Implications of Transient Receptor Potential Cation Channels in Migraine Pathophysiology
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
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 anti-migraine 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.
Keywords
Migraine; TRPV1; TRPM8; TRPA1; TRPV4; Calcitonin gene-related peptide; Trigeminal ganglion; Neurogenic inflammation
