An axonic action potential occurs due to rapid transient changes in gNa or gK, or both. In axons, there is a brief rise in gNa followed by a decline back to baseline levels. In some cases, gNa changes while gK remains constant, but in others, both gNa and gK change. Therefore, the action potential depends on the opposing tendencies of the Na+ gradient and K+ gradient, but unlike the resting membrane potential, the gK/gNa ratio continuously changes. Additionally, a capacitative current exists because the membrane potential is changing, which needs to be taken into account when describing the membrane potential quantitatively during an action potential. 

The early phase of the action potential is a result of a rapid increase in gNa and Na+ current (INa), causing the membrane potential to move towards the equilibrium potential for Na+ (ENa). However, the peak of the action potential does not reach ENa because the rise in gNa is not infinite. The rise in gNa is transient due to the nature of the underlying Na+ channels. In many cases, depolarization leads to a rise in gK, causing the gK/gNa ratio to stop falling and start increasing. As a result, the membrane potential is driven back towards EK and repolarizes towards its resting value. If repolarization involves a rise in gK, the membrane potential may temporarily hyperpolarize beyond its normal rest value. This afterhyperpolarization occurs because gK remains elevated for a period of time after the action potential. As gK returns to its baseline level, the membrane potential returns to its rest value. 

The changes in conductance during an action potential are explained by the properties of Na+ and K+ ion channels. Early studies indicated that ion currents pass through separate Na+ and K+ channels, each with distinct characteristics. Subsequent research has supported this finding and provided detailed knowledge about the amino acid sequences and functional characteristics of these channels. 

A voltage-gated Na+ channel consists of four α subunits and two β subunits. The α subunit has four repeated motifs with six transmembrane helices surrounding a central ion pore. The pore walls are formed by the six helices in each motif. Most voltage-gated K+ channels are composed of four separate subunits, each consisting of a polypeptide with six membrane-spanning segments, similar to the motifs in the α subunit of the Na+ channel. 

Voltage-gated channels, such as those involved in the action potential, are gated by the membrane voltage. These channels sense the membrane potential and either open or close the pore accordingly. The gates are formed by groups of charged amino acid residues, and the voltage dependence of the Na+ and K+ channel gates account for the complex changes in gNa and gK during an action potential. 

By using standard intracellular recording and voltage-clamp techniques, researchers have characterized the underlying ionic currents and conductance changes during an action potential.
An axonic action potential is, in fact, the result of a rapid sequence of transient changes in gNa or gK, or both. In all axons there is a brief rise in gNa, followed by a decline back to baseline levels. In some axons, this change in gNa occurs against a fixed resting gK (because of leak channels, which are not voltage-gated; discussed later). In many other cases, however, both gNa and gK change. Thus as with the resting membrane potential, the action potential depends on the opposing tendencies of (1) the Na+ gradient to bring the resting membrane potential toward the Nernst potential for Na+ and (2) the K+ gradient to bring the resting membrane potential toward the Nernst potential for K+; but in contrast to when the neuron is at rest, the gK/gNa ratio is not constant but is changing continuously. One additional difference is that because the membrane potential is changing, a capacitative current also exists, and this must also be taken into account to describe the membrane potential quantitatively during an action potential (as a corollary, note that the chord conductance equation is valid only when the membrane potential is constant because then there is no capacitative current).
The early phase of the action potential (the positive deflection of the membrane potential toward ENa) is a result of a rapid increase in gNa and thus of the Na+ current (INa). These changes cause the membrane potential to move toward the equilibrium potential for Na+ . The peak of the action potential does not reach ENa because the rise in gNa is not infinite (i.e., the gK/gNa ratio does not fall to zero).
Because of the nature of the underlying Na+ channels (described later), the rise in gNa with depolarization is transient. Moreover, in many cases, the depolarization leads to a rise in gK. These two factors cause the gK/gNa ratio to stop falling and start increasing; as a result, the membrane potential is driven back toward EK and thus repolarizes toward its resting value. In cases in which the repolarization involves a rise in gK, the membrane potential hyperpolarizes temporarily beyond its normal rest value (if gK does not change, the drop in gNa causes the membrane simply to return to its resting potential). This afterhyperpolarization occurs because gK remains elevated for a period of time after the action potential. As gK returns to its baseline level, the membrane potential returns to its rest value.
These changes in conductance can be explained by the properties of Na+ and K+ ion channels, which are described next.
Early studies of the mechanism underlying action potentials indicated that ion currents pass through separate Na+ and K+ channels, each with distinct characteristics, in the cell membrane. Subsequent research has supported this interpretation. The amino acid sequences of the channel proteins and many of the functional and structural characteristics of the channels are now known in detail.
The structure of a voltage-gated Na+ channel (
Fig. 5.5 ) consists of four α subunits and two β subunits. The α subunit has four repeated motifs each of six transmembrane helices that surround a central ion pore. The pore walls are partly formed by the six helices in each motif. Most voltage-gated K+ channels are composed of four separate subunits, each consisting of a polypeptide with six membrane-spanning segments, similar to the motifs that make up the α subunit of the Na+ channel.
An important characteristic of some channels, such as those that underlie the action potential, is that they are gated by the membrane voltage. These voltage-gated channels sense the potential across the membrane and then act to either open or close the pore according to the membrane potential. The gates are formed by groups of charged amino acid residues, and the voltage dependence of the Na+ and K+ channel gates can account for the complex changes in gNa and gK that occur during an action potential.
The Characteristics of the Na+ and K+ Channels Explain the Conductance Changes During the Action Potential
Use of standard intracellular recording along with voltage-clamp techniques enabled investigators to characterize the underlying ionic currents and conductance changes