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Comment
. 2017 Nov 21:8:623.
doi: 10.3389/fneur.2017.00623. eCollection 2017.

Commentary: Cholinergic Nociceptive Mechanisms in Rat Meninges and Trigeminal Ganglia: Potential Implications for Migraine Pain

Karl Messlinger  1
Affiliations
Comment

Commentary: Cholinergic Nociceptive Mechanisms in Rat Meninges and Trigeminal Ganglia: Potential Implications for Migraine Pain

Karl Messlinger. Front Neurol. .
No abstract available

Keywords: cholinergic receptors; dura mater; headache; in vitro recordings; meningeal nociceptors.

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Figures

Figure 1
Figure 1
Scheme of proposed parasympathetic and trigeminal signaling in the dura mater mediated by acetylcholine (Ach) and calcitonin gene-related peptide (CGRP). Signaling by solid arrows is derived from the reviewed paper, broken arrows denote additionally discussed effects. Ach is likely to cause degranulation of mast cells (MCs) via muscarinic (possibly M3) Ach receptors (mAch-R) and activation of trigeminal fibers via mAch-R and nicotinic Ach receptors (nAch-R) but not via TRPA1 receptors. Activation of parasympathetic nerve fibers has previously been shown to cause plasma extravasation from venous blood vessels (VV) and to increase meningeal blood flow, most likely by dilating arterial vessels (AV). The latter may be mediated by endothelial mAch-R (possibly M3) via nitric oxide signaling or by vasoactive intestinal polypeptide binding to VPAC receptors on smooth arterial muscle cells, which also express CGRP receptors. Besides its prominent vasodilatory effect, CGRP may be considered to act on Schwann cells, some of which express CGRP receptors.
See this image and copyright information in PMC

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