Skip to main content
. 2002 Mar 19;99(7):4325–4330. doi: 10.1073/pnas.072073399

Figure 3.

Figure 3

Functional role of endogenous PIP3 in the voltage-dependent relaxation of KG currents in atrial myocytes. (A) Voltage-dependent relaxation of ACh-induced KG current in atrial myocytes. Voltage-clamp protocol (Upper) and a typical ACh-induced KG current (Lower) recorded during a prepulse to +40 mV followed by stepping to −100 mV. Inward current upon stepping to −100 mV changes first instantaneously (Iins) and then slowly increases to a steady-state (Imax); the time-dependent decay is called “relaxation”. (B) KG currents were evoked by 10−7 M (Left) or 10−6 M (Right) ACh when control antibody (a) or anti-PIP3 antibody (c) were contained in the pipette. Currents at −100 mV were recorded after prepulses to between −100 and +40 mV in steps of 20 mV (Inset, voltage protocol ). (b and d) Relationship between the prepulse voltage and the Iins/Imax ratio for currents elicited by either 10−7 M (open circles) or 10−6 M (closed circles) ACh, with either control antibody (b) or anti-PIP3 antibody (d) in the pipette. n = 5 for each. In each family of currents arrowheads indicate the zero current level, and horizontal scale bars represent 1 s, and vertical scale bars represent 500 pA.