ArticleBritish journal of pharmacology2009
Activation of iGluR5 kainate receptors inhibits neurogenic dural vasodilatation in an animal model of trigeminovascular activation.
Article in British journal of pharmacology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 43 citations in OpenAlex.
- 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
- Kainate Receptor Antagonists: Recent Advances and Therapeutic Perspective.International journal of molecular sciences · 2023Review
- Sensory Nerve Maintains Intervertebral Disc Extracellular Matrix Homeostasis Via CGRP/CHSY1 Axis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Article
- Peripheral role of glutamate in orofacial pain.Frontiers in neuroscience · 2022Review
- Dysregulation of the peripheral glutamatergic system: A key player in migraine pathogenesis?Cephalalgia : an international journal of headache · 2021Review
- Mechanisms of migraine as a chronic evolutive condition.The journal of headache and pain · 2019Review
- Plasma Calcitonin Gene-Related Peptide: A Potential Biomarker for Diagnosis and Therapeutic Responses in Pediatric Migraine.Frontiers in neurology · 2019Article
- The α6 subunit-containing GABANeuropharmacology · 2018Article
- Glutamate and Its Receptors as Therapeutic Targets for Migraine.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2018Review
- Age-Dependent Anti-migraine Effects of Valproic Acid and Topiramate in Rats.Frontiers in pharmacology · 2018Article
- Article
- Review
- 5-HT7 receptors are involved in neurogenic dural vasodilatation in an experimental model of migraine.Journal of molecular neuroscience : MN · 2014Article
- Kainate receptor signaling in pain pathways.Molecular pharmacology · 2013Review
- Pathophysiology of migraine.Annals of Indian Academy of Neurology · 2012Article
- Glutamate pharmacology and metabolism in peripheral primary afferents: physiological and pathophysiological mechanisms.Pharmacology & therapeutics · 2011Review
- Acute migraine therapy: new drugs and new approaches.Current treatment options in neurology · 2011Article
- CGRP and its receptors provide new insights into migraine pathophysiology.Nature reviews. Neurology · 2010Review
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
background and purposeMigraine is a disabling neurological disorder involving activation, or the perception of activation, of trigeminovascular afferents containing calcitonin gene-related peptide (CGRP). Released CGRP from peripheral trigeminal afferents causes dilatation of dural blood vessel, and this is used to measure trigeminal nerve activation. Kainate receptors with the GluR5 subunit (iGluR5, ionotropic glutamate receptor) are present in the trigeminal ganglion and may be involved in nociception. We investigated the possible involvement of prejunctional iGluR5 kainate receptors on CGRP release from trigeminal afferents. EXPERIMENTAL APPROACH: We used neurogenic dural vasodilatation, which involves reproducible vasodilatation in response to CGRP release after electrical stimulation of the dura mater surrounding the middle meningeal artery. The effects of the specific iGluR5 receptor antagonist UBP 302 and agonist (S)-(-)-5-iodowillardiine were investigated on neurogenic and CGRP-induced dural vasodilatation in rats, by using intravital microscopy. KEY
resultsAdministration of 10 and 20 mg.kg(-1) of iodowillardiine inhibited electrically induced dural vessel dilatation, an effect blocked by pretreatment with 50 mg.kg(-1) UBP 302. Administration of the iGluR5 receptor antagonist UBP 302 alone had no significant effect. CGRP (1 mg.kg(-1))-induced dural vasodilatation was not inhibited by the iGluR5 receptor agonist iodowillardiine. CONCLUSIONS AND IMPLICATIONS: This study demonstrates that activation of the iGluR5 kainate receptors with the selective agonist iodowillardiine is able to inhibit neurogenic dural vasodilatation probably by inhibition of prejunctional release of CGRP from trigeminal afferents. Taken together with recent clinical studies the data reinforce CGRP mechanisms in primary headaches and demonstrate a novel role for kainate receptor modulation of trigeminovascular activation.
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