BEGAIN and peripheral nerve injury: Our findings suggest that NMDAR and BEGAIN mutually interacted for the maintenance of pathological pain in spinal lamina IIi because BEGAIN expression in the PSD was increased by NMDAR activity accompanying the phosphorylation of GluN2B at Y1472 after peripheral nerve injury (Table 1), and also because BEGAIN modulated the EPSCs of NMDAR (Fig. 6).