ArticleHeadache2010
DHE repression of ATP-mediated sensitization of trigeminal ganglion neurons.
Article in Headache, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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.
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.
Who cites it
13 citing papers in PubMed, 27 citations in OpenAlex.
- MAP0004, orally inhaled dihydroergotamine for acute treatment of migraine: efficacy of early and late treatments.Mayo Clinic proceedings · 2011Trial
- The cornea-trigeminal axis: potassium channels as master regulators of ocular surface homeostasis and sensory transduction.Frontiers in cell and developmental biology · 2026Review
- Calcitonin gene-related peptide differentially modulates intracellular calcium levels in response to depolarizing stimuli in trigeminal ganglion neurons and glial cells.Neuroscience · 2025Article
- Intervening in the Premonitory Phase to Prevent Migraine: Prospects for Pharmacotherapy.CNS drugs · 2024Review
- Method for cryopreservation of trigeminal ganglion for establishing primary cultures of neurons and glia.Journal of neuroscience methods · 2024Article
- A link between gastrointestinal disorders and migraine: Insights into the gut-brain connection.Headache · 2021Review
- P2X7 receptors exert a permissive effect on the activation of presynaptic AMPA receptors in rat trigeminal caudal nucleus glutamatergic nerve terminals.The journal of headache and pain · 2020Article
- Migraine Treatment: Current Acute Medications and Their Potential Mechanisms of Action.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2018Review
- The role of purinergic signaling in the etiology of migraine and novel antimigraine treatment.Purinergic signalling · 2015Review
- Ion channels and migraine.Headache · 2014Review
- Advances in drug development for acute migraine.Drugs · 2012Article
- Acute treatment of migraines.CNS drugs · 2012Review
- Meeting acute migraine treatment needs through novel treatment formulations.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2010Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
objectiveTo investigate the mechanism by which adenosine triphosphate (ATP) causes sensitization of trigeminal neurons and how dihydroergotamine (DHE) represses this modulatory effect.
backgroundDihydroergotamine is an effective treatment of migraine. The cellular mechanisms of action of DHE in treating migraine attacks remain unclear.
methodsIn this study, neonatal rat trigeminal ganglia cultures were used to investigate effects of ATP, alpha, beta-methyl ATP (α,β-meATP), and DHE on intracellular calcium levels and calcitonin gene-related peptide (CGRP) secretion.
resultsPretreatment with ATP or α,β-meATP caused sensitization of neurons, via P2X(3) receptors, such that a subthreshold amount of potassium chloride (KCl) significantly increased intracellular calcium levels and CGRP secretion. Pretreatment with DHE repressed increases in calcium and CGRP secretion in response to ATP-KCl or α,β-meATP-KCl treatment. Importantly, these inhibitory effects of DHE were blocked with an α(2) -adrenoceptor antagonist and unaffected by a 5HT(1B/D) receptor antagonist. DHE also decreased neuronal membrane expression of the P2X(3) receptor.
conclusionsOur findings provide evidence for a novel mechanism of action for DHE that involves blocking ATP-mediated sensitization of trigeminal neurons, repressing stimulated CGRP release, and decreasing P2X(3) membrane expression via activation of α(2) -adrenoceptors.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.