Figure 4.

ER stores are not involved in shaping α₂δ-1 HA prolonged responses. A, Preincubation of DRGs in Ca²⁺ free bathing solution during the period shown by the gray shading abolished high K⁺-induced transients. The response was recovered after a subsequent application of extracellular 2 mm Ca²⁺. B, The Ca²⁺ hump observed in high K⁺-evoked signal of α₂δ-1 HA overexpressing neurons is not affected by perfusion with 0 mm Ca²⁺ after the initiation of the peak response (representative of n = 4). C, D, High K⁺-evoked Ca²⁺ transients imaged before and after store depletion by CPA pretreatment (right trace; 5 μm, 15 min) in control (C) and α₂δ-1 HA overexpressing neurons (D). E, Ca²⁺ transients evoked in α₂δ-1 HA overexpressing DRGs (striped bars) were not altered by CPA preapplication (gray bars; n = 14) when compared with neurons processed in parallel without the drug (white bars; n = 15). By contrast, in control neurons, CPA pretreatment (n = 14) resulted in responses with a slower recovery than those from untreated neurons (n = 14; interaction: p = 0.001, two-way ANOVA and Bonferroni post hoc test, *p < 0.05, **p < 0.01). F, G, Application of CPA in Ca²⁺-free solution (gray bar; 20 μm, 5 min). Caffeine (Caff; 5 mm) was then applied, and the lack of response indicated store depletion. Adding Ca²⁺ into the extracellular solution (white bar) triggered a similar store-operated calcium channel response in both control DRG neurons (F) and those overexpressing α₂δ-1 HA (G).