Evidence map›Paper›PMID 27189587›Full record

ArticleThe journal of headache and pain2016

Endovanilloids are potential activators of the trigeminovascular nocisensor complex.

Mária Dux, Éva Deák, Noémi Tassi, Péter Sántha, Gábor Jancsó

Open access · goldAbstract read
In one paragraph

Article in The journal of headache and pain, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.0field-weighted citation impact, top 27% 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

11 citing papers in PubMed, 23 citations in OpenAlex.

  1. Review
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  7. Review
  8. Article
  9. Cannabinoid control of neurogenic inflammation.British journal of pharmacology · 2020
    Review
  10. Review
  11. Emerging Role of (Endo)Cannabinoids in Migraine.Frontiers in pharmacology · 2018
    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

5 authors at 1 institution in 1 country.

Mária DuxDepartment of Physiology, University of Szeged, Dóm tér 10, H-6720, Szeged, Hungary. dux.maria@med.u-szeged.hu.
Éva DeákDepartment of Physiology, University of Szeged, Dóm tér 10, H-6720, Szeged, Hungary.
Noémi TassiDepartment of Physiology, University of Szeged, Dóm tér 10, H-6720, Szeged, Hungary.
Péter SánthaDepartment of Physiology, University of Szeged, Dóm tér 10, H-6720, Szeged, Hungary.
Gábor JancsóDepartment of Physiology, University of Szeged, Dóm tér 10, H-6720, Szeged, Hungary.
University of Szeged · HU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIn the dura mater encephali a significant population of trigeminal afferents coexpress the nociceptive ion channel transient receptor potential vanilloid type 1 (TRPV1) receptor and calcitonin gene-related peptide (CGRP). Release of CGRP serves the central transmission of sensory information, initiates local tissue reactions and may also sensitize the nociceptive pathway. To reveal the possible activation of meningeal TRPV1 receptors by endogenously synthetized agonists, the effects of arachidonylethanolamide (anandamide) and N-arachidonoyl-dopamine (NADA) were studied on dural vascular reactions and meningeal CGRP release.

methodsChanges in meningeal blood flow were measured with laser Doppler flowmetry in a rat open cranial window preparation following local dural applications of anandamide and NADA. The release of CGRP evoked by endovanilloids was measured with ELISA in an in vitro dura mater preparation.

resultsTopical application of NADA induced a significant dose-dependent increase in meningeal blood flow that was markedly inhibited by pretreatments with the TRPV1 antagonist capsazepine, the CGRP antagonist CGRP8-37, or by prior systemic capsaicin desensitization. Administration of anandamide resulted in minor increases in meningeal blood flow that was turned into vasoconstriction at the higher concentration. In the in vitro dura mater preparation NADA evoked a significant increase in CGRP release. Cannabinoid CB1 receptors of CGRP releasing nerve fibers seem to counteract the TRPV1 agonistic effect of anandamide in a dose-dependent fashion, a result which is confirmed by the facilitating effect of CB1 receptor inhibition on CGRP release and its reversing effect on the blood flow.

conclusionsThe present findings demonstrate that endovanilloids are potential activators of meningeal TRPV1 receptors and, consequently the trigeminovascular nocisensor complex that may play a significant role in the pathophysiology of headaches. The results also suggest that prejunctional CB1 receptors may modulate meningeal vascular responses.

Indexed as

Dura MaterAnimalsArachidonic AcidsCalcitonin Gene-Related PeptideCannabinoid Receptor AgonistsCapsaicinDisease Models, AnimalDopamineDose-Response Relationship, DrugEndocannabinoidsEnzyme-Linked Immunosorbent AssayLaser-Doppler FlowmetryNociceptorsPeptide FragmentsPolyunsaturated AlkamidesRatsanandamideArachidonic Acidsarachidonyl dopamineCalcitonin Gene-Related Peptidecalcitonin gene-related peptide (8-37)Cannabinoid Receptor AgonistsCapsaicincapsazepineDopamineEndocannabinoidsPeptide FragmentsPolyunsaturated AlkamidesReceptor, Cannabinoid, CB1Receptors, Calcitonin Gene-Related PeptideTRPV1 receptorTRPV Cation ChannelsDura mater encephaliEndovanilloidHeadacheMeningeal blood flowTransient receptor potential vanilloid 1Trigeminovascular nocisensor complex

Identifiers

PMID27189587
PMCPMC4870586
OpenAlexW2403997537

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.