As you go about thinking about this case study, you should consider first the membrane kinetics of potassium.
As I am sure you are well aware, K+ concentration is vastly higher within the membrane than without (and in fact near a factor of 10 higher).
So the basic way of thinking of what would happen to neurotransmission is visualizing what would occur at the ion channels.
When a neuron depolarizes, it is due to a quick influx of sodium through NA+ channels. as more sodium influxes it depolarises the membrane opening more channels. (this produces the peak in the action potential) (in other words the membrane approaches electrochemical balance for sodium.
Now think about how the cell recovers after depolarization.
The large influx of sodium has produced an energetically unstable concentration of ions within the cell. the high voltage produces an opening of voltage gated potassium channels. It is through these channels that the neuron effluxes K+ and stabilizes its electrochemical gradient.
So what would happen to the rate of K+ efflux, if the membrane potential for potassium was in homeostatic balance?
--- you should predict a decreased rate of efflux
If there is no drive to move potassium outside the cell, after initial depolarization the electrochemical balance would stabilize much closer to sodium homeostasis.n (~+150 sodium, as opposed to ~-85 K+).
--- a simple prediction to derive from this would be that cells are not firing at a quicker rate, but lose the ability to repolarise and slow down.
To follow up from what you were concluding. In essence the neuron would skip the refractory phase entirely (the refractory phase is when the cell overshoots to close to K+ equilibrium) but skip the repolarization phase as well.
---- I don't want to mislead you by laying out additional mechanisms that may facilitate repolarization, but if you need clarification or elaboration let me know.