Before we begin ... just a few notes about permeability and conductance. High permeability indicates that particle mass moves easily through a membrane. High conductance indicates that electrical charge moves easily through a membrane. (Conductance is the inverse of electrical resistance. If the conductance of the membrane to a particular ion is low, then the resistance to movement of that ion across the membrane is high.)
For ions, which are charged particles, movement of mass and movement of electrical charge occur simulataneously. So higher permeability indicates higher conductance. However, the relationship is not linear. Doubling of permeability does not mean that conductance exactly doubles.
In the following discussion, we look carefully at how each ion contributes to changes in membrane potential during an "action potential" by following what happens to sodium, potassium, and chloride conductances.
At rest (1), the sodium conductance is very low relative to either potassium or chloride conductances. (Typically, sodium conductance is 1/100 of potassium conductance.)
But, after initiation of the action potential, the sodium conductance rises very rapidly, quickly becoming much larger than either the potassium or chloride conductance. Remember that membrane potential is determined by the relative conductances or permeabilities of the membrane to various ions, not the actual values of conductances or permeabilities. So, when the sodium conductance becomes very large relative to the other conductances, the membrane potential approaches the sodium Nernst potential, VNa (2).
The membrane never quite reaches the actual sodium Nernst potential because of electrical capacitance - The sodium conductance is falling rapidly after its peak and the membrane potential never quite "catches up" to the conductance changes - There is a time lag between the two.
During the initial phase of the action potential, potassium conductance, gK has been rising. Notice that after the peak of sodium conductance, the ratio of gK/gNa is increasing very rapidly as the result of the simultaneous increase of gK and decrease of gNa (3). So, the increase in gK causes the action potential to decrease back towards the resting potential more rapidly than it would be expected to if gK did not change. Experimentally, we find that if the membrane channels for potassium are blocked by a chemical inhibitor, the action potential is prolonged!
Finally, notice that gK remains high for awhile. Since the potassium and chloride Nernst potentials are not quite the same - the potassium Nernst potential is somewhat lower than the resting potential - the effect of high gK, with gCl remaining constant, is to produce an "afterpotential" (4). The membrane potential is near the Nernst potential for the ion to which the membrane is primarily permeable - potassium! This particular type of afterpotential is called a positive afterpotential because a long time ago, people used to make the recordings of membrane potential upside down - They didn't have intracellular electrodes and had to measure potentials with two electrodes on the outside of the cell - one near where the potential was changing and one some distance away where the potential was constant!