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. 2022 Jul 23;23(1):87. doi: 10.1186/s10194-022-01464-2

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© The Author(s) 2022

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 1 — cAMP-dependent pathways in migraine pathophysiology. The cell is a vascular smooth muscle cell within the walls of intracranial arteries. Experimental studies have shown that binding of calcitonin gene-related peptide (CGRP), adrenomedullin (ADM), amylin (AMY), Pituitary adenylate cyclase-activating polypeptide (PACAP), vasoactive intestinal polypeptide (VIP), prostaglandin E₂ (PGE₂), and prostaglandin I₂ (PGI₂) to their G protein-coupled receptors increases the intracellular concentration of cyclic adenosine monophosphate (cAMP) and thereby activates the cAMP-dependent pathway. This will then activate protein kinase A which, in turn, results in outflow of potassium via opening of adenosine triphosphate-sensitive potassium (K_ATP) channels and large conductance calcium-activated potassium (BK_Ca) channels. The end result is hyperpolarization of the vascular smooth muscle and accompanying vasodilation which is hypothesized to provide the necessary chemical and mechanical stimuli needed to activate and sensitize perivascular nociceptors [2]. AC, adenylate cyclase; ADM, adrenomedullin; AMY, amylin; ATP, adenosine triphosphate; BK_CA, large conductance calcium-activated potassium channels; cAMP, cyclic adenosine monophosphate; CGRP, calcitonin-gene related peptide; K_ATP-channels, adenosine triphosphate-sensitive potassium channels; PACAP, pituitary adenylate cyclase activating polypeptide; PGE₂, prostaglandin E₂; PGI₂, prostaglandin I₂; Protein kinase A, cAMP-dependent protein kinase; VIP, vasoactive intestinal polypeptide