulating Clinically Relevant Opiod ActionsR01DA023132 · NIDA · UNIVERSITY OF COLORADO · PI WATKINS, LINDA · 2008 to 2012
$1.9M
Models and mechanisms for the transition of acute-to-chronic orofacial painRC1DE020247 · NIDCR · UNIVERSITY OF COLORADO · PI WATKINS, LINDA · 2009 to 2010
$679k
NIDA NIH HHS R01 DA017670NIDA NIH HHS R01 DA023132NIDCR NIH HHS R01 DE021966NIDCR NIH HHS RC1 DE020247
6 · The paper itself

Abstract

Central neuropathic pain (CNP) is a pervasive, debilitating problem that impacts thousands of people living with central nervous system disorders, including spinal cord injury (SCI). Current therapies for treating this type of pain are ineffective and often have dose-limiting side effects. Although opioids are one of the most commonly used CNP treatments, recent animal literature has indicated that administering opioids shortly after a traumatic injury can actually have deleterious effects on long-term health and recovery. In order to study the deleterious effects of administering morphine shortly after trauma, we employed our low thoracic (T13) dorsal root avulsion model (Spinal Neuropathic Avulsion Pain, SNAP). Administering a weeklong course of 10mg/kg/day morphine beginning 24h after SNAP resulted in amplified mechanical allodynia. Co-administering the non-opioid toll-like receptor 4 (TLR4) antagonist (+)-naltrexone throughout the morphine regimen prevented morphine-induced amplification of SNAP. Exploration of changes induced by early post-trauma morphine revealed that this elevated gene expression of TLR4, TNF, IL-1β, and NLRP3, as well as IL-1β protein at the site of spinal cord injury. These data suggest that a short course of morphine administered early after spinal trauma can exacerbate CNP in the long term. TLR4 initiates this phenomenon and, as such, may be potential therapeutic targets for preventing the deleterious effects of administering opioids after traumatic injury.

Indexed as

Analgesics, OpioidAnimalsHyperalgesiaMaleMorphineNaltrexoneNeuralgiaRats, Sprague-DawleySpinal Cord InjuriesToll-Like Receptor 4Analgesics, OpioidMorphineNaltrexoneTlr4 protein, ratToll-Like Receptor 4InflammasomeInterleukin-1β(+)-NaltrexoneNeuropathic painNLRP3Proinflammatory cytokinesRatsTLR4Tumor necrosis factor

Identifiers

PMID27519154
PMCPMC5067205
OpenAlexW2507193047

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.