TRP Channels in the Focus of Trigeminal Nociceptor Sensitization Contributing to Primary Headaches

Language
en
Document Type
Article
Issue Date
2022-10-24
First published
2020-01-04
Issue Year
2020
Authors
Dux, Mária
Rosta, Judit
Messlinger, Karl
Editor
Publisher
MDPI
Abstract

Pain in trigeminal areas is driven by nociceptive trigeminal afferents. Transduction molecules, among them the nonspecific cation channels transient receptor potential vanilloid 1 (TRPV1) and ankyrin 1 (TRPA1), which are activated by endogenous and exogenous ligands, are expressed by a significant population of trigeminal nociceptors innervating meningeal tissues. Many of these nociceptors also contain vasoactive neuropeptides such as calcitonin gene-related peptide (CGRP) and substance P. Release of neuropeptides and other functional properties are frequently examined using the cell bodies of trigeminal neurons as models of their sensory endings. Pathophysiological conditions cause phosphorylation, increased expression and trafficking of transient receptor potential (TRP) channels, neuropeptides and other mediators, which accelerate activation of nociceptive pathways. Since nociceptor activation may be a significant pathophysiological mechanism involved in both peripheral and central sensitization of the trigeminal nociceptive pathway, its contribution to the pathophysiology of primary headaches is more than likely. Metabolic disorders and medication-induced painful states are frequently associated with TRP receptor activation and may increase the risk for primary headaches.

Journal Title
International Journal of Molecular Sciences
Volume
21
Issue
1
Citation
International Journal of Molecular Sciences 21.1 (2020): 342. <https://www.mdpi.com/1422-0067/21/1/342>
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