Figure 4.

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 [20] 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
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