Implications of Transient Receptor Potential Cation Channels in Migraine Pathophysiology
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REVIEW
Implications of Transient Receptor Potential Cation Channels in Migraine Pathophysiology Mamoru Shibata1,2 • Chunhua Tang1,3
Received: 4 February 2020 / Accepted: 11 May 2020 Ó Shanghai Institutes for Biological Sciences, CAS 2020
Abstract Migraine is a common and debilitating headache disorder. Although its pathogenesis remains elusive, abnormal trigeminal and central nervous system activity is likely to play an important role. Transient receptor potential (TRP) channels, which transduce noxious stimuli into pain signals, are expressed in trigeminal ganglion neurons and brain regions closely associated with the pathophysiology of migraine. In the trigeminal ganglion, TRP channels co-localize with calcitonin gene-related peptide, a neuropeptide crucially implicated in migraine pathophysiology. Many preclinical and clinical data support the roles of TRP channels in migraine. In particular, activation of TRP cation channel V1 has been shown to regulate calcitonin gene-related peptide release from trigeminal nerves. Intriguingly, several effective antimigraine therapies, including botulinum neurotoxin type A, affect the functions of TRP cation channels. Here, we discuss currently available data regarding the roles of major TRP cation channels in the pathophysiology of migraine and the therapeutic applicability thereof.
Mamoru Shibata and Chunhua Tang have contributed equally to this review. & Mamoru Shibata [email protected] 1
Department of Neurology, Keio University School of Medicine, Tokyo 160-8582, Japan
2
Department of Neurology, Tokyo Dental College Ichikawa General Hospital, Chiba 272-8513, Japan
3
Department of Neurology and Center for Clinical Neuroscience, Daping Hospital, Third Military Medical University, Chongqing 400042, China
Keywords Migraine TRPV1 TRPM8 TRPA1 TRPV4 Calcitonin gene-related peptide Trigeminal ganglion Neurogenic inflammation
Introduction Migraine is one of the most debilitating neurological disorders, characterized by recurrent headache attacks [1, 2]. The concept that migraine is a channelopathy has been substantiated by the fact that familial hemiplegic migraine types 1 and 3 are caused by mutations in the genes encoding the a1 subunit of the CaV2.1 P/Q-type voltage-gated Ca2? channel (CACNA1A) [3] and the a1 subunit of the neuronal NaV1.1 voltage-gated Na? channel (SCN1A) [4], respectively. Furthermore, genetic abnormalities of the two-pore-domain K? channel, TRESK, have been shown to cause a familial form of migraine with aura. Unlike the CaV2.1 and NaV1.1 channels, the TRESK channel is strongly expressed in trigeminal ganglion (TG) neurons, pointing to the importance of peripheral trigeminal nociception in migraine pathophysiology. Transient receptor potential (TRP) channels are non-selective cation channels that transduce various noxious stimuli into pain signals [5]. They are expressed in TG neurons, and some are associated with the functions of calcitonin gene-related peptide (CGRP) [6, 7], a key target mo
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