When an action potential occurs, the neuron reaches the maximum voltage of +40mV. It then begins to repolarise, with potassium ions diffusing back in to the neuron, down the concentration gradient. This makes the neuron more negative. The section which is being repolarised undergoes the process, and has to undergo this fully due to the voltage gated channel proteins ( see diagram ). This means, that as the action potential passes forward and causes depolarisation, it cannot flow backwards as there is the influx of potassium. This means it cannot pass backwards, once the impulse is in the axon. Also, if a little bit flowed back, it wouldn't even make a difference as there are no vesicles containing neurotransmitters at that end. It's not something to worry about!Thinking about how we can see why it doesn't go back, we can look as to why it goes forward. So as we can see with the initial diagram of an action potential, if sufficient depolarisation happens (due to a stimulus), then an action potential always happens. It always reaches +40mV. So, when one section is being depolarised, it can trigger the voltage gated channels next to the initial area as there is more na+. If they get depolarised to -40mV, an action potential will be triggered and all the voltage gated Na+ channels will open, causing an action potential there. This then continues all the way along the axon, until the impulse reaches the pre-synaptic knob, where it can then trigger the synapse. How might this be different if we have a myelin sheath?