Table 2.
Inhibition of nicotinic currents by different pharmacological agents
| Agent | Peak current amplitude % Inhibition (mean ± SE) | |||
|---|---|---|---|---|
| Type IA (peak) | n | Type IB (steady-state) | n | |
| MLA (10 nm) | 74.2 ± 2.3 | 6 | ||
| MLA (50 nm) | 100 | 6 | 4.5 ± 1.0 | 4 |
| Choline (25 μm) | 34.2 ± 3.2 | 4 | ||
| Choline (50 μm) | 58.0 ± 4.8 | 5 | ||
| Choline (100 μm) | 97.8 ± 1.1 | 6 | 6.2 ± 1.4 | 5 |
| α-BGT (100 nm) | 100 | 6 | 5.7 ± 1.5 | 4 |
| DHβE (10 μm) | 39.2 ± 3.9 | 4 | 87.2 ± 4.6 | 5 |
Steady-state current was measured as the difference between the baseline and the current at the end of a 6 sec agonist pulse. The amplitudes of the currents recorded in the presence of each antagonist were significantly (p < 0.05 according to the paired Student’s t test) different from those measured in the absence of the antagonists.