Recept Channels 1993 Jan 01;14:279-86.

Block of delayed rectifier (DRK1) K+ channels by internal 2,3-butanedione monoxime in Xenopus oocytes.

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Inhibition of delayed rectifier (DRK1) potassium channels by 2,3-butanedione monoxime (BDM) was investigated in inside-out membrane patches from Xenopus oocytes previously injected with in vitro transcribed DRK1 cRNA. Internally applied BDM (20 mM) rapidly and reversibly reduced peak macroscopic DRK1 current. 20 mM internal BDM increased the time constant of activation at all voltages (from 8.0 +/- 0.9 ms to 19.8 +/- 2.0 ms at zero mV, n = 6). Fluctuation analyses, and direct measurement of single channel currents, indicated that BDM reduced open probability (P0), and single channel current, at all voltages. The peak P0-voltage (V) relationship (estimated with a Boltzman equation) was shifted (from V0 = -29.3 +/- 4.6 to -9.4 +/- 2.7 mV) and shallowed (from Z = 2.8 +/- 0.2 to 1.8 +/- 0.15, n = 4) by BDM. In a simple sequential kinetic model of DRK1, the peak P0-V relationship, both in control and in BDM, was well fitted with the same V0 and Z (1.51 +/- 0.1 and -37.1 +/- 4 mV, respectively; n = 4) but with different voltage-independent rate constants. Thus, the effects of BDM on the kinetics of activation, the voltage-dependence of activation, and the rate of inactivation could be accounted for by assuming changes only in voltage-independent parameters.

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Species referenced: Xenopus
Genes referenced: kcnb1