ATP1A2 and migraine disorder: Interestingly, FHM2 knock-in mice, having reduced rate of glutamate clearance at cortical excitatory synapses (Leo et al., 2011; Capuani et al., 2016; Parker et al., 2021), show facilitation of NMDA spikes in L5 PC tuft dendrites in cingulate cortex slices, which is correlated with enhanced sensitivity to a migraine-relevant head pain trigger (Romanos et al., 2020); they also show enhanced activation of extrasynaptic GluN1-N2B NMDA receptors in L2/3 PC apical dendrites in barrel cortex slices, whose inhibition rescues the facilitation of experimental CSD (Crivellaro et al., 2021).