They both stay open.
If sodium channels were to remain closed, there wouldn't be any repolarization. The Potassium concentration gradient would keep pumping Potassium ions out of the cell and the Potassium electrical gradient would drive Potassium ions into the cell, thus maintaining the equilibrium potential of -90 mV.
No repolarization would occur if the sodium channels are closed.
The above is not correct.
During the depolarization phase, BOTH VOLTAGE-GATED SODIUM & POTASSIUM channels open.
Once the cell reaches close to sodium's equilibrium potential, the VOLTAGE-GATED sodium channel closes.
The VOLTAGE-GATED potassium channel opens around this time
(The voltage gated potassium channel is very slow to open; it fully opens around the same time the voltage gated sodium channel closes) causing repolarization.
The cell experiences hyperpolarization because the voltage gated potassium is also slow to close.
Once fully closed, the cell depolarizes back to resting potential.
Also, the picture is a picture of the AP in cardiac muscle which differ from skeletal muscle.
The plateau is due to voltage-gated calcium channel that opens during the AP.
It has to do with what types of channels are open during this phase. In the repolarization phase the number of potassium channels are increased and the number of sodium channels are decreased. This allows for action potentials to not occur. Otherwise, the action potentials would add up and produce tetany.
potassium ions diffusion to the outside of the cell membrain,
During resting potential, the Sodium-Potassium pump is inactive. Therefore, it is indirectly responsible for the resting potential. However, Potassium diffuses outside the membrane via "leakage" channels, and causes the resting potential.
As the action potential passes an area on the axon, sodium channels are closed, preventing influx of more sodium ions. At the same time, voltage-sensitive potassium channels open, allowing the membrane potential to fall quickly. After this repolarization phase, membrane permeability to potassium remains high, allowing for the "afterhyperpolarization" phase. During this entire period, while the sodium ion channels are forced closed, another action potential cannot be generated except by a much larger input signal. This helps to prevent the action potential from moving backwards along the axon.
Sodium and potassium voltage gated ion channels.
...repolarization
It has to do with what types of channels are open during this phase. In the repolarization phase the number of potassium channels are increased and the number of sodium channels are decreased. This allows for action potentials to not occur. Otherwise, the action potentials would add up and produce tetany.
potassium ions diffusion to the outside of the cell membrain,
During resting potential, the Sodium-Potassium pump is inactive. Therefore, it is indirectly responsible for the resting potential. However, Potassium diffuses outside the membrane via "leakage" channels, and causes the resting potential.
As the action potential passes an area on the axon, sodium channels are closed, preventing influx of more sodium ions. At the same time, voltage-sensitive potassium channels open, allowing the membrane potential to fall quickly. After this repolarization phase, membrane permeability to potassium remains high, allowing for the "afterhyperpolarization" phase. During this entire period, while the sodium ion channels are forced closed, another action potential cannot be generated except by a much larger input signal. This helps to prevent the action potential from moving backwards along the axon.
As the action potential passes an area on the axon, sodium channels are closed, preventing influx of more sodium ions. At the same time, voltage-sensitive potassium channels open, allowing the membrane potential to fall quickly. After this repolarization phase, membrane permeability to potassium remains high, allowing for the "afterhyperpolarization" phase. During this entire period, while the sodium ion channels are forced closed, another action potential cannot be generated except by a much larger input signal. This helps to prevent the action potential from moving backwards along the axon.
Sodium and potassium voltage gated ion channels.
voltage-sensitive potassium channels
Action Potential
Membrane potential - a nerve cell set and ready to fire;"The wave of reverse polarity" i.e. sodium versus potassium trans-cell-membrane ion passaging - a nerve cell firing; andRecharge period - the regeneration time.
The action potential has 5 main phases:1) stimulation/rising phase - depolarization caused by influx of sodium ions at the axon hillock; potential increases from a resting potential of -70 mV2) peak phase - depolarization and membrane potential reaches a peak, with sodium channels open maximally, at about +40 mV3) falling phase - potassium channels open in response, causing a subsequent reduction in membrane potential, and the neuron begins to repolarize4) hyperpolarization/undershoot phase - more potassium channels stay open after sodium channels close, causing a hyperpolarization of the neuronal membrane, bringing the potential down below its initial resting potential (below -70 mV)5) refractory phase - potassium channels begin to close, allowing the membrane potential to revert back to the resting potential of -70 mV; during this phase, the probability of the nerve being able to refire is extremely low, thus allowing for a delay between action potentials
repolarization