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. 2004 May;123(5):521–531. doi: 10.1085/jgp.200409011

Figure 7.

Figure 7.

Inhibition of homomeric (CNGA1) rod channels by 200 nM ATR in saturating (2 mM) cGMP showed no significant voltage dependence other than that expected with voltage-dependent changes in open probability. For the top panel, an inside-out, multichannel patch was maintained at a holding potential of +50 mV in 200 nM ATR and 2 mM cGMP and monitored to steady-state. A double exponential provided the best fit to the time course of the inhibition, with τfast = 206 s and τslow = 3,779 s. After steady-state was achieved, the holding potential was changed to −50 mV. The time course of the resulting decrease in current (increase in inhibition) was best fit with a single exponential, with τ = 44 s. For the lower panel, the same experiment was performed on another patch, except that the initial membrane potential was −50 mV, and it was then switched to +50 mV. A double exponential provided the best fit to the initial time course of inhibition, with τfast = 77 s and τslow = 769 s. The time course of the increase in current (decrease in inhibition) after switching the voltage to +50 mV was best fit with a single exponential, with τ = 64 s. These changes in ATR inhibition with voltage are consistent with the expected voltage-dependent changes in open probability and the greater ATR inhibition of closed versus open channels.