Figure 4. NK-1R activation inhibits Bdel2 currents. HEK-M1 cells were transiently transfected with Bdel2, α2δ-1, CaVβ2a, or CaVβ3 and NK-1R. (A) Averaged current–voltage plot measured before and after application of SP. (B and C) Individual traces from CaVβ2a-containing Bdel2 channels (B) or CaVβ3-containing wt channels (C) taken before and 2 min after application of SP (red) before (P1) or after a prepulse (P2). (D) Prepulse facilitation (ratio of P2/P1) for wt CaV2.2 (▪), Bdel1 (•), and Bdel2 with either CaVβ2a (▴) or CaVβ3 (▾); *, P < 0.05 compared with Bdel1. (E) Summary of modulation of wt CaV2.2 (▪), Bdel1 (•), and Bdel2 with either CaVβ2a (▴) or CaVβ3 (▾) by SP before (closed) and after (open) a prepulse; *, P < 0.05 compared with control currents (n = 4–9). Error bars represent SEM. Bars, 10 ms and 200 pA.
Figure 4.

NK-1R activation inhibits Bdel2 currents. HEK-M1 cells were transiently transfected with Bdel2, α2δ-1, CaVβ2a, or CaVβ3 and NK-1R. (A) Averaged current–voltage plot measured before and after application of SP. (B and C) Individual traces from CaVβ2a-containing Bdel2 channels (B) or CaVβ3-containing wt channels (C) taken before and 2 min after application of SP (red) before (P1) or after a prepulse (P2). (D) Prepulse facilitation (ratio of P2/P1) for wt CaV2.2 (▪), Bdel1 (•), and Bdel2 with either CaVβ2a (▴) or CaVβ3 (▾); *, P < 0.05 compared with Bdel1. (E) Summary of modulation of wt CaV2.2 (▪), Bdel1 (•), and Bdel2 with either CaVβ2a (▴) or CaVβ3 (▾) by SP before (closed) and after (open) a prepulse; *, P < 0.05 compared with control currents (n = 4–9). Error bars represent SEM. Bars, 10 ms and 200 pA.

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