This would probably require high-frequency repetitive or synchronous activity of a sufficient number of excitatory synapses in which glutamatergic transmission is potentiated, e.g. as a consequence of increased glutamate release as in FHM1 or reduced expression of astrocytic α2 NKA and glutamate transporters, as in FHM2, or as a consequence of other mechanisms in common migraine. This evidence concerns the gene ATP1A2 and migraine disorder.