The magnitude of the resting membrane and graded potentials depends upon the concentration gradients of and membrane permeabilities to different ions, particularly sodium and potassium. This is true for the action potential as well. The action potential is initiated by a transient change in membrane ion permeability, which allows sodium and potassium ions to move down their concentration gradients. In the resting state, the leak channels in the plasma membrane are predominantly those that are permeable to potassium ions. Very few sodium ion channels are open, and the resting potential is therefore close to the potassium equilibrium potential. The action potential begins with depolarization of the membrane in response to a stimulus.
This initial depolarization opens voltage-gated sodium channels, which increases the membrane permeability to sodium ions several hundredfold. This allows more sodium ions to move into the cell, and the cell becomes more and more depolarized until a threshold is reached to trigger the action potential. This is called the threshold potential. After the threshold potential is reached, more voltage-gated sodium channels open. The membrane potential overshoots, becoming positive on the inside and negative on the outside of the membrane. In this phase, the membrane potential approaches but does not quite reach the sodium equilibrium potential (+60 mV).
At the peak of the action potential, sodium permeability abruptly decreases and voltage-gated potassium channels open. The membrane potential begins to rapidly repolarize to its resting level. The timing of the movements of sodium and potassium can be seen. Closure of the sodium channels alone would restore the membrane potential to its resting level since potassium flux out would then exceed sodium flux in. However, the process is speeded up by the simultaneous increase in potassium permeability. Potassium diffusion out of the cell becomes much greater than the sodium diffusion in, rapidly returning the membrane potential to its resting level. In fact, after the sodium channels have closed, some of the voltage-gated potassium channels are still open, and in nerve cells there is generally a small hyperpolarization of the membrane potential beyond the resting level called the afterhyperpolarization. Once the voltage-gated potassium channels close, the resting membrane potential is restored. Chloride permeability does not change during the action potential.