Migraine: Calcium Channels and Glia

Migraine is a common neurological disease that affects about 11% of the adult population. The disease is divided into two main clinical subtypes: migraine with aura and migraine without aura. According to the neurovascular theory of migraine, the activation of the trigeminovascular system (TGVS) and the release of numerous neuropeptides, including calcitonin gene-related peptide (CGRP) are involved in headache pathogenesis. TGVS can be activated by cortical spreading depression (CSD), a phenomenon responsible for the aura. The mechanism of CSD, stemming in part from aberrant interactions between neurons and glia have been studied in models of familial hemiplegic migraine (FHM), a rare monogenic form of migraine with aura. The present review focuses on those interactions, especially as seen in FHM type 1, a variant of the disease caused by a mutation in CACNA1A, which encodes the alpha 1A subunit of the P/Q-type voltage-gated calcium channel.

Automated summary

Migraine is a common neurological disease divided into two main types: with aura and without aura. Research shows that the activation of the trigeminovascular system and release of neuropeptides play crucial roles in headache pathogenesis. Cortical spreading depression, responsible for aura, stems from aberrant interactions between neurons and glia, particularly studied in FHM models.