The structure and function of myelinated motor neurones. The establishment of a resting potential in terms of differential membrane permeability, electrochemical gradients and the movement of sodium and potassium ions. Changes in membrane permeability that lead to depolarisation and the generation of an action potential, the all-or-nothing principle, the passage of a wave of depolarisation along a neurone, saltatory conduction in myelinated neurones, and the nature and importance of the refractory period.

What this dot point is asking

AQA wants you to explain how a neurone maintains a resting potential, how an action potential is generated and propagated, the all-or-nothing principle, why myelination speeds conduction, and the role of the refractory period.

The answer

Structure of a myelinated motor neurone

A motor neurone carries impulses from the central nervous system to an effector. It has a cell body (with the nucleus), many dendrites that receive impulses, and one long axon that carries the impulse to the effector. The axon is wrapped in a myelin sheath made by Schwann cells, with gaps called nodes of Ranvier between adjacent Schwann cells.

The resting potential

When a neurone is not transmitting an impulse, the inside of the axon is negative relative to the outside, at about -70 mV. The membrane is said to be polarised.

This is established by:

• The sodium-potassium pump, which actively transports 3 Na+ out for every 2 K+ in using ATP.
• The resulting gradients: high Na+ outside, high K+ inside.
• Differential permeability: the membrane is more permeable to K+ (more potassium channels open) than to Na+, so K+ leaks out faster than Na+ leaks in.

The net loss of positive ions from inside makes the inside negative, giving the resting potential.

The action potential and depolarisation

A stimulus that is large enough triggers an action potential, a brief reversal of the membrane potential. The stages are:

1. Resting state (-70 mV). Voltage-gated Na+ and K+ channels are closed.
2. Depolarisation. The stimulus opens some voltage-gated sodium channels; Na+ diffuses in and the inside becomes less negative. If the threshold (about -55 mV) is reached, more sodium channels open (positive feedback), Na+ floods in and the potential rises to about +40 mV.
3. Repolarisation. Voltage-gated sodium channels close and voltage-gated potassium channels open; K+ diffuses out, restoring the negative inside.
4. Hyperpolarisation. K+ channels are slow to close, so slightly too much K+ leaves and the potential overshoots below -70 mV.
5. Return to rest. The sodium-potassium pump and channels restore the resting potential.

The all-or-nothing principle

An action potential is all-or-nothing. If the stimulus reaches the threshold, a full action potential of the same size is always produced; if it does not reach threshold, no action potential occurs. A bigger stimulus does not make a bigger action potential; instead it increases the frequency of action potentials. This is how the nervous system codes stimulus strength.

Propagation: the wave of depolarisation

An action potential propagates because the influx of Na+ at one point sets up local currents that depolarise the next region of membrane to threshold, opening its sodium channels. A wave of depolarisation therefore travels along the axon. The region just behind is in its refractory period and cannot fire again immediately, so the impulse travels in one direction only.

Saltatory conduction

In a myelinated neurone the myelin sheath acts as an electrical insulator, so the membrane can only depolarise at the nodes of Ranvier. The action potential therefore jumps from node to node, which is called saltatory conduction. This makes conduction much faster than in a non-myelinated axon, where depolarisation must occur continuously along the whole membrane.

The refractory period

After an action potential there is a short refractory period during which the sodium channels are recovering and the membrane cannot be stimulated again. Its importance is:

• It ensures action potentials travel in one direction only (the region behind cannot re-fire).
• It separates discrete action potentials so they do not merge.
• It limits the frequency of action potentials, setting an upper limit on impulse frequency.

Examples in context

Example 1. Multiple sclerosis and demyelination. In multiple sclerosis the immune system destroys the myelin sheath around neurones in the central nervous system. Without myelin, saltatory conduction is lost, action potentials must travel continuously and conduction slows or fails, producing the muscle weakness, numbness and coordination problems seen in patients. This directly illustrates why myelin is essential for fast conduction.

Example 2. Local anaesthetics blocking sodium channels. Drugs such as lidocaine block voltage-gated sodium channels in sensory neurones. Without Na+ influx the membrane cannot reach threshold, no action potential is generated, and pain impulses cannot reach the brain. This medical application shows the central role of voltage-gated sodium channels in generating the action potential.

Try this

Q1. Explain how the resting potential of about -70 mV is established and maintained. [4 marks]

• Cue. Sodium-potassium pump moves 3 Na+ out for 2 K+ in; sets up gradients; membrane more permeable to K+; K+ diffuses out faster than Na+ in, leaving inside negative.

Q2. Explain what is meant by the all-or-nothing principle and how stimulus strength is coded. [3 marks]

• Cue. Below threshold no action potential; at or above threshold a full, fixed-size action potential. A stronger stimulus increases the frequency of action potentials, not their size.

Q3. Explain why an action potential travels faster in a myelinated than a non-myelinated neurone. [3 marks]

• Cue. Myelin insulates the membrane so depolarisation only occurs at the nodes of Ranvier; the impulse jumps node to node (saltatory conduction), which is faster than continuous depolarisation along the whole membrane.