Let us now consider what happens when a neurone generates an action potential. As well as the Na+/ K + pump, the membrane also has ion channels through which ions can pass under certain conditions; one of these is called the sodium channel. This allows sodium to move into the cell driven by the concentration difference on both sides of the membrane. However, it is usually closed in a resting nerve cell. When a nerve cell becomes activated, this sodium channel opens up and sodium flows into the cell due to diffusion. As the positively charged sodium rushes into the cell it brings with it its positive charge and the inside of the cell changes from being negative, when compared with the outside, to actually being positive. The membrane potential rises to +30 mV. This change in polarity from negative to positive is called depolarisation (Fig. 6). As the membrane potential becomes more positive, eventually the sodium channel closes.

 

 

As the membrane potential becomes more positive, a second channel, this time for potassium, opens up. This allows potassium to flow out of the cell, again due to diffusion. As potassium carries its positive charge to the outside of the cell, the membrane potential then returns to -70 mV. This is called repolarisation as the original charge differential between the inside and outside of the cell is re-established. An action potential is the sum of depolarisation and repolarisation.

Figure 7 shows an animation illustrating how the action potential spreads along the axon. When we measure membrane potential at a particular point on the axon, we first see the resting potential is at -70 mV. When the nerve impulse arrives, ion channels for sodium open, sodium flows into the cell and the membrane potential is locally reversed to +30 mV. This is depolarisation. Immediately afterwards repolarisation occurs and the membrane potential returns to -70 mV. This is due to the opening of the potassium channels. The cell has regained its resting potential. A nerve impulse is conveyed along the axon when such an action potential spreads through the axon.

So how is an action potential initiated? The trigger for the opening of the sodium channels that drive the action potential is a small change in membrane potential to about -50 mV, the sodium channels then open spontaneously. When sodium flows into the cell or axon, the membrane potential in this particular region increases. We say that the membrane is depolarised. This depolarised region, being very positive compared to its neighbouring regions, tends to attract the negative ions and proteins away from those surrounding areas. This causes a small rise in their membrane potential.  When this small rise reaches about -50mV, then the sodium channels in these surrounding regions open up and an action potential begins here also. In this way, depolarisation is spreading along the axon toward the axon terminals.

 

 

The nerve impulse thus consists of a local depolarisation that spreads along the axon, followed by a corresponding local repolarisation which restores resting potential and prepares the neurone for a new nerve impulse.

At any one time a nerve cell is either resting or sending a nerve impulse (action potential). They are either ”on” or ”off”. In other words, there are no strong or weak nerve impulses, either the nerve cell is activated or not. This is sometimes called the ‘all or nothing response’, an action potential cannot be “half activated”. The strength of a signal that a nerve cell sends lies in the frequency of impulses that it conveys. A nerve cell could send numerous nerve impulses in a second, only a few or none. The perception of a strong flavour or a loud sound is not due to the strength of nerve impulses, but rather a high frequency of impulses in a short time.

As mentioned previously, an axon with a myelin sheath around it transmits a nerve impulse faster than axon without a myelin sheath. The reason for this increase in speed can be understood when we consider the arrangement of the ion channels in these axons. There are no ion channels to exchange sodium and potassium with the outside of the cell where the axon is covered in myelin. Instead, these are concentrated into the small gaps in the myelin called the Nodes of Ranvier (see Fig.2). Therefore the positive membrane potential generated by an action potential at one node draws negative ions from along the axon between itself and the next node and the sodium channels are destabilised at the next node, leading to the triggering of an action potential here, instead of in the area directly adjacent to the first node.  In this way the action potential “jumps” along the axon (see Fig. 8).  This is known as saltatory conduction. In addition to myelin, the diameter of the axon matters with respect to signal speed. The larger the diameter, the faster the nerve impulse travels. The fastest nerve cells have speeds of up to 130 m / s.

 

 

Think about a time when you have stubbed your toe. First you feel a sharp stabbing pain and probably shout “ouch”, then afterwards you feel a long dull throbbing feeling. The reason for this is that the type of pain receptors that send the sharp stabbing pain that alerts you that you have hit something convey signals via large, myelinated nerves whereas the pain signals associated with the dull ache travel in smaller, non-myelinated nerves. Therefore, the sharp pain reaches the brain first, causing you to shout “ouch” and then this is followed by the dull aching pain.

 

Summary
An axon transmits a nerve impulse when the membrane potential at the start of the axon is destabilised sufficiently to generate an action potential. This action potential then propagates along the axon by destabilising the membrane potential in the adjacent part of the axon or at the next Node of Ranvier. What determines whether the membrane potential will be destabilised at the beginning of the axon is the sum of the stimulatory and inhibitory inputs on the dendrites and cell body. Inhibitory inputs actually make it less likely that the resting potential will be destabilised because they actually make the resting potential more negative, making it harder for the threshold value of minus (-)50mV that triggers depolarisation through opening of the sodium channels to be achieved.