Role of Kv1 Potassium Channels in Regulating Dopamine Release and Presynaptic D2 Receptor Function
Figure 2
Effect of broad-spectrum potassium channel blockers on evoked DA overflow.
(A) A 30 min perfusion of the broad-spectrum potassium channels blocker 4-AP (100 µM) (n = 10;4) increased DA overflow kinetics compared to control (n = 8;6). Data were normalized to the first 6 recordings (10 min) of their respective control period (means ± SEM). (B) A 30 min perfusion of the broad-spectrum potassium channels blocker TEA (10 mM) (n = 10;3) drastically increased DA overflow kinetics compared to control (n = 8;6). Data were normalized to the first 6 recordings (10 min) of their respective control period (means ± SEM). (C) Time-course of the effect of a 30 min application of 100 µM 4-AP (n = 10;4) in comparison to control (n = 8;6). DA was electrically evoked at intervals of 2 min. Each group is normalized to the first 6 recordings (10 min) of its respective control period and graphically plotted against time (means ± SEM). After 10 min of stable recordings, 4-AP was superfused for 30 min. (D) Time-course of the effect of a 30 min application of 10 mM TEA (n = 10;3) in comparison to control (n = 8;6). (E) After a 30 min application of 100 µM 4-AP, 1 µM ConoTX was applied and caused a ∼ 90% decrease in evoked DA release. (F) After a 30 min application of 10 mM TEA, 1 µM ConoTX was applied and failed to inhibit DA overflow. Abbreviations: 4-AP, 4-aminopyridine; TEA, tetraethylammonium; ConoTX, ω-conotoxin GVIA.