ArticlePain2015
Modulation of nociceptive dural input to the trigeminocervical complex through GluK1 kainate receptors.
Article in Pain, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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
18 citing papers in PubMed, 27 citations in OpenAlex.
- From bench to bedside: relevant animal models across the migraine attack phases.The journal of headache and pain · 2026Review
- Emerging pharmacological targets in migraine therapy: CGRP and beyond.Frontiers in pharmacology · 2026Review
- Glutamate as a Therapeutic Substrate in Migraine.International journal of molecular sciences · 2025Review
- The Potential Role of Glutamate Receptors and their Antagonists or Modulators in Migraine Therapy.Current neuropharmacology · 2025Review
- The 5-HTNature reviews. Neurology · 2023Review
- HCN2 Ion Channels Drive Pain in Rodent Models of Migraine.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- Kynurenine Pathway of Tryptophan Metabolism in Migraine and Functional Gastrointestinal Disorders.International journal of molecular sciences · 2021Review
- Clinical relevance of depressed kynurenine pathway in episodic migraine patients: potential prognostic markers in the peripheral plasma during the interictal period.The journal of headache and pain · 2021Article
- Distinct Activity of Endocannabinoid-Hydrolyzing Enzymes MAGL and FAAH in Key Regions of Peripheral and Central Nervous System Implicated in Migraine.International journal of molecular sciences · 2021Article
- Double-Binding Botulinum Molecule with Reduced Muscle Paralysis: Evaluation in In Vitro and In Vivo Models of Migraine.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2021Article
- Mechanisms of migraine as a chronic evolutive condition.The journal of headache and pain · 2019Review
- Meningeal Mast Cells Contribute to ATP-Induced Nociceptive Firing in Trigeminal Nerve Terminals: Direct and Indirect Purinergic Mechanisms Triggering Migraine Pain.Frontiers in cellular neuroscience · 2019Article
- Glutamate and Its Receptors as Therapeutic Targets for Migraine.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2018Review
- Pathophysiology of Migraine: A Disorder of Sensory Processing.Physiological reviews · 2017Review
- Inhibitory effect of high-frequency greater occipital nerve electrical stimulation on trigeminovascular nociceptive processing in rats.Journal of neural transmission (Vienna, Austria : 1996) · 2017Article
- Cholinergic Nociceptive Mechanisms in Rat Meninges and Trigeminal Ganglia: Potential Implications for Migraine Pain.Frontiers in neurology · 2017Article
- Pharmacology of reflex blinks in the rat: a novel model for headache research.The journal of headache and pain · 2016Article
- Transcranial magnetic stimulation and potential cortical and trigeminothalamic mechanisms in migraine.Brain : a journal of neurology · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Migraine is a common and disabling neurologic disorder, with important psychiatric comorbidities. Its pathophysiology involves activation of neurons in the trigeminocervical complex (TCC). Kainate receptors carrying the glutamate receptor subunit 5 (GluK1) are present in key brain areas involved in migraine pathophysiology. To study the influence of kainate receptors on trigeminovascular neurotransmission, we determined the presence of GluK1 receptors within the trigeminal ganglion and TCC with immunohistochemistry. We performed in vivo electrophysiologic recordings from TCC neurons and investigated whether local or systemic application of GluK1 receptor antagonists modulated trigeminovascular transmission. Microiontophoretic application of a selective GluK1 receptor antagonist, but not of a nonspecific ionotropic glutamate receptor antagonist, markedly attenuated cell firing in a subpopulation of neurons activated in response to dural stimulation, consistent with selective inhibition of postsynaptic GluK1 receptor-evoked firing seen in all recorded neurons. In contrast, trigeminovascular activation was significantly facilitated in a different neuronal population. The clinically active kainate receptor antagonist LY466195 attenuated trigeminovascular activation in all neurons. In addition, LY466195 demonstrated an N-methyl-d-aspartate receptor-mediated effect. This study demonstrates a differential role of GluK1 receptors in the TCC, antagonism of which can inhibit trigeminovascular activation through postsynaptic mechanisms. Furthermore, the data suggest a novel, possibly presynaptic, modulatory role of trigeminocervical kainate receptors in vivo. Differential activation of kainate receptors suggests unique roles for this receptor in pro- and antinociceptive mechanisms in migraine pathophysiology.
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.