Depolarization is the first step in an action potential. In this step the voltage-gated sodium channels open due to an external stimulus. These channels permit rapid flow of sodium ions into the cell. This changes the polarity of the cell and causes the membrane potential to increase. The increase in membrane potential is attributed to the increased amounts of positive ions inside the cell. Recall that the membrane potential is defined as the potential inside the cell minus the potential outside the cell. An increase in positive ions inside the cell will increase the potential inside the cell and, subsequently, increase the membrane potential.

Absolute refractory period occurs because of the inactivation of sodium channels. Since the sodium channels are inactivated, the neuron can’t depolarize and initiate another action potential. Relative refractory period occurs due to the slow inactivation of potassium channels. The voltage-gated potassium channels take a longer time to inactivate, which causes the cell to hyperpolarize. The cell becomes more negative than resting membrane potential as positive potassium ions exit the cell down their gradient. Since the cell has a more negative membrane potential, a larger stimulus is required to reach the threshold.

The absolute refractory period results from the initial gating of voltage-gated sodium channels. This initial mechanism ensures that the channel is incapable of opening, even when stimulated. The channel then shifts to a different gating mechanisms, which can be opened by a large enough electrical stimulus.

Absolute refractory period of a neuron is the period of time during which no amount of external stimulus will generate an action potential. Relative refractory period is the period of time during which only a large stimulus will generate an action potential.

In this question the neuron initially generated an action potential when 20mV was applied; however, five seconds after the initial stimulus the neuron only generated the action potential when a large stimulus (60mV) was applied. We can conclude that the neuron was in its relative refractory period. If the neuron was in its absolute refractory period, then a stimulus of 60mV shouldn’t have generated an action potential.

A neuron never becomes temporarily dead. Also, remember that once the neuron is out of its relative refractory period, the required stimulus for action potential will revert back to normal. At a later time (for example ten seconds after the initial stimulus) the neuron will only require 20mV to generate an action potential. Increasing time doesn’t necessarily increase the magnitude of the external stimuli required to produce an action potential.

All three channels provided in the question are open during depolarization. Open voltage-gated sodium channels characterize depolarization. The flow of sodium ions into the cytosol (facilitated by these channels) causes the cell to depolarize.

The sodium and potassium leak channels are also open during depolarization. Sodium leak channels further enhancing the influx of sodium ions, while potassium leak channels allow potassium ions to diffuse out of the cell. It doesn’t matter if the neuron is at the resting membrane potential, depolarizing, repolarizing, or hyperpolarizing; the leak channels are always open.

Remember that the sodium potassium pump is an integral membrane protein that is essential in maintaining the resting membrane potential in neurons. This protein pumps three sodium ions out of the cell and two potassium ions into the cell, creating an electrochemical gradient. The activity of this pump creates a higher concentration of sodium ions outside the cell and a higher concentration of potassium ions inside the cell. This creates a chemical gradient for sodium to flow into the cell and potassium to flow out of the cell. The net transfer of three ions out of the cell and two ions into the cell also generates an electrical gradient, increasing the potential for positive ions to enter the cell. Together, the chemical gradient and electrical gradient are called an electrochemical gradient, and are responsible for the influx of sodium during the depolarization of an axon.

The axon hillock is the region that is the first to respond to changing sodium levels by triggering an action potential, should threshold potential be reached. This is due to the presence of voltage-gated channels that can detect the voltage difference caused by the influx of sodium making the inside of the cell more positive.

Axons are responsible for the propagation of the action potential down to the axon terminal, but do not initiate the signal. The cell body has no voltage-gated channels, and therefore cannot respond to the influx of sodium ions. Myelin sheaths also do not have voltage-gated channels, and only assist in speeding up the conduction of the signal. Axon terminals form the interface used to innervate a muscle, a gland, or another neuron.

The period of time immediately after an action potential passes will be characterized by an immediate reduction in membrane potential, followed by hyperpolarization. At this point in time, the sodium voltage-gated channels are inactivated, halting the overshoot and influx of sodium ions into the cell. These channels remain inactivated, in order to avoid having the voltage-gated sodium channels open again to trigger another action potential. This is considered the absolute refractory period. The voltage-gated potassium channels are slower to open than the voltage-gated sodium channels. By the time the sodium overshoot has peaked, the voltage-gated potassium channels are open, allowing an efflux of potassium out of the cell. The efflux is responsible for lowering the membrane potential and eventually causing hyperpolarization.

An electrical stimulus causes voltage-gated sodium channels in a neuron to open. Sodium then travels down its concentration gradient through the channels, into the cell. With the movement of sodium into the cell, the cell depolarizes (its membrane potential becomes more positive). The gradient that drives depolarization is established by the sodium-potassium pump, which causes two primary effects: the resting membrane potential is negative and there is a large concentration of sodium outside of the cell. When sodium channels open, sodium ions flow down both the electrical gradient formed by the negative membrane potential and the chemical gradient formed by ion concentrations.

During the generation of an action potential, the cell will undergo two refractory periods. The first is referred to as the absolute refractory period, during which no stimulus, regardless of size, will generate another action potential. This is followed by the relative refractory period, during which an action potential will be generated only if an abnormally large stimulus is encountered. During the relative refractory period, the cell is hyperpolarized due to the removal of potassium ions from the cell interior, which results in a more negative membrane potential than the cell would have at rest.

The resting potential of a cell is roughly –70mV. When the potential rises above this level, the cell is considered "depolarized." When the potential delves below this level, the cell is considered "hyperpolarized." If the cell is depolarized above –55mV, the threshold potential, then an action potential is triggered.

Hyperpolarization occurs because potassium channels are slow to open and close, and thus the cell polarizes itself beyond its usual membrane potential. After an action potential depolarizes a cell there is a build-up of positive charge in the cell interior. The late opening of potassium channels causes an abrupt rush of potassium out of the cell, propelled by its electrochemical gradient. This rush lowers the cell potential below its normal resting state, resulting in hyperpolarization. The cell then returns to its resting state via repolarization. Sodium is removed from the cell and potassium is reintroduced through action of the sodium-potassium pump.