however, once a stimulus activates the voltage-gated sodium channels to open, positive sodium ions flood into the cell and the voltage increases. this process can also be initiated by ligand or neurotransmitter binding to a ligand-gated channel. more sodium is outside the cell relative to the inside, and the positive charge within the cell propels the outflow of potassium ions through delayed-rectifier voltage-gated potassium channels. since the potassium channels within the cell membrane are delayed, any further entrance of sodium activates more and more voltage-gated sodium channels. depolarization above threshold results in an increase in the conductance of na sufficient for inward sodium movement to swamp outward potassium movement immediately. if the influx of sodium ions fails to reach threshold, then sodium conductance does not increase a sufficient amount to override the resting potassium conductance. in that case, subthreshold membrane potential oscillations are observed in some type of neurons. if successful, the sudden influx of positive charge depolarizes the membrane, and potassium is delayed in re-establishing, or hyperpolarizing, the cell. sodium influx depolarizes the cell in attempt to establish its own equilibrium potential (about +52 mv) to make the inside of the cell more positive relative to the outside.