Evidence map›Paper›PMID 30967775›Full record

ArticleFrontiers in pharmacology2019

Repeated Sigma-1 Receptor Antagonist MR309 Administration Modulates Central Neuropathic Pain Development After Spinal Cord Injury in Mice.

Sílvia Castany, Xavier Codony, Daniel Zamanillo, Manuel Merlos, Enrique Verdú, Pere Boadas-Vaello

Open access · goldAbstract read
In one paragraph

Article in Frontiers in pharmacology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

18 citing papers in PubMed, 31 citations in OpenAlex.

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  16. Botulinum Toxin Type A Possibly Affects CaDrug design, development and therapy · 2020
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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

6 authors at 2 institutions in 1 country.

Sílvia CastanyResearch Group of Clinical Anatomy, Embryology and Neuroscience (NEOMA), Department of Medical Sciences, Universitat de Girona, Girona, Spain.
Xavier CodonyEsteve Pharmaceuticals, Drug Discovery and Preclinical Development, Parc Científic de Barcelona, Barcelona, Spain.
Daniel ZamanilloEsteve Pharmaceuticals, Drug Discovery and Preclinical Development, Parc Científic de Barcelona, Barcelona, Spain.
Manuel MerlosEsteve Pharmaceuticals, Drug Discovery and Preclinical Development, Parc Científic de Barcelona, Barcelona, Spain.
Enrique VerdúResearch Group of Clinical Anatomy, Embryology and Neuroscience (NEOMA), Department of Medical Sciences, Universitat de Girona, Girona, Spain.
Pere Boadas-VaelloResearch Group of Clinical Anatomy, Embryology and Neuroscience (NEOMA), Department of Medical Sciences, Universitat de Girona, Girona, Spain.
Esteve Química (Spain) · ESUniversity of Girona · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Up to two-thirds of patients affected by spinal cord injury (SCI) develop central neuropathic pain (CNP), which has a high impact on their quality of life. Most of the patients are largely refractory to current treatments, and new pharmacological strategies are needed. Recently, it has been shown that the acute administration of the σ1R antagonist MR309 (previously developed as E-52862) at 28 days after spinal cord contusion results in a dose-dependent suppression of both mechanical allodynia and thermal hyperalgesia in wild-type CD-1 Swiss female mice. The present work was addressed to determine whether MR309 might exert preventive effects on CNP development by repeated administration during the first week after SCI in mice. To this end, the MR309 (16 or 32 mg/kg i.p.) modulation on both thermal hyperalgesia and mechanical allodynia development were evaluated weekly up to 28 days post-injury. In addition, changes in pro-inflammatory cytokine (TNF-α, IL-1β) expression and both the expression and activation (phosphorylation) of the N-methyl-D-aspartate receptor subunit 2B (NR2B-NMDA) and extracellular signal-regulated kinases (ERK1/2) were analyzed. The repeated treatment of SCI-mice with MR309 resulted in significant pain behavior attenuation beyond the end of the administration period, accompanied by reduced expression of central sensitization-related mechanistic correlates, including extracellular mediators (TNF-α and IL-1β), membrane receptors/channels (NR2B-NMDA) and intracellular signaling cascades (ERK/pERK). These findings suggest that repeated MR309 treatment after SCI may be a suitable pharmacologic strategy to modulate SCI-induced CNP development.

Indexed as

central neuropathic paincentral sensitization-related biomarkersMR309pro-inflammatory cytokinesspinal cord injury

Identifiers

PMID30967775
PMCPMC6439356
OpenAlexW2922599850

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Registered trials

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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.