(1) At resting potential, some potassium voltage-gated channels are permanently open, but sodium voltage-gated channels are closed.
(2) The energy from a stimulus causes some sodium voltage-gated channels to open, allowing Na+ ions to diffuse into the axon along the electrochemical gradient. Since sodium ions are positive, they trigger a reversal in potential difference across the membrane.
(3) As Na+ diffuses into the axon, more sodium channels open, causing an influx of sodium ions via facilitateddiffusion.
(4) Once the 40mV action potential has been established, the voltage gates on the sodium ion channels close to prevent further influx. The voltage gates on the potassium ion channels begin to open.
(5) Once some potassium voltage-gated channels are open, the electrical gradient is reversed, causing more potassium voltage-gated channels to open. Therefore, more potassium ions diffuse out of the axon, starting repolarisation of the axon.
(6) The outwarddiffusion of the potassium ions causes a temporary overshoot of the electrical gradient, with the inside of the axon being more negative than usual (hyperpolarisation). Some gates in the potassium voltage-gated channels then close, and the original activities of the sodium-potassium pump resume. The axon is repolarised and the resting potential is reestablished.
The movement of sodium ions inwards is a passive process (facilitated diffusion), whereas the resting potential is maintained via active transport.