Evidence map›Paper›PMID 10212302›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience1999

Regulation of calcitonin gene-related peptide secretion by a serotonergic antimigraine drug.

P L Durham, A F Russo

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
74citing papers in PubMed, 1 pooled it
4.4field-weighted citation impact, top 5% 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

74 citing papers in PubMed, 1 synthesis or guideline pooled it, 193 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Molecular Mechanisms of Migraine: Nitric Oxide Synthase and Neuropeptides.International journal of molecular sciences · 2023
    Review
  12. Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Review
  18. Article
  19. Anti-migraine agents from an immunological point of view.Journal of translational medicine · 2021
    Review
  20. Cross-talk signaling in the trigeminal ganglion: role of neuropeptides and other mediators.Journal of neural transmission (Vienna, Austria : 1996) · 2020
    Review

14 more citing papers are in PubMed but not listed here.

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

2 authors at 1 institution in 1 country.

P L DurhamDepartment of Physiology and Biophysics, University of Iowa, Iowa City, Iowa 52242, USA.
A F Russo
University of Iowa · US

Funding

VASOPRESSIN IN CARDIOVASCULAR REGULATIONP01HL014388 · NHLBI · UNIVERSITY OF IOWA · PI SANFORD, L PHILLIP · 1985 to 2018
$40.3M
INTERDISCIPLINARY CARDIOVASCULAR RESEARCH FELLOWSHIPT32HL007121 · NHLBI · UNIVERSITY OF IOWA · PI LONDON, BARRY · 1985 to 2020
$15.1M
NEURONAL CONTROL OF CGRP GENE EXPRESSIONR01HD025969 · NICHD · UNIVERSITY OF IOWA · PI RUSSO, ANDREW F · 1991 to 2003
$999k
CGRP IN SUBARACHNOID HEMORRHAGER01NS037386 · NINDS · UNIVERSITY OF IOWA · PI RUSSO, ANDREW F · 1998 to 2001
$375k
NHLBI NIH HHS HL14388NHLBI NIH HHS P01 HL014388NHLBI NIH HHS T32 HL007121NICHD NIH HHS HD25969NICHD NIH HHS R01 HD025969NINDS NIH HHS NS37386
6 · The paper itself

Abstract

We have investigated the regulation of calcitonin gene-related peptide (CGRP) release from trigeminal neurons by the serotonergic antimigraine drug sumatriptan. Serum levels of the neuropeptide CGRP are elevated during migraine. Treatment with the drug sumatriptan returns CGRP levels to normal coincident with the alleviation of headache. However, despite this clinical efficacy, the cellular target and mechanism of sumatriptan action are not well understood beyond the pharmacology of its recognition of the 5-HT1 class of serotonin receptors. We have used cultured trigeminal neurons to demonstrate that sumatriptan can directly repress CGRP secretion from sensory neurons. The stimulated secretion in response to depolarization or inflammatory agents was inhibited, but not the basal secretion rate. Unexpectedly, sumatriptan did not lower cAMP levels, in contrast to the classical role ascribed to the 5-HT1 receptors. Instead, activation of 5-HT1 receptors caused a slow and remarkably prolonged increase in intracellular calcium. The inhibition of CGRP secretion is attenuated by the phosphatase inhibitor okadaic acid, suggesting that sumatriptan action is mediated by calcium-recruited phosphatases. These results suggest that 5-HT1 agonists may block a deleterious feedback loop in migraine at the trigeminal neurons and provide a general mechanism by which this class of drugs can attenuate stimulated neuropeptide release.

Indexed as

AnimalsAnimals, NewbornCalcitonin Gene-Related PeptideCells, CulturedColforsinCyclic AMPHeLa CellsHumansInflammationKineticsModels, NeurologicalNeuronsOkadaic AcidOxadiazolesPotassium ChlorideQuinoxalinesCalcitonin Gene-Related PeptideCGS 12066BColforsinCyclic AMPHTR1B protein, humanL 694247Okadaic AcidOxadiazolesPotassium ChlorideQuinoxalinesReceptor, Serotonin, 5-HT1BReceptors, SerotoninReceptors, Serotonin, 5-HT1Recombinant ProteinsSerotonin Receptor AgonistsSumatriptanTryptamines

Identifiers

PMID10212302
PMCPMC6782229
OpenAlexW2153751480

What OpenQuestion holds

Textmetadata
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.