MCU contributes to generate the Ca2+ hump in DRGs overexpressing α2δ-1 HA. A, High K+-induced Ca2+ transients in control DRG neurons, in the absence (left; n = 31) or presence (right; n = 22) of MCUD260N,E263Q. B, No change in the peak amplitude after MCUD260N,E263Q overexpression (checked bar compared with open bar) in control DRG neurons (p = 0.4, t test). C, High K+-induced Ca2+ transients in α2δ-1 HA overexpressing (left; n = 28) and α2δ-1 HA + MCUD260N,E263Q overexpressing (right; n = 23) DRGs. D, Cotransfection of MCUD260N,E263Q and α2δ-1 HA subunit increased the peak amplitude of high K+-induced Ca2+ transients (gray checked bar compared with solid gray bar, *p < 0.05, t test). E, Following MCUD260N,E263Q overexpression, α2δ-1 HA neurons did not display prolonged Ca2+ response in response to 50 mm K+ (gray checked bar compared with solid gray bar; p = 0.01 two-way ANOVA and Bonferroni post hoc test, *p < 0.05). There was no effect of MCUD260N,E263Q on the response width in control DRG neurons (checked bar compared with open bar). F, MtPericam responses stimulated by the application of 20 and 100 APs at 10 Hz in control (n = 26; black trace) and α2δ-1 HA neurons (n = 31; top gray trace). G, Increase of 100 AP-induced mitochondrial Ca2+ uptake in the presence of α2δ-1 HA and normalized to [Ca2+]mt in control neurons (p = 0.034; Kruskal–Wallis one-way ANOVA and Dunn's multiple-comparison test, *p < 0.05).