ATP1A2 and migraine disorder: We will summarize some of our findings supporting the conclusions that i) excessive cortical excitatory synaptic transmission and excessive activation of NMDA receptors, due either to enhanced glutamate release in FHM1 or impaired glutamate clearance in FHM2, are the main mechanisms underlying facilitation of experimental CSD in the genetic migraine models; ii) the dynamic regulation of the excitatory-inhibitory balance during thalamocortical activity is dysfunctional in FHM1 mice.