Figure 5. Bdel2 current inhibition by SP is voltage independent, BAPTA sensitive, and antagonized by BSA similar to slow pathway modulation of CaV2.2. HEK-M1 cells were transiently transfected with NK-1R, either Bdel2 or wt CaV2.2, α2δ-1, and either CaVβ2a or CaVβ3. (A and B) Individual traces from wt CaV2.2/β3 (left) and Bdel2/β2a currents (right) taken before and 90 s after application of SP with 0.1 mM BAPTA (A) or 20 mM BAPTA (B) in the pipette solution. (C) Schematic showing BSA's site of action. (D) 1 mg/ml BSA in the external bath medium. Left, wt CaV2.2/β3; right, Bdel2/β2a. (E) Summary of the percent current remaining after SP from CaV2.2/β3 and Bdel2/β2a channels; *, P < 0.05 compared with control currents (n = 6–9); †, P < 0.05 using a one-way paired t test compared with unstimulated current amplitudes. Error bars represent SEM. Bars, 10 ms and 200 pA.
Figure 5.

Bdel2 current inhibition by SP is voltage independent, BAPTA sensitive, and antagonized by BSA similar to slow pathway modulation of CaV2.2. HEK-M1 cells were transiently transfected with NK-1R, either Bdel2 or wt CaV2.2, α2δ-1, and either CaVβ2a or CaVβ3. (A and B) Individual traces from wt CaV2.2/β3 (left) and Bdel2/β2a currents (right) taken before and 90 s after application of SP with 0.1 mM BAPTA (A) or 20 mM BAPTA (B) in the pipette solution. (C) Schematic showing BSA's site of action. (D) 1 mg/ml BSA in the external bath medium. Left, wt CaV2.2/β3; right, Bdel2/β2a. (E) Summary of the percent current remaining after SP from CaV2.2/β3 and Bdel2/β2a channels; *, P < 0.05 compared with control currents (n = 6–9); †, P < 0.05 using a one-way paired t test compared with unstimulated current amplitudes. Error bars represent SEM. Bars, 10 ms and 200 pA.

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