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Repolarization typically results from the movement of positively charged K + ions out of the cell. The repolarization phase of an action potential initially results in hyperpolarization, attainment of a membrane potential, termed the afterhyperpolarization, that is more negative than the resting potential. Repolarization usually takes several ...
Hyperpolarization is a change in a cell's membrane potential that makes it more negative. Cells typically have a negative resting potential, with neuronal action potentials depolarizing the membrane. Cells typically have a negative resting potential, with neuronal action potentials depolarizing the membrane.
The process of repolarization causes an overshoot in the potential of the cell. Potassium ions continue to move out of the axon so much that the resting potential is exceeded and the new cell potential becomes more negative than the resting potential. The resting potential is ultimately re-established by the closing of all voltage-gated ion ...
After the action potential peak is reached, the neuron begins repolarization (3), where the sodium channels close and potassium channels open, allowing potassium ions to cross the membrane into the extracellular fluid, returning the membrane potential to a negative value.
Hyperpolarization by the delayed-rectifier potassium channels causes a relative refractory period that makes it much more difficult to reach threshold. The delayed-rectifier potassium channels are responsible for the late outward phase of the action potential, where they open at a different voltage stimulus compared to the quickly activated ...
During repolarization, the sodium channels begin to become inactivated, causing a net efflux of potassium ions. This causes the membrane potential to drop down to its resting membrane potential of -100mV. Hyperpolarization occurs because the slow-acting potassium channels take longer to deactivate, so the membrane overshoots the resting ...
This causes brief hyperpolarization of the membrane, that is, the membrane potential becomes transiently more negative than the normal resting potential. Until the potassium conductance returns to the resting value, a greater stimulus will be required to reach the initiation threshold for a second depolarization.
Transient outward K+ currents following action potentials can cause hyperpolarization, allowing for low-threshold spikes. An initial ohmic leakage current composed of K+ and Na+ ions characterizes the first phase. This is followed by a hyperpolarization-activated "sag" current that contributes to slowly depolarizing the membrane potential.