Synaptic GluA1, but not GluA2/3, is upregulated in the insular cortex during neuropathic pain. A, The schematic diagram of the behavioral and biochemical experiments. B, Fractionation of the insular cortex was probed for PSD95, synaptophysin, and Rab3A to confirm the accuracy of the subcellular fractionation procedure. H, Homogenate; S2, cytosome; P2, crude synaptosome; Non-PSD, non-PSD enriched fraction; PSD, PSD-enriched fraction. C, Representative Western blots for GluA1 and GluA2/3 in the PSD fraction of the insular cortex obtained on postsurgical day 7. S, Sham; N, nerve ligation. D, Representative Western blots for GluA1 and GluA2/3 in the PSD fraction of the insular cortex obtained on postsurgical days 3 and 14. E, The abundance of GluA1 in the PSD fraction was significantly increased on postsurgical days 7 and 14 but not on day 3 (n = 4–7 mice for each group). The abundance of GluA2/3 in the PSD fraction showed no changes after nerve ligation (n = 4–5 mice for each group). F, Representative Western blots for GluA1 and GluA2/3 in the non-PSD fraction of the insular cortex obtained on postsurgical days 3, 7, and 14. G, The abundance of GluA1 or GluA2/3 showed no change after nerve ligation (n = 4–5 mice for each group). *p < 0.05, **p < 0.01 compared with sham control.