(A) Neurons were preincubated with vehicle, PHE, and the indicated kinase inhibitors before seal formation. (B) Ten consecutive traces from representative cell-attached single-channel recordings of LTCCs with vehicle (0.1% DMSO; black) and PHE either alone (red) or with the PKC inhibitors chelerythrine (Chel; 10 µM; bright brown) and bisindolylmaleimide I (Bis I; 100 nM; dark brown), the Pyk2 inhibitor PF-719 (1 µM; green), or the Src inhibitors PP2 (10 µM; blue) and SU6656 (10 µM; purple). (C) The increase in NPo by PHE was blocked by all inhibitors. F6,108 = 6.434. Control vs. PHE, p = 0.0076; PHE vs. Chel + PHE, p = 0.0001; PHE vs. Bis I + PHE, p = 0.0076; PHE vs. PF-719 + PHE, p = 0.0018; PHE vs. PP2 + PHE, p = 0.0003; PHE vs. SU6656 + PHE, p = 0.0022. (D) Ensemble averages during depolarization. (E) The increase in ensemble average peak currents by PHE was blocked by PKC inhibitors chelerythrine, bisinolylmaleimide I, and Src inhibitor PP2. F6,108 = 4.839. Control vs. PHE, p = 0.0242; PHE vs. Chel + PHE, p = 0.0004; PHE vs. Bis I + PHE, p = 0.0242; PHE vs. PF-719 + PHE, p = 0.0723; PHE vs. PP2 + PHE, p = 0.0006; PHE vs. SU6656 + PHE, p = 0.0723. (C, E) Data are presented as means ± standard error of the mean (SEM). n represents the number of cells (*p ≤ 0.05, **p ≤ 0.01, ***p ≤ 0.001; analysis of variance [ANOVA] with post hoc Holm–Sidak’s multiple comparisons test). Panel A was created using Biorender.com.