Latest Insights into the Pathophysiology of Migraine: the ATP-Sensitive Potassium Channels
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EPISODIC MIGRAINE (S NAHAS, SECTION EDITOR)
Latest Insights into the Pathophysiology of Migraine: the ATP-Sensitive Potassium Channels Lili Kokoti 1
&
Mohammad Al-Mahdi Al-Karagholi 1 & Messoud Ashina 1,2
Accepted: 15 November 2020 # Springer Science+Business Media, LLC, part of Springer Nature 2020
Abstract Purpose of Review Migraine remains a challenging condition to treat, thus highlighting the need for a better understanding of its molecular mechanisms. This review intends to unravel a new emerging target in migraine pathophysiology, the adenosine 5′triphosphate-sensitive K+ (KATP) channel. Recent Findings KATP channel is a common denominator in the cyclic adenosine monophosphate (cAMP) and cyclic guanosine monophosphate (cGMP) mediated intracellular cascades, both of which are involved in migraine. Intravenous infusion of KATP channel opener, levcromakalim, provoked migraine attack associated with dilation of extracerebral arteries in all persons with migraine. Summary Preclinical and clinical studies implicate KATP channels in migraine initiation. KATP channel is a novel therapeutic target for the acute and preventive treatment of migraine. Future studies are warranted to provide a better understanding of the role of KATP channel subgroups in migraine. Keywords KATP channel . Headache . Human models . Cromakalim . Migraine
Introduction The pathophysiology of migraine is complex and the underlying cause initiating migraine attacks remains unknown. Over the past two decades, advances in basic and clinical research in migraine have led to the development of new migraine-specific treatments [1–3]. Targeting extracellular calcitonin gene-related peptide (CGRP) and cell membrane CGRP receptors may abort and prevent migraine attacks in This article is part of the Topical Collection on Episodic Migraine * Messoud Ashina [email protected] Lili Kokoti [email protected] Mohammad Al-Mahdi Al-Karagholi [email protected] 1
Danish Headache Center, Department of Neurology, Rigshospitalet Glostrup, Faculty of Health and Medical Sciences, University of Copenhagen, Valdemar Hansen Vej 5, Glostrup, DK-2600 Copenhagen, Denmark
2
Danish Headache Knowledge Center, Rigshospitalet – Glostrup, Valdemar Hansens Vej 5, DK-2600 Glostrup, Denmark
many patients but variability of response in patients has been reported [4]. These data suggest the heterogeneous pathogenesis of migraine [5] and reveal the unmet need of a deeper understanding of the molecular pathways underlying migraine. A key feature of migraine is that various trigger factors have been demonstrated to initiate migraine attacks [6]. This provides a unique opportunity to identify the complex interplay between different molecular signaling pathways causing migraine attacks. Human provocation models allocate persons with migraine and non-migraine volunteers to receive a putative “trigger” molecule [6]. A repeated observation from these studies was that only individuals with migraine developed provoked migraine attacks, whereas non-migraine volunteers dev
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