ArticleBritish journal of pharmacology2003
Voltage-dependent calcium channels are involved in neurogenic dural vasodilatation via a presynaptic transmitter release mechanism.
Article in British journal of pharmacology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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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
27 citing papers in PubMed, 99 citations in OpenAlex.
- Hallmarks of primary headache: part 3 - cluster headache.The journal of headache and pain · 2025Review
- Current and Novel Therapies for Cluster Headache: A Narrative Review.Pain and therapy · 2025Review
- Sensitization of meningeal afferents to locomotion-related meningeal deformations in a migraine model.eLife · 2024Article
- Sensitization of meningeal afferents to locomotion-related meningeal deformations in a migraine model.bioRxiv : the preprint server for biology · 2023Article
- Cluster headache pathophysiology - insights from current and emerging treatments.Nature reviews. Neurology · 2021Review
- Migraine: Calcium Channels and Glia.International journal of molecular sciences · 2021Review
- Pharmacotherapy for Cluster Headache.CNS drugs · 2020Review
- Electrical stimulation of the superior sagittal sinus suppresses A-type KThe journal of headache and pain · 2019Article
- 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
- Resolution of Persistent Post-Stapedotomy Vertigo With Migraine Prophylactic Medication.Otology & neurotology : official publication of the American Otological Society, American Neurotology Society [and] European Academy of Otology and Neurotology · 2017Article
- Efficacy of (Pain reports · 2016Article
- Riboflavin and vitamin E increase brain calcium and antioxidants, and microsomal calcium-ATP-ase values in rat headache models induced by glyceryl trinitrate.The Journal of membrane biology · 2015Article
- The proteome of mouse cerebral arteries.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2014Article
- Review
- A PEPTIDE UNCOUPLING CRMP-2 FROM THE PRESYNAPTIC Ca(2+) CHANNEL COMPLEX DEMONSTRATES EFFICACY IN ANIMAL MODELS OF MIGRAINE AND AIDS THERAPY-INDUCED NEUROPATHY.Translational neuroscience · 2012Article
- Trigeminal ganglion neuron subtype-specific alterations of Ca(V)2.1 calcium current and excitability in a Cacna1a mouse model of migraine.The Journal of physiology · 2011Article
- CaV2.1 channelopathies.Pflugers Archiv : European journal of physiology · 2010Review
- Insights into migraine mechanisms and CaV2.1 calcium channel function from mouse models of familial hemiplegic migraine.The Journal of physiology · 2010Review
- Headache-type adverse effects of NO donors: vasodilation and beyond.British journal of pharmacology · 2010Review
- Biological correlates of migraine and cluster headaches: an overview of their potential use in diagnosis and treatment.Pragmatic and observational research · 2010Review
Corrections and comments
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Authors and funding
3 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Amissense mutation of the CACNA1A gene that encodes the alpha1A subunit of the voltage-dependent P/Q-type calcium channel has been discovered in patients suffering from familial hemiplegic migraine. This suggested that calcium channelopathies may be involved in migraine more broadly, and established the importance of genetic mechanisms in migraine. Channelopathies share many clinical characteristics with migraine, and thus exploring calcium channel functions in the trigeminovascular system may give insights into migraine pathophysiology. It is also known that drugs blocking the P/Q- and N-type calcium channels have been successful in other animal models of trigeminovascular activation and head pain. In the present study, we used intravital microscopy to examine the effects of specific calcium channel blockers on neurogenic dural vasodilatation and calcitonin gene-related peptide (CGRP)-induced dilation. The L-type voltage-dependent calcium channel blocker calciseptine significantly attenuated (20 microg kg(-1), n=7) the dilation brought about by electrical stimulation, but did not effect CGRP-induced dural dilation. The P/Q-type voltage-dependent calcium channel blocker omega-agatoxin-IVA (20 microg kg-1, n=7) significantly attenuated the dilation brought about by electrical stimulation, but did not effect CGRP-induced dural dilation. The N-type voltage-dependent calcium channel blocker omega-conotoxin-GVIA (20 microg kg(-1), n=8 and 40 microg kg(-1), n=7) significantly attenuated the dilation brought about by electrical stimulation, but did not effect CGRP-induced dural dilation. It is thought that the P/Q-, N- and L-type calcium channels all exist presynaptically on trigeminovascular neurons, and blockade of these channels prevents CGRP release, and, therefore, dural blood vessel dilation. These data suggest that the P/Q-, N- and L-type calcium channels may be involved in trigeminovascular nociception.
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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.