The rate of h-erg channel inactivation was strongly voltage dependent at depolarized potentials and modulated by increasing [K+]0, suggesting an intrinsic voltage sensor.
The inactivation of h-erg channels has its own intrinsic voltage sensor, distinguishing it from C-type inactivation in other voltage-gated K+ channels.
The rapid delayed rectifier, IKr, is believed to have h-erg (human ether-à-go-go related gene) as its molecular basis. A recent study has shown that rectification of h-erg involves a rapid inactivation process that involves rapid closure of the external mouth of the pore or C-type inactivation. We measured the instantaneous current to voltage relationship for h-erg channels using the saponin permeabilized variation of the cut-open oocyte clamp technique. In contrast to C-type inactivation in other voltage-gated K+ channels, the rate of inactivation was strongly voltage dependent at depolarized potentials. This voltage dependence could be modulated independently of activation by increasing K+0 from 2 to 98 mM. These results suggest that inactivation of h-erg has its own intrinsic voltage sensor.
Wang et al. (1996) studied this question. Increasing [K+]0 vs. 2 mM [K+]0 was evaluated on Instantaneous current to voltage relationship and rate of inactivation. The rate of h-erg channel inactivation was strongly voltage dependent at depolarized potentials and modulated by increasing [K+]0, suggesting an intrinsic voltage sensor.