Phosphorylation of GluA1 at the Ser845 site is required for neuropathic pain-induced upregulation of GluA1. A, Mechanical allodynia was significantly increased in the GluA1–S831A mice with nerve ligation compared with sham control on postsurgical day 7 (n = 5 mice for each group) but not in the GluA1–S845A mice (n = 8 mice for each group). *p < 0.05. B, In the PSD fraction of the insular cortex from GluA1–S831A mice, the abundance of GluA1 and its phosphorylation at the Ser845 site was significantly increased on day 7 after nerve ligation compared with sham control (n = 5 mice for each group). C, In the non-PSD fraction of the insular cortex from the GluA1–S831A mice, the phosphorylation of GluA1 at the Ser845 site was significantly reduced on day 7 after nerve ligation compared with sham control, whereas no change was observed for GluA1 (n = 4 mice for each group). D, In the PSD fraction of the insular cortex from GluA1–S845A mice with nerve ligation, the abundance of GluA1 and its phosphorylation at the Ser845 site showed no change compared with sham control (n = 5 mice for each group). E, No change was observed for GluA1 or its phosphorylation at the Ser845 site in the non-PSD fraction of the insular cortex from GluA1–S845A mice with nerve ligation compared with sham control (n = 3 mice for each group). **p < 0.01 compared with sham control.