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. 2003 Apr 1;23(7):2686–2695. doi: 10.1523/JNEUROSCI.23-07-02686.2003

Fig. 5.

Fig. 5.

Dopamine D1 receptor-mediated inhibition of VGKC.A, Activation of D1 receptors by the selective agonist SKF 81297 (0.1 and 1 μm) failed to alterIK (n = 5). Theinset shows two traces ofIK in the presence and absence of SKF 81297 (0.1 μm), clearly indicating the lack of effect of D1 receptor stimulation on this current. B, Activation of D1 receptors with SKF 81297 produced a dose-dependent suppression of ID(n = 25), which was prevented by the D1 receptor antagonist SCH 23390 (n = 5). Inset traces clearly show the dose-dependent modulation.C, Activation of D1 receptors by SKF 81297 (1 μm) failed to alterIA (n = 5).Inset traces show the overall effect of SKF 81297 and the effect on the isolated IA. D, The late component of VGKC (mostlyID) was measured at the open circle in inset; peak VGKC (mostlyIA) was measured at the beginning of the current, as indicated by the filled circle ininset. Perfusion of DA (20 μm) failed to alter peak VGKC (mostly IA) (n = 5; filled circles) but significantly inhibited the late component of VGKC (mostlyID) (n = 6;open circles). E, The effects of DA and SKF 81297 on the various components of VGKC are summarized in a box–whisker plot. Concentrations of 0.1 μm SKF 81297 (n = 5), 1 μm SKF 81297 (n = 5), or 0.1 μm SKF 81297 with 1 μm SCH 23390 (n = 3) failed to alter the amplitude of IK. Perfusion of 0.1 μm SKF 81297 produces a 19 ± 3% inhibition of ID(n = 15). Perfusion of 1 μm SKF 81297 produces a 34 ± 17% inhibition ofID (n = 10). Perfusion of 0.1 μm SKF 81297 together with 1 μm SCH 23390 does not alter the amplitude ofID(IRelative = 0.96 ± 0.03;n = 5). Perfusion of 0.1 (n = 3) or 1 μm SKF 81297 (n = 5), or SKF 81297 (0.1 μm) with SCH 23390 (1 μm) (n = 3), does not alter the amplitude of IA. Perfusion of DA does not alter IA(IRelative = 0.93 ± 0.09;n = 5) but inhibitsID(IRelative = 0.78 ± 0.06;n = 6.).