ArticleBritish journal of pharmacology2010
Effects of ionotropic glutamate receptor antagonists on rat dural artery diameter in an intravital microscopy model.
Article in British journal of pharmacology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
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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.
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Who cites it
14 citing papers in PubMed, 28 citations in OpenAlex.
- Headache and mechanical sensitization of human pericranial muscles after repeated intake of monosodium glutamate (MSG).The journal of headache and pain · 2013Trial
- 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
- Animal Models of Chronic Migraine: From the Bench to Therapy.Current pain and headache reports · 2024Review
- Functional Analysis of TRPA1, TRPM3, and TRPV1 Channels in Human Dermal Arteries and Their Role in Vascular Modulation.Pharmaceuticals (Basel, Switzerland) · 2024Article
- Review
- Testing the Role of Glutamate NMDA Receptors in Peripheral Trigeminal Nociception Implicated in Migraine Pain.International journal of molecular sciences · 2022Article
- Effects of Calcitonin-Gene-Related-Peptide on Auditory Nerve Activity.Frontiers in cell and developmental biology · 2021Article
- 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 · 2019Article
- Inhibition of NMDAR reduces bladder hypertrophy and improves bladder function in cyclophosphamide induced cystitis.The Journal of urology · 2015Article
- Review
- Review
- Glutamate pharmacology and metabolism in peripheral primary afferents: physiological and pathophysiological mechanisms.Pharmacology & therapeutics · 2011Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
background and purposeDuring migraine, trigeminal nerves may release calcitonin gene-related peptide (CGRP), inducing cranial vasodilatation and central nociception; hence, trigeminal inhibition or blockade of craniovascular CGRP receptors may prevent this vasodilatation and abort migraine headache. Several preclinical studies have shown that glutamate receptor antagonists affect the pathophysiology of migraine. This study investigated whether antagonists of NMDA (ketamine and MK801), AMPA (GYKI52466) and kainate (LY466195) glutamate receptors affected dural vasodilatation induced by alpha-CGRP, capsaicin and periarterial electrical stimulation in rats, using intravital microscopy. EXPERIMENTAL APPROACH: Male Sprague-Dawley rats were anaesthetized and the overlying bone was thinned to visualize the dural artery. Then, vasodilator responses to exogenous (i.v. alpha-CGRP) and endogenous (released by i.v. capsaicin and periarterial electrical stimulation) CGRP were elicited in the absence or presence of the above antagonists. KEY
resultsalpha-CGRP, capsaicin and periarterial electrical stimulation increased dural artery diameter. Ketamine and MK801 inhibited the vasodilator responses to capsaicin and electrical stimulation, while only ketamine attenuated those to alpha-CGRP. In contrast, GYKI52466 only attenuated the vasodilatation to exogenous alpha-CGRP, while LY466195 did not affect the vasodilator responses to endogenous or exogenous CGRP. CONCLUSIONS AND IMPLICATIONS: Although GYKI52466 has not been tested clinically, our data suggest that it would not inhibit migraine via vascular mechanisms. Similarly, the antimigraine efficacy of LY466195 seems unrelated to vascular CGRP-mediated pathways and/or receptors. In contrast, the cranial vascular effects of ketamine and MK801 may represent a therapeutic mechanism, although the same mechanism might contribute, peripherally, to cardiovascular side effects.
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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.