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CGRP and migraine: neurogenic inflammation revisited.

Abstract
For more than a century neurogenic inflammation has been proposed to have a role in various human diseases. The present review will cover the conceptual steps of the itinerary that has led to the conclusion that neurogenic inflammation is important in migraine. Of particular relevance for the object of this article is the observation that tachykin-independent neurogenic inflammatory responses are evident in rodents, but much less pronounced or absent in other mammal species, including man, whereas neurogenic vasodilatation, most likely mediated by CGRP, occurs in most mammalian species and also in man. Recent evidence that a CGRP receptor antagonist was effective in the treatment of migraine attack supports the hypothesis that neurogenic vasodilatation is a major underlying mechanism of migraine.
AuthorsPierangelo Geppetti, Jay Guido Capone, Marcello Trevisani, Paola Nicoletti, Giovanni Zagli, Maria Rosalia Tola
JournalThe journal of headache and pain (J Headache Pain) Vol. 6 Issue 2 Pg. 61-70 (Apr 2005) ISSN: 1129-2369 [Print] Italy
PMID16362644 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Review)
Chemical References
  • Receptors, Calcitonin Gene-Related Peptide
  • TRPV Cation Channels
  • TRPV1 receptor
  • Calcitonin Gene-Related Peptide
Topics
  • Animals
  • Calcitonin Gene-Related Peptide (metabolism)
  • Cerebral Arteries (innervation, metabolism, physiopathology)
  • Humans
  • Migraine Disorders (drug therapy, etiology, physiopathology)
  • Neurogenic Inflammation (complications, metabolism, physiopathology)
  • Nociceptors (drug effects, physiology)
  • Receptors, Calcitonin Gene-Related Peptide (antagonists & inhibitors, physiology)
  • Sensory Receptor Cells (metabolism, physiopathology)
  • TRPV Cation Channels (drug effects, physiology)
  • Vasodilation (physiology)

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