Table 2. Properties of membrane currents evoked by step depolarizations to −10 mV with potassium gluconate-containing intracellular solution, in the presence of picrotoxin (50 μm)
| Control | Nifedipine | |
|---|---|---|
| Data were obtained from 17 control terminals and nine terminals in the presence of the L-type Ca2+ channel antagonist nifedipine (100 μm; three terminals were recorded from in both conditions). Step depolarizations in control conditions evoked an initial inward ICa followed rapidly by net outward current, which exhibited a biphasic profile. The degree of outward current inactivation during the first ∼25 ms was variable between recordings (no inactivation, n= 6; partial inactivation, n= 9; complete inactivation, n= 2). Nifedipine inhibited ICa and both the rapidly activated component and a slowly developing component of the outward current (IK(Ca)). | ||
| Peak inward current (pA) | −112 ± 11 | −13 ± 3 |
| Outward current at 3 ms (pA) | 109 ± 10 | 4 ± 3 |
| Outward current at 25 ms (pA) | 76 ± 10 | 35 ± 9 |
| Outward current at 200 ms (pA) | 120 ± 12 | 37 ± 8 |
| Outward current at 1 s (pA) | 176 ± 20 | 41 ± 13 |