Evidence map›Paper›PMID 24618941›Full record

ArticlePloS one2014

Molecular mechanisms underlying the enhanced analgesic effect of oxycodone compared to morphine in chemotherapy-induced neuropathic pain.

Karine Thibault, Bernard Calvino, Isabelle Rivals, Fabien Marchand, Sophie Dubacq, Stephen B McMahon, Sophie Pezet

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 2 pooled it
3.8field-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

23 citing papers in PubMed, 2 syntheses or guidelines pooled it, 54 citations in OpenAlex.

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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

7 authors at 5 institutions in 2 countries.

Karine ThibaultBrain Plasticity Unit, ESPCI-ParisTech, Paris, France; Centre National de la Recherche Scientifique, UMR 8249, Paris, France; Neurorestoration Group, The Wolfson Centre for Age-Related Diseases, King's College London, London, United Kingdom.
Bernard CalvinoBrain Plasticity Unit, ESPCI-ParisTech, Paris, France; Centre National de la Recherche Scientifique, UMR 8249, Paris, France.
Isabelle RivalsEquipe de Statistique Appliquée, ESPCI-ParisTech, Paris, France.
Fabien MarchandInstitut National de la Santé et de la Recherche Médicale, Unité 1107, NEURO-DOL, Clermont-Ferrand, France; Clermont Université, Université d'Auvergne, Pharmacologie Fondamentale et Clinique de la Douleur, Clermont-Ferrand, France.
Sophie DubacqBrain Plasticity Unit, ESPCI-ParisTech, Paris, France; Centre National de la Recherche Scientifique, UMR 8249, Paris, France.
Stephen B McMahonNeurorestoration Group, The Wolfson Centre for Age-Related Diseases, King's College London, London, United Kingdom.
Sophie PezetBrain Plasticity Unit, ESPCI-ParisTech, Paris, France; Centre National de la Recherche Scientifique, UMR 8249, Paris, France.
Centre National de la Recherche Scientifique · FRKing's College London · GBESPCI Paris · FRInserm · FRParisTech · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Oxycodone is a μ-opioid receptor agonist, used for the treatment of a large variety of painful disorders. Several studies have reported that oxycodone is a more potent pain reliever than morphine, and that it improves the quality of life of patients. However, the neurobiological mechanisms underlying the therapeutic action of these two opioids are only partially understood. The aim of this study was to define the molecular changes underlying the long-lasting analgesic effects of oxycodone and morphine in an animal model of peripheral neuropathy induced by a chemotherapic agent, vincristine. Using a behavioural approach, we show that oxycodone maintains an optimal analgesic effect after chronic treatment, whereas the effect of morphine dies down. In addition, using DNA microarray technology on dorsal root ganglia, we provide evidence that the long-term analgesic effect of oxycodone is due to an up-regulation in GABAB receptor expression in sensory neurons. These receptors are transported to their central terminals within the dorsal horn, and subsequently reinforce a presynaptic inhibition, since only the long-lasting (and not acute) anti-hyperalgesic effect of oxycodone was abolished by intrathecal administration of a GABAB receptor antagonist; in contrast, the morphine effect was unaffected. Our study demonstrates that the GABAB receptor is functionally required for the alleviating effect of oxycodone in neuropathic pain condition, thus providing new insight into the molecular mechanisms underlying the sustained analgesic action of oxycodone.

Indexed as

Analgesics, OpioidAnimalsAntineoplastic AgentsBehavior, AnimalDisease Models, AnimalGanglia, SpinalGene Expression ProfilingGene Expression RegulationMaleMorphineNeuralgiaOxycodoneProtein TransportReceptors, GABA-BSpinal CordAnalgesics, OpioidAntineoplastic AgentsMorphineOxycodoneReceptors, GABA-B

Identifiers

PMID24618941
PMCPMC3949760
OpenAlexW2089458218

What OpenQuestion holds

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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.