Evidence map›Paper›PMID 18416824›Full record

ArticleMolecular pain2008

Release of glutamate and CGRP from trigeminal ganglion neurons: Role of calcium channels and 5-HT1 receptor signaling.

Yan Xiao, Judith A Richter, Joyce H Hurley

Open access · goldAbstract read
In one paragraph

Article in Molecular pain, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed, 1 pooled it
4.8field-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

45 citing papers in PubMed, 1 synthesis or guideline pooled it, 93 citations in OpenAlex.

  1. Pooled it
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  17. Review
  18. Trigeminovascular calcitonin gene-related peptide function in Cacna1a R192Q-mutated knock-in mice.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2019
    Article
  19. Review
  20. Verapamil Inhibits TRESK (KInternational journal of molecular sciences · 2018
    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

3 authors at 2 institutions in 1 country.

Yan XiaoDepartment of Biochemistry and Molecular Biology, Stark Neurosciences Research Institute, Indiana University School of Medicine, 950 West Walnut Street, Indianapolis, Indiana, 46202, USA. yaxiao@iupui.edu
Judith A Richter
Joyce H Hurley
Indiana University School of MedicineIndiana University – Purdue University Indianapolis · US

Funding

EXTRAMURAL RESEARCH FACILITIES CONSTRUCTIONC06RR015481 · NCRR · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI FIFE, ROSE S · 2001 to 2001
$1.6M
Sensitization in Trigeminal Neurons: A Role in Migraine?R01NS046503 · NINDS · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI HURLEY, JOYCE H · 2005 to 2008
$731k
NCRR NIH HHS C06 RR015481NCRR NIH HHS C06 RR015481-01NINDS NIH HHS NS 46503NINDS NIH HHS R01 NS046503
6 · The paper itself

Abstract

backgroundThe aberrant release of the neurotransmitters, glutamate and calcitonin-gene related peptide (CGRP), from trigeminal neurons has been implicated in migraine. The voltage-gated P/Q-type calcium channel has a critical role in controlling neurotransmitter release and has been linked to Familial Hemiplegic Migraine. Therefore, we examined the importance of voltage-dependent calcium channels in controlling release of glutamate and CGRP from trigeminal ganglion neurons isolated from male and female rats and grown in culture. Serotonergic pathways are likely involved in migraine, as triptans, a class of 5-HT1 receptor agonists, are effective in the treatment of migraine and their effectiveness may be due to inhibiting neurotransmitter release from trigeminal neurons. We also studied the effect of serotonin receptor activation on release of glutamate and CGRP from trigeminal neurons grown in culture.

resultsP/Q-, N- and L-type channels each mediate a significant fraction of potassium-stimulated release of glutamate and CGRP. We determined that 5-HT significantly inhibits potassium-stimulated release of both glutamate and CGRP. Serotonergic inhibition of both CGRP and glutamate release can be blocked by pertussis toxin and NAS-181, a 5-HT1B/1D antagonist. Stimulated release of CGRP is unaffected by Y-25130, a 5-HT3 antagonist and SB 200646, a 5-HT2B/2C antagonist.

conclusionThese data suggest that release of both glutamate and CGRP from trigeminal neurons is controlled by calcium channels and modulated by 5-HT signaling in a pertussis-toxin dependent manner and probably via 5-HT1 receptor signaling. This is the first characterization of glutamate release from trigeminal neurons grown in culture.

Indexed as

Signal TransductionAnimalsCalcitonin Gene-Related PeptideCalcium ChannelsCells, CulturedFemaleGlutamic AcidMaleNeuronsRatsRats, Sprague-DawleyReceptors, Serotonin, 5-HT1Trigeminal GanglionCalcitonin Gene-Related PeptideCalcium ChannelsGlutamic AcidReceptors, Serotonin, 5-HT1

Identifiers

PMID18416824
PMCPMC2359740
OpenAlexW2086537685

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.