New insight in migraine pathogenesis: Vasoactive intestinal peptide (VIP) and pituitary adenylate cyclase-activating polypeptide (PACAP) in the circulation after sumatriptan

New insight in migraine pathogenesis: Vasoactive intestinal peptide (VIP) and pituitary adenylate... In this issue of the Scandinavian Journal of Pain Jakob Møller Hansen and coworkers [1] report the effect of sumatriptan on circulating levels of two neuropeptides, vasoactive intestinal peptide (VIP) and pituitary adenylate cyclase activating peptide-38 (PACAP-38) to provide new insights into migraine pathogenesis.1Trigeminovascular system in migraineDysfunction of the trigeminovascular system is one of many factors that have been considered in the pathogenesis of migraine [2]. It has long been known that the headache phase of migraine, at least in part, is associated with release of vasoactive substances and neuropeptides [3]. The role of several neuropeptides (e.g. substance P, calcitonin gene-related peptide (CGRP) and VIP) and a possible impact of these peptides on vascular and neuronal mechanisms associated with migraine have already been investigated [4, 5]. Neuropeptides can cause dural neurogenic vasodilatation, plasma protein extravasation and sensitization of nociceptors, which have been documented in animal studies [6, 7]. In humans, elevated concentrations of neuropeptides such as CGRP, VIP, and neurokinin A (NKA) have been found in plasma samples during migraine attacks [4, 8, 9, 10]. Hence, one strategy to abort migraine is to block the release of neuropeptides or their receptor activation. Abortive agents in acute migraine management exert http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Scandinavian Journal of Pain de Gruyter

New insight in migraine pathogenesis: Vasoactive intestinal peptide (VIP) and pituitary adenylate cyclase-activating polypeptide (PACAP) in the circulation after sumatriptan

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Publisher
de Gruyter
Copyright
© 2013 Scandinavian Association for the Study of Pain
ISSN
1877-8860
eISSN
1877-8879
D.O.I.
10.1016/j.sjpain.2013.07.001
Publisher site
See Article on Publisher Site

Abstract

In this issue of the Scandinavian Journal of Pain Jakob Møller Hansen and coworkers [1] report the effect of sumatriptan on circulating levels of two neuropeptides, vasoactive intestinal peptide (VIP) and pituitary adenylate cyclase activating peptide-38 (PACAP-38) to provide new insights into migraine pathogenesis.1Trigeminovascular system in migraineDysfunction of the trigeminovascular system is one of many factors that have been considered in the pathogenesis of migraine [2]. It has long been known that the headache phase of migraine, at least in part, is associated with release of vasoactive substances and neuropeptides [3]. The role of several neuropeptides (e.g. substance P, calcitonin gene-related peptide (CGRP) and VIP) and a possible impact of these peptides on vascular and neuronal mechanisms associated with migraine have already been investigated [4, 5]. Neuropeptides can cause dural neurogenic vasodilatation, plasma protein extravasation and sensitization of nociceptors, which have been documented in animal studies [6, 7]. In humans, elevated concentrations of neuropeptides such as CGRP, VIP, and neurokinin A (NKA) have been found in plasma samples during migraine attacks [4, 8, 9, 10]. Hence, one strategy to abort migraine is to block the release of neuropeptides or their receptor activation. Abortive agents in acute migraine management exert

Journal

Scandinavian Journal of Painde Gruyter

Published: Oct 1, 2013

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