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.

• Authors: Pierangelo Geppetti, Jay Guido Capone, Marcello Trevisani, Paola Nicoletti, Giovanni Zagli, Maria Rosalia Tola
• Journal: The journal of headache and pain (J Headache Pain) Vol. 6 Issue 2 Pg. 61-70 (Apr 2005) ISSN: 1129-2369 [Print] England
• PMID: 16362644 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Review)

Chemical References

• Calcitonin Gene-Related Peptide Receptor Antagonists
• Receptors, Calcitonin Gene-Related Peptide
• TRPV Cation Channels
• TRPV1 receptor
• Calcitonin Gene-Related Peptide

Topics

• Animals
• Calcitonin Gene-Related Peptide (metabolism)
• Calcitonin Gene-Related Peptide Receptor Antagonists
• 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 (physiology)
• Sensory Receptor Cells (metabolism, physiopathology)
• TRPV Cation Channels (drug effects, physiology)
• Vasodilation (physiology)