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.

偏头痛是一种常见且令人衰弱的头痛疾病。尽管其发病机制仍然难以捉摸，但异常的三叉神经和中枢神经系统活动可能发挥重要作用。瞬时受体电位（TRP）通道将有害刺激转变成疼痛信号，在三叉神经节神经元和与偏头痛病理生理学密切相关的大脑区域中表达。在三叉神经节中，TRP 通道与降钙素基因相关肽共定位，降钙素基因相关肽是一种与偏头痛病理生理学密切相关的神经肽。许多临床前和临床数据支持 TRP 通道在偏头痛中的作用。特别是，TRP 阳离子通道 V1 的激活已被证明可以调节三叉神经降钙素基因相关肽的释放。有趣的是，几种有效的抗偏头痛疗法，包括 A 型肉毒杆菌神经毒素，会影响 TRP 阳离子通道的功能。在这里，我们讨论有关主要 TRP 阳离子通道在偏头痛病理生理学中的作用及其治疗适用性的当前可用数据。