Implications of Transient Receptor Potential Cation Channels in Migraine Pathophysiology

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.

Automated summary

Migraine is a common and debilitating headache disorder with elusive pathogenesis, likely involving abnormal trigeminal and central nervous system activity. TRP channels, which transduce noxious stimuli into pain signals, play important roles in migraine pathophysiology by co-localizing with calcitonin gene-related peptide in the trigeminal ganglion and regulating its release. Effective anti-migraine therapies, such as botulinum neurotoxin type A, also impact TRP cation channel functions.