Final answer:
The state of delayed rectifier K+ channels is primarily dependent on membrane potential. The channels' single gate opens in response to a membrane voltage of -50 mV, although with a delay, and they close upon repolarization, ensuring the cell's membrane potential is restored with the help of the Na+/K+ ATPase and non-gated channels.
Step-by-step explanation:
The state of the delayed rectifier K+ channels is dependent on the membrane potential. After depolarization, during repolarization, these channels work to restore the resting membrane potential. The voltage-gated K+ channel is equipped with a single gate that is sensitive to a membrane voltage of -50 mV. Unlike voltage-gated Na+ channels, the K+ channel opens with a delay after this voltage threshold is reached, coinciding with the peak of Na+ influx and subsequent inactivation of Na+ channels. When the membrane potential repolarizes past -50 mV, the K+ channel slowly closes, resulting in a brief continuation of K+ efflux, hyperpolarizing the cell and causing an overshoot. Ultimately, the ongoing activity of non-gated channels and the Na+/K+ ATPase restore the resting potential.
Delayed rectifier potassium (K+) channels exhibit voltage-dependent gating. The state of these channels depends on the membrane potential. In the closed state, they maintain resting membrane potential. When the membrane undergoes depolarization, the channels slowly open, allowing potassium efflux, contributing to repolarization. The voltage sensitivity of delayed rectifier K+ channels plays a critical role in regulating action potential duration, influencing cellular excitability, and maintaining electrochemical balance across cell membranes.