Fig 2: a2d-1’s C terminus is critically involved in the dominance of synaptic CP-AMPARs in spinal cords in neuropathic pain(A) Effect of lentiviral vector-mediated expression of the a2d-1 C terminus peptide on nerve-injury-induced chronic pain in rats. The lentiviral vector expressing the C-terminal sequence of a2d-1 (CT vector, n = 8 rats) and a Cont vector (n = 7 rats) were intrathecally injected in rats 2 weeks after spinal nerve ligation (SNL). *p < 0.05, **p < 0.01, ***p < 0.001 versus baselines. One-way ANOVA followed by Dunnett test.(B) Effect of intrathecal injection of a lentiviral vector expressing wild-type a2d-1 or a2d-1 chimera (a2d-1CT(a2d-3)) vector on withdrawal thresholds in Cacna2d1 KO mice (n = 10 mice per group). **p < 0.01, ***p < 0.001 versus baselines. One-way ANOVA followed by Dunnett test.(C–E) Original traces (C), I-V plots (D), and rectification index (E) of AMPAR-EPSCs of lamina II neurons before and during bath application of 100 µM IEM-1460. AMPAR-EPSCs were recorded in Cacna2d1 KO mice 5 weeks after intrathecal injection of a lentiviral vector expressing wild-type a2d-1 (n = 15 neurons) or a2d-1 chimera (a2d-1CT(a2d-3), n = 16 neurons). *p < 0.05 versus the wild-type a2d-1 vector group; #p < 0.05 versus baseline control. One-way ANOVA followed by Tukey test.