Meningeal mast cells, inflammation and migraine pain

Abstract

Migraine is a debilitating, throbbing headache that afflicts about 15% of the Western population. While the underlying cause of migraine is still a matter of speculation, the intracranial throbbing pain of migraine is largely attributed to an episode of local sterile meningeal inflammation that promote activation of trigeminal mechanosensitive nociceptive afferents that supply the meninges. The key players responsible for triggering such nociceptive neuronal events remain poorly defined, however. Mast cells, resident inflammatory cells that populate the meninges, particularly the dura mater, were implicated in the pathophysiology of migraine more than 50 years ago. Additional clinical and preclinical data that further support their role in migraine have recently emerged. This review highlights these findings, examines the evidence of a neuroimmune interaction between meningeal nociceptors and mast cells, in particular their involvement in promoting the activation and sensitization of the trigeminovascular systems, and will finally discuss the notion that in some migraine attacks, mast cells serve as an intermediate between various migraine triggers and the persistent activation of meningeal nociceptors. Drug Dev Res 68: 412-418, 2007.

Mast Cell Degranulation Mediates Compound 48/80-İnduced Meningeal Vasodilatation Underlying Migraine Pain

“…When the sensory nerve fibers are stimulated by mechanical or chemical stimuli, SP, NKA and CGRP are released from these fibers terminals and in turn these neuropeptides cause vasodilatation, increased vascular permeability, and plasma protein extravasation in the dura mater. It was reported that plasma levels of some mast cell mediators including histamine, triptase, TNF-α and interleukin-1 (IL-1) were increased during migraine attack (18). First of all, testing of mast cell stabilizing agents in rodent models of migraine pain may promise hope for the next big things in the treatment of migraine headaches.…”