Ethanol Causes Neurogenic Vasodilation by TRPV1 Activation and CGRP Release in the Trigeminovascular System of The Guinea Pig
Ethanol stimulating transient receptor potential vanilloid 1 (TRPV1) on primary sensory neurons promotes neurogenic inflammation, including calcitonin gene-related peptide (CGRP)-mediated coronary dilation. Alcoholic beverages trigger migraine attacks and activation of trigeminal neurons plays a rol...
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Published in | Cephalalgia Vol. 28; no. 1; pp. 9 - 17 |
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Main Authors | , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
London, England
SAGE Publications
01.01.2008
Blackwell Publishing Ltd |
Subjects | |
Online Access | Get full text |
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Summary: | Ethanol stimulating transient receptor potential vanilloid 1 (TRPV1) on primary sensory neurons promotes neurogenic inflammation, including calcitonin gene-related peptide (CGRP)-mediated coronary dilation. Alcoholic beverages trigger migraine attacks and activation of trigeminal neurons plays a role in migraine. We have investigated in guinea pigs whether ethanol by TRPV1 stimulation causes neurogenic inflammation in the trigeminovascular system. Ethanolevoked release of neuropeptides from slices of dura mater was abolished by Ca2+ removal, capsaicin pretreatment and the TRPV1 antagonist, capsazepine. Intragastric ethanol increased plasma extravasation in dura mater, an effect abolished by capsazepine and the NK1 receptor antagonist, SR140333, and caused vasodilation around the middle meningeal artery, an effect abolished by capsazepine and the CGRP receptor antagonist, BIBN4096BS. Vasodilation of meningeal vessels by TRPV1 activation and CGRP release may be relevant to the mechanism by which alcohol ingestion triggers migraine attacks. |
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Bibliography: | P.N. and M.T. contributed equally to this work. ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0333-1024 1468-2982 |
DOI: | 10.1111/j.1468-2982.2007.01448.x |