Inhibition of metabotropic glutamate receptor subtype 1 (mGluR1) attenuates chronic constriction injury (CCI)–induced alterations in firing number, fast afterhyperpolarization (fAHP), and action potential (AP) width via disinhibiting voltage-gated potassium channel subunit 2 (Kv2) current. (A) Expanded view of the representative traces showing the firing response to a depolarizing current stimulus (+300 pA, 500 ms). (B, left) AP number of CCI neurons decreases significantly to the sham level after application of 10 μM 9-(dimethylamino)-3-(hexahydro-1H-azepin-1-yl)pyrido[3′,2′:4,5]thieno[3,2-d]pyrimidin-4(3H)-one (A841720). One-way ANOVA and post hoc Bonferroni multiple comparison tests, CCI n = 12, all other groups n = 10. (B, middle) CCI neurons show comparable fAHP potentials to sham neurons after application of 10 μM A841720. Two-way repeated-measures ANOVA and post hoc Bonferroni multiple comparison tests, all groups n = 12. (B, right) CCI neurons also have comparable AP waveforms to sham neurons after application of 10 μM A841720. Two-way repeated-measures ANOVA and post hoc Bonferroni multiple comparison tests, all groups n = 12. (C) Expanded view of the representative traces showing the firing response to a depolarizing current stimulus (+300 pA, 500 ms). (D) After preapplication of 100 nM guangxitoxin-1E (GxTX), the 10 μM A841720 cannot down-regulate the AP number, fAHP potentials, and AP widths of CCI cholera toxin subunit B (CT-B)+ neurons. One-way ANOVA (for AP number) or two-way repeated-measures ANOVA (for fAHP and AP width) and post hoc Bonferroni multiple comparison tests, all groups n = 12. n.s. = no significant difference, *P < 0.05, **P < 0.01.