Evidence map›Paper›PMID 27023421›Full record

ArticlePain2016

Neuropeptide Y inhibits the trigeminovascular pathway through NPY Y1 receptor: implications for migraine.

Margarida-Martins Oliveira, Simon Akerman, Isaura Tavares, Peter J Goadsby

Erratum issuedOpen access · hybridAbstract read
In one paragraph

Article in Pain, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
5.1field-weighted citation impact, top 4% 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

30 citing papers in PubMed, 54 citations in OpenAlex.

  1. Trial
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  6. Hallmarks of primary headache: part 3 - cluster headache.The journal of headache and pain · 2025
    Review
  7. Review
  8. Neuropeptide Y and Pain: Insights from Brain Research.ACS pharmacology & translational science · 2024
    Review
  9. Review
  10. Review
  11. Review
  12. Genetic Mechanisms of Migraine: Insights from Monogenic Migraine Mutations.International journal of molecular sciences · 2023
    Review
  13. Molecular Mechanisms of Migraine: Nitric Oxide Synthase and Neuropeptides.International journal of molecular sciences · 2023
    Review
  14. Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

4 authors at 2 institutions in 3 countries.

Margarida-Martins OliveiraHeadache Group, Basic and Clinical Neuroscience, Institute of Psychology, Psychiatry and Neuroscience, King's College London, London, United Kingdom.
Simon AkermanDepartment of Neurology, University of California, San Francisco, San Francisco, CA, USA.
Isaura TavaresDepartment of Experimental Biology, Faculty of Medicine of University of Porto, and Institute of Investigation and Innovation in Health (I3S), University of Porto, Porto, Portugal.
Peter J GoadsbyHeadache Group, Basic and Clinical Neuroscience, Institute of Psychology, Psychiatry and Neuroscience, King's College London, London, United Kingdom.
University of California, San Francisco · USi3S - Instituto de Investigação e Inovação em Saúde, Universidade do Porto · PT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Migraine is a painful neurologic disorder with premonitory symptomatology that can include disturbed appetite. Migraine pathophysiology involves abnormal activation of trigeminocervical complex (TCC) neurons. Neuropeptide Y (NPY) is synthesized in the brain and is involved in pain modulation. NPY receptors are present in trigeminal ganglia and trigeminal nucleus caudalis suggesting a role in migraine pathophysiology. The present study aimed to determine the effect of systemic administration of NPY on TCC neuronal activity in response to dural nociceptive trigeminovascular activation. We performed in vivo electrophysiology in anesthetized rats, administered NPY (10, 30, and 100 µg·kg), and investigated the receptors involved by studying NPY Y1 (30 µg·kg), Y2 (30 µg·kg), and Y5 receptor agonists (100·µg·kg), and NPY Y1 receptor antagonist (30 µg·kg). NPY (30 and 100 µg·kg) significantly reduced TCC neuronal firing in response to dural-evoked trigeminovascular activation, but only NPY (30 µg·kg) significantly reduced spontaneous trigeminal firing. NPY Y1 receptor agonist also significantly reduced dural-evoked and spontaneous TCC neuronal firing. NPY (10 µg·kg), NPY Y2, and Y5 receptor agonists, and the NPY Y1 receptor antagonist had no significant effects on nociceptive dural-evoked neuronal firing in the TCC or spontaneous trigeminal firing. This study demonstrates that NPY dose dependently inhibits dural-evoked trigeminal activity, through NPY Y1 receptor activation, indicating antinociceptive actions of NPY in a migraine animal model. Based on the role of NPY in appetite regulation, it is possible that disruption of the NPY system might explain changes of appetite in migraineurs.

Indexed as

Action PotentialsAnimalsDisease Models, AnimalMaleMigraine DisordersNeuronsNeuropeptide YRatsRats, Sprague-DawleyReceptors, Neuropeptide YTrigeminal GanglionTrigeminal NucleiNeuropeptide Yneuropeptide Y-Y1 receptorReceptors, Neuropeptide Y

Identifiers

PMID27023421
PMCPMC4949002
OpenAlexW2320537959

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.