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. Author manuscript; available in PMC: 2017 Mar 1.
Published in final edited form as: Nature. 2016 Aug 24;537(7618):117–121. doi: 10.1038/nature19102

Extended Data Figure 1. Biophysical characterization of CaVAb I199S.

Extended Data Figure 1

a, Ba2+ currents recorded from a holding potential of −120 mV to test potentials from −60 mV to 20 mV in 10 mV steps for I199S. b, GV curves of CaVAb and CaVAb I199S derived from peak IV relationships. The voltages for half-maximal activation and slopes are: CaVAb: V1/2 = − 18.8±0.3, k =3.68±0.43, n = 7; CaVAb I199S: V1/2 = −18.8±0.3, k =3.88±0.47 (n = 5). c, Repetitive depolarization to 0 mV at 1 Hz from a holding potential of − 120mV (n 5). d, Steady-state inactivation of CaVAb and CaVAb I199S. Two pulses were applied: a 300-ms conditioning pulse to the indicated potentials followed by 50-ms test pulse to 0 mV (n =3). e, State-dependent block of CaVAb I199S by 10 nM (green), 100 nM (blue), or 1.5 μM (red) amlodipine during repetitive depolarizations to 0 mV (left, n = 3–5 cells). Ba2+ currents in 100 nM amlodipine for CaVAb I199S (right). f, Concentration-dependent block of CaVAb I199S by nimodipine at 100 nM (blue), 1 μM (red), 5 μM (brown), 10 μM (grey) and 50 μM (black) (left, n = 4–5 cells for each curve). Ba2+ currents in the presence of 5 μM nimodipine for CaVAb I199S (right).