Remarkably, chemogenetic silencing of the CeA PKC-δ positive neurons could reverse these behavioral and biochemical CM-like phenotypes (Fig. 5) while repetitive chemogenetic activation of these neurons in naïve mice recapitulated similar phenotypes observed after chronic NTG infusion (Fig. 7), suggesting a potential causal relationship between these neurons and migraine chronification. This evidence concerns the gene PRKCD and migraine disorder.