Pharmacological characterization defines two permeation pathways in N.at-Kv3.2. A. Treatment of the wild-type N.at-Kv3.2 with 4-aminopyridine (4-AP) blocked the inward rectifying omega current in a dose-dependent fashion, while treatment with 10 mM tetraethylammonium (TEA) failed to block this permeation pathway. Pharmacological block was calculated for each individual experiment as % control current, where the control was ND96 (n = 7). B. Treatment of the G331K delayed-rectifier mutant demonstrated TEA block (10 mM) of the canonical pore. This mutant channel was insensitive to 10 mM 4-AP (n = 6). The slow onset of the TEA block does not reflect slow intrinsic binding kinetics, but rather the time it takes the perfusate to come to equilibrium (See Taglialatela and colleagues  for a similar result with the rat drk1 channel). Error bars denote s.e.m.
Klassen et al. BMC Neuroscience 2008 9:52 doi:10.1186/1471-2202-9-52