The creation and conduction of action potentials represents a fundamental means of communication in the nervous system. Action potentials represent rapid reversals in voltage across the cell membrane of axons. These rapid reversals are mediated by voltage-gated ion channels found in the cell membrane. The distribution of voltage-gated channels along the axon enables the conduction of the action potential from the nerve cell body to the axon terminal. At the synapse, the electrical signal is converted to a chemical signal that is then propagated to the postsynaptic neuron.
An action potential is a rapid change in membrane potential that is governed by the opening and closing of ion channels in the cell membrane of a neuron. When the action potential is recorded, with mV on the y-axis and time on the x-axis, the result is a characteristic shape, with a starting resting potential of about -60 mV, to a peak of about +50 mV. The membrane potential then rapidly returns to its resting potential.
We begin with the neuron at rest, with a resting potential of about -60 mV. Here a small number of potassium channels are open. These are potassium leak channels, and they permit potassium ions to enter and exit the cell based on electrochemical forces. Note that there is no net movement of potassium ions. For each potassium ion that leaves the cell, another returns, maintaining the membrane potential at a constant value.
As a depolarizing stimulus arrives at our segment of the membrane, a few sodium channels open, permitting sodium ions to enter the neuron. The increase in positive ions inside the cell depolarizes the membrane potential (making it less negative), and brings it closer to the threshold at which an action potential is generated.
If the depolarization reaches the threshold potential, additional voltage-gated sodium channels open. As positive sodium ions rush into the cell, the voltage across the membrane rapidly reverses and reaches its most positive value.
At the peak of the action potential, two processes occur simultaneously. First, many of the voltage-gated sodium channels begin to close. Second, many more potassium channels open, allowing positive charges to leave the cell. This causes the membrane potential to begin to shift back toward the resting membrane potential.
As the membrane potential approaches the resting potential, voltage-gated potassium channels are maximally activated and open.
The membrane actually repolarizes beyond the resting membrane voltage. This undershoot occurs because more potassium channels are open at this point than during the membrane's resting state, allowing more positively charged potassium ions to leave the cell.
The return to steady state continues as the additional potassium channels that opened during the action potential now close. The membrane potential is now determined by the subset of potassium channels that are normally open during the membrane's resting state. The membrane potential is back to the resting potential.
When the neuronal membrane becomes depolarized, either via the delivery of an electric current or from a signal passing from an adjacent patch of membrane, voltage-gated sodium channels open and positively charged sodium ions—which are in much higher concentration outside of the cell—rush into the cell, producing a rapid reversal of the charge across the membrane. This spike of depolarization represents the action potential. The depolarization spreads to adjacent regions of the membrane, bringing these regions to threshold and thus propagating the signal along the axon. There is thus no loss of signal as an action potential travels along an axon.
When the axon potential reaches the nerve terminal, it triggers the release of neurotransmitter across the synaptic cleft, propagating the signal to the next neuron in the circuit.