Fig. 2: Nerve injury increased the AMPAR/NMDAR-mediated current.

A Schematic diagram of experimental design. B The whole-cell patch recording of ACC L3 pyramidal neurons. C Representative traces showing the light-evoked AMPAR current input-output relationship. D Summary plots of the AMPAR currents in (C) (Two-way ANOVA, Interaction, F(5, 100) = 6.29, P < 0.0001; Sham vs. CPN: F(1, 20) = 6.28, P = 0.02; n = 13 neurons/4 mice, n = 9 neurons/3 CPN mice). E Representative traces of light-evoked AMPAR current in Sham and CPN groups when the holding potentials were increased from −80 to 40 mV at a step of 20 mV. F Current–voltage plots of the light-evoked AMPAR currents in (E). Current amplitudes were normalized to that recorded at −80 mV (Two-way ANOVA, Interaction, F(6, 120) = 1.38, P = 0.23; Sham vs. CPN: F(1, 20) = 0.13, P = 0.72; n = 9 neurons/3 Sham mice, n = 13 neurons/4 CPN mice). G Representative traces show the light-evoked NMDAR current input-output relationship. H Summary plots of the NMDAR currents in (G) (Two-way ANOVA, Interaction, F(5, 90) = 7.19, P < 0.0001, Sham vs. CPN, F(1, 18) = 5.46, P = 0.03; n = 9 neurons/3 sham mice, n = 11 neurons/3 CPN mice). I Representative traces of light-evoked NMDAR current in Sham and CPN group when the holding potentials were increased from −80 to + 40 mV at a step of 20 mV. J Current–voltage plots of the light-evoked NMDAR current in (I). Current amplitudes were normalized to that recorded at +40 mV (Two-way ANOVA, Interaction, F(6, 174) = 0.41, P = 0.87; Sham vs. CPN, F(1, 29) = 0.47, P = 0.50; n = 13 neurons/4 Sham mice, n = 18 neurons/5 CPN mice). All data were mean ± SEM. *P < 0.05, **P < 0.01, ***P < 0.001.