Abstract
Migraine is a primary headache disorder ranked as the leading cause of years lived with disability among individuals younger than 50 years. The aetiology of migraine is complex and might involve several molecules of different signalling pathways. Emerging evidence implicates potassium channels, predominantly ATP-sensitive potassium (K(ATP)) channels and large (big) calcium-sensitive potassium (BK(Ca)) channels in migraine attack initiation. Basic neuroscience revealed that stimulation of potassium channels activated and sensitized trigeminovascular neurons. Clinical trials showed that administration of potassium channel openers caused headache and migraine attack associated with dilation of cephalic arteries. The present review highlights the molecular structure and physiological function of K(ATP) and BK(Ca) channels, presents recent insights into the role of potassium channels in migraine pathophysiology, and discusses possible complementary effects and interdependence of potassium channels in migraine attack initiation.