Evidence map›Paper›PMID 40886229›Full record

ArticleJournal of neural transmission (Vienna, Austria : 1996)2025

The effect of recombinant botulinum neurotoxin A on neuropathic pain in the spared nerve injury mouse model.

Rasmus E Hammer, Akinyemi A Omoniyi, Mette Richner, Stephane Lezmi, Christian B Vaegter, Mikhail Kalinichev, Pall Karlsson, Jens R Nyengaard

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of neural transmission (Vienna, Austria : 1996), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. Review
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

8 authors.

Rasmus E HammerCore Center for Molecular Morphology, Section for Stereology and Microscopy, Department of Clinical Medicine, Aarhus University, Aarhus, Denmark.
Akinyemi A OmoniyiCore Center for Molecular Morphology, Section for Stereology and Microscopy, Department of Clinical Medicine, Aarhus University, Aarhus, Denmark.
Mette RichnerDanish Research Institute of Translational Neuroscience (DANDRITE), Nordic-EMBL Partnership for Molecular Medicine, Department of Biomedicine, Aarhus University, Aarhus, 8000, Denmark.
Stephane LezmiIpsen Innovation, Avenue Du Canada, Les Ulis, 91940, France.
Christian B VaegterDanish Research Institute of Translational Neuroscience (DANDRITE), Nordic-EMBL Partnership for Molecular Medicine, Department of Biomedicine, Aarhus University, Aarhus, 8000, Denmark.
Mikhail KalinichevIpsen Innovation, Avenue Du Canada, Les Ulis, 91940, France. mikhail.kalinichev@icloud.com.
Pall KarlssonCore Center for Molecular Morphology, Section for Stereology and Microscopy, Department of Clinical Medicine, Aarhus University, Aarhus, Denmark.
Jens R NyengaardCore Center for Molecular Morphology, Section for Stereology and Microscopy, Department of Clinical Medicine, Aarhus University, Aarhus, Denmark.

Funding

Ipsen Ipsen
6 · The paper itself

Abstract

Neuropathic pain following traumatic nerve injury is a disabling chronic pain disorder characterized by sensory abnormalities such as mechanical allodynia. Botulinum neurotoxin type A (BoNT/A) has shown analgesic properties in a range of clinical pain conditions and in animal models. Here, we investigated analgesic efficacy of recombinant BoNT/A1 (rBoNT/A1; IPN10260) in the spared nerve injury (SNI) mouse model of neuropathic pain. Potential tissue site and mechanisms of action were explored by analyzing a series of pain biomarkers in the ipsilateral dorsal root ganglion (DRG) and the spinal cord. C57Bl6 mice received either SNI- or a sham surgery 14 days before being treated with either rBoNT/A1 or vehicle. Mechanical sensitivity was evaluated in von Frey tests performed at baseline and throughout the experiment. DRGs and spinal cords were collected for quantitative microscopy of immunohistochemically labelled pain-related targets. rBoNT/A1-injection resulted in significant and prolonged (up to 14 days) increases in mechanical threshold compared to vehicle in SNI-operated mice. Volume of type B DRG neurons and number density of Iba1-positive cells in DRG were significantly increased in the SNI-operated animals in comparison to the sham-operated controls, however no significant effect of rBoNT/A1 could be demonstrated. Among spinal cord biomarkers, no effects were observed. These results demonstrate that rBoNT/A1 reduces mechanical allodynia following peripheral nerve injury, but the mechanisms remain elusive. Investigating these biomarkers in a challenged system (diabetes, chemotherapy, etc.) might extend the window of activation, possibly better exposing analgesic mechanisms of rBoNT/A1.

Indexed as

AnalgesicsBotulinum Toxins, Type ANeuralgiaPeripheral Nerve InjuriesAnimalsCalcium-Binding ProteinsDisease Models, AnimalGanglia, SpinalHyperalgesiaMaleMiceMice, Inbred C57BLMicrofilament ProteinsPain ThresholdRecombinant ProteinsSpinal CordAif1 protein, mouseAnalgesicsBotulinum Toxins, Type ACalcium-Binding ProteinsMicrofilament ProteinsRecombinant ProteinsAnalgesiaAnimal modelAntinociceptive efficacyChronic painvon Frey

Identifiers

PMID40886229
PMCPMC12669262

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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.