Figure 5.

CICR is increased in TALK-1 KO δ-cells. (A, B) Average increase in ${\mathrm{C}{\mathrm{a}}^{2+}}_{\mathrm{c}}$ following high K⁺ (45 mM)-induced depolarization in WT and TALK-1 KO δ-cells, treated with vehicle or with 5 μM thapsigargin (Tg). SERCAs were energized with 11 mM glucose and K_ATP was activated with 125 μM diazoxide. Subtraction of the signal obtained from Tg treated cells from vehicle treated cells reveals the contribution of the ER to the ${\mathrm{C}{\mathrm{a}}^{2+}}_{\mathrm{c}}$ signal (C) (N = 3 mice per genotype). (D) Average change in ${\mathrm{C}{\mathrm{a}}^{2+}}_{\mathrm{c}}$ in response to treatment with diazoxide (125 μM) and depolarization with 45 mM K⁺ in WT and TALK-1 KO δ-cells (N = 3 mice per genotype); *P < 0.05. (E) Representative ${\mathrm{C}{\mathrm{a}}^{2+}}_{\mathrm{c}}$ transients in WT and TALK-1 KO δ-cells subjected to short depolarizing pulses. The fold increase in δ-cell Ca²⁺ in response to increasingly long depolarizations in the presence or absence of CPA (25 μM) is quantified in (F) (N = 9 cells (WT); 7 cells (TALK-1 KO); 3 mice per genotype). (G) ${\mathrm{C}{\mathrm{a}}^{2+}}_{\mathrm{c}}$ in WT and TALK-1 KO δ-cells was assessed before and after treatment with CPA. (N = 3 mice per genotype); *P < 0.05, **P < 0.005.