Evidence map›Paper›PMID 35189809›Full record

ArticleThe journal of headache and pain2022

Dual action of the cannabinoid receptor 1 ligand arachidonyl-2'-chloroethylamide on calcitonin gene-related peptide release.

Isabella Mai Christiansen, Jacob C A Edvinsson, Philip V Reducha, Lars Edvinsson, Kristian Agmund Haanes

Open access · goldAbstract read
In one paragraph

Article in The journal of headache and pain, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

12 citing papers in PubMed, 29 citations in OpenAlex.

  1. Review
  2. Overlapping pathways of migraine and the endocannabinoid system: Potential therapeutic targets.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026
    Review
  3. Article
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  11. Expression of Cannabinoid Receptors in the Trigeminal Ganglion of the Horse.International journal of molecular sciences · 2023
    Article
  12. 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

5 authors at 2 institutions in 2 countries.

Isabella Mai ChristiansenDepartment of Clinical Experimental Research, Glostrup Research Institute, Rigshospitalet, Glostrup, Denmark.
Jacob C A EdvinssonDepartment of Clinical Experimental Research, Glostrup Research Institute, Rigshospitalet, Glostrup, Denmark.
Philip V ReduchaDepartment of Clinical Experimental Research, Glostrup Research Institute, Rigshospitalet, Glostrup, Denmark.
Lars EdvinssonDepartment of Clinical Experimental Research, Glostrup Research Institute, Rigshospitalet, Glostrup, Denmark.
Kristian Agmund HaanesDepartment of Clinical Experimental Research, Glostrup Research Institute, Rigshospitalet, Glostrup, Denmark. khaa0039@regionh.dk.ORCID http://orcid.org/0000-0001-5182-8957
University of Copenhagen · DKLund University · SE

Funding

Lundbeckfonden R345-2020-1977
6 · The paper itself

Abstract

backgroundBased on the current understanding of the role of neuropeptide signalling in migraine, we explored the therapeutic potential of a specific cannabinoid agonist. The aim of the present study was to examine the effect of the synthetic endocannabinoid (eCB) analogue, arachidonyl-2'-chloroethylamide (ACEA), on calcitonin gene-related peptide (CGRP) release in the dura and trigeminal ganglion (TG), as cannabinoids are known to activate G

methodsThe experiments were performed using the hemi-skull model and dissected TGs from male Sprague-Dawley rats. CGRP release was induced by either 60 mM K

resultsCB1 was predominantly expressed in neuronal somas in which colocalization with CGRP was observed. Furthermore, CB1 exhibited colocalization with RAMP1 in neuronal Aδ-fibres but was not clearly expressed in the CGRP-immunoreactive C-fibres. CB2 was mainly expressed in satellite glial cells and did not show substantial colocalization with either CGRP or RAMP1. Without stimulation, 140 nM ACEA per se caused a significant increase in CGRP release in the dura but not TG, compared to vehicle. Furthermore, 140 nM ACEA did not significantly modify neither K

conclusionsResults from the present study indicate that ACEA per se does not exhibit antimigraine potential due to its dual agonistic properties, resulting in activation of both CB1 and TRPV1, and thereby inhibition and stimulation of CGRP release, respectively.

Indexed as

Calcitonin Gene-Related PeptideAnimalsArachidonic AcidsLigandsMaleRatsRats, Sprague-DawleyReceptors, CannabinoidArachidonic Acidsarachidonyl-2-chloroethylamideCalcitonin Gene-Related PeptideLigandsReceptors, CannabinoidACEACannabinoid receptorsCGRPImmunohistochemistryTrigeminal ganglion

Identifiers

PMID35189809
PMCPMC8903492
OpenAlexW4213314318

What OpenQuestion holds

Textmetadata
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.