Action Potential Generation & Propagation Revision Notes | A Level AQA Biology

1. The Electrical Life of a Neurone

Your nervous system transmits information at speeds of up to 120 metres per second — faster than a Formula 1 car. That speed depends entirely on a brief, violent reversal of electrical charge across a membrane. Understanding how that reversal is generated, and how it travels, is the core of this lesson.

At rest, a neurone is not doing nothing. It is actively maintaining a resting potential of approximately −70 mV across its axon membrane — inside negative relative to outside. This is sustained by the sodium-potassium pump, which moves 3 Na⁺ out and 2 K⁺ in per ATP molecule, and by the fact that the membrane is far more permeable to K⁺ than to Na⁺ at rest.

The resting potential is the baseline from which everything else launches. When a stimulus arrives, it disturbs this balance — and the consequences are dramatic.

2. Generating an Action Potential: Changes in Membrane Permeability

Here is where the specification requirement lands: changes in membrane permeability lead to depolarisation and the generation of an action potential. The key players are voltage-gated ion channels — protein channels that open or close in response to changes in the potential difference across the membrane.

When a stimulus reaches the axon membrane, it causes a small depolarisation. If this depolarisation reaches the threshold potential (approximately −55 mV for most neurones), voltage-gated Na⁺ channels open rapidly. Sodium ions flood inward down their electrochemical gradient — both the concentration gradient and the electrical gradient favour their entry. The inside of the membrane becomes positive, reaching around +30 to +40 mV. This is depolarisation.

After roughly 1 millisecond, the voltage-gated Na⁺ channels close and become temporarily inactivated. Simultaneously, voltage-gated K⁺ channels open — more slowly than the Na⁺ channels. Potassium ions rush outward, restoring the negative charge inside. This is repolarisation. The membrane briefly overshoots the resting potential, becoming more negative than −70 mV — a phase called hyperpolarisation — before the sodium-potassium pump gradually restores the original resting potential.

During hyperpolarisation, the membrane is in its refractory period. The absolute refractory period (while Na⁺ channels are inactivated) makes it impossible to generate another action potential at all. The relative refractory period follows, during which a stronger-than-normal stimulus is required. This ensures action potentials travel in one direction only and limits the maximum frequency of firing.

3. The All-or-Nothing Principle

Now that you can picture the action potential, there is a crucial rule governing whether it fires at all. A stimulus either reaches threshold and triggers a full-sized action potential, or it falls short and nothing happens. There is no such thing as a 'half' action potential. This is the all-or-nothing principle.

The magnitude of the action potential is always the same for a given neurone — approximately 100 mV of change. A stronger stimulus does not produce a larger action potential; instead, it produces a higher frequency of action potentials. This is how the nervous system encodes stimulus intensity: not by varying the size of each impulse, but by varying how many fire per second.

The all-or-nothing principle has a direct consequence for how the nervous system works: information about stimulus intensity is coded in the pattern of impulses, not in the size of individual ones. A painful stimulus and a gentle touch both produce action potentials of identical magnitude in their respective neurones — the difference lies in frequency and which neurones are recruited.

4. Propagation Along Non-Myelinated Axons

Generating an action potential at one point is only useful if that signal can travel. The mechanism by which it does so in a non-myelinated axon relies on local circuits of ionic current.

Picture the axon membrane laid out flat. At the site of an action potential, the inside is positive. The adjacent region ahead is still at resting potential — inside negative. This potential difference drives a local current: positive ions flow along the inside of the axon from the depolarised region toward the resting region, and in the opposite direction on the outside. This local current depolarises the adjacent membrane to threshold, triggering a new action potential there. The process repeats continuously along the entire length of the axon.

Crucially, the region behind the active zone is in its refractory period — it cannot be re-excited. This is why, after an action potential is initiated at a certain point on the axon, the action potential propagates away from the site of initiation in one direction only: the region just behind is in its refractory period and cannot generate a new action potential.

Conduction in non-myelinated axons is continuous along the entire membrane surface. This makes it relatively slow — typically 0.5 to 2 metres per second — because every patch of membrane must depolarise in sequence. The axon diameter also matters: wider axons have lower internal resistance, so local currents spread further and faster.

5. Propagation Along Myelinated Axons and Saltatory Conduction

Many vertebrate neurones, including the large motor and sensory neurones in your body, are wrapped in a myelin sheath — a fatty insulating layer formed by Schwann cells. The sheath is interrupted at regular intervals by gaps called nodes of Ranvier, where the axon membrane is exposed and densely packed with voltage-gated ion channels.

Myelin acts as an electrical insulator. Ion exchange across the membrane can only occur at the nodes of Ranvier, not along the myelinated internodal segments. The local current generated at one node therefore spreads rapidly along the inside of the axon — with very little resistance and no ion leakage through the insulated sections — to the next node, where it triggers a new action potential. The action potential effectively 'jumps' from node to node.

Saltatory conduction is dramatically faster than continuous conduction — myelinated axons conduct at 70 to 120 metres per second compared with under 2 metres per second for small non-myelinated fibres. It is also more energy-efficient: because ion exchange is restricted to the nodes, far fewer ions cross the membrane per impulse, so the sodium-potassium pump does less work to restore the resting potential.

Worked example: Explaining Action Potential Propagation: Exam-Style Worked Answer

Explain how an action potential is propagated along a myelinated axon. [5 marks]

1. An action potential is generated at a node of Ranvier when the membrane depolarises to threshold. — Always anchor your answer at the node — this is where ion exchange occurs in a myelinated axon. [B1]
2. The depolarised node (inside positive) creates a potential difference with the adjacent resting node (inside negative). Positive ions flow along the inside of the axon toward the next node. — Describe the direction of current flow explicitly — examiners look for this. [B1]
3. The myelin sheath insulates the internodal segments, preventing ion leakage. Local currents therefore spread rapidly to the next node with minimal resistance. — Linking myelin to insulation and reduced resistance is a mark-winning explanation. [B1]
4. The local current depolarises the next node of Ranvier to threshold, opening voltage-gated Na⁺ channels and generating a new action potential there. — State that threshold must be reached — this links back to the all-or-nothing principle. [B1]
5. The previous node is in its refractory period and cannot be re-excited, so the action potential travels in one direction only — toward the axon terminal. — Unidirectionality via the refractory period is frequently tested and often missed. [B1]

Answer: 5 marks: node of Ranvier as site of depolarisation; local current flows to next node; myelin insulates and reduces resistance; next node reaches threshold and fires; refractory period ensures unidirectional travel.

6. Factors Affecting Conduction Velocity

Two structural variables determine how fast an axon conducts: the presence of a myelin sheath and the diameter of the axon. You have already seen how myelination enables saltatory conduction. Axon diameter matters because a wider axon has a larger cross-sectional area, which reduces the internal electrical resistance of the cytoplasm. Lower resistance means local currents spread further and faster, so adjacent regions reach threshold more quickly.

Temperature also affects conduction velocity, though it is not a structural factor. Higher temperatures increase the rate of ion channel opening and closing, speeding up each stage of the action potential. This is why nerve conduction studies in clinical settings are temperature-sensitive.

7. Exam Technique and Common Mistakes

Action potential questions appear regularly in AQA papers and follow predictable patterns. The most common errors are not factual gaps — they are precision failures. Here is how to avoid them.

When asked to explain depolarisation, always state that voltage-gated Na⁺ channels open and that Na⁺ moves into the axon down its electrochemical gradient. Saying 'sodium moves in' without specifying the channel type or the gradient will lose marks. Similarly, for repolarisation, specify that voltage-gated K⁺ channels open and K⁺ moves out.

When asked to compare myelinated and non-myelinated axons, structure your answer as a direct comparison: name the feature, state what it is in each type, and link it to the consequence for conduction speed. Avoid writing two separate descriptions — the examiner is looking for explicit comparative language.

Together, the all-or-nothing principle, the ionic basis of depolarisation, and the structural differences between myelinated and non-myelinated axons form a coherent picture: the nervous system generates fixed-magnitude signals, encodes intensity through frequency, and uses myelin to transmit those signals at speeds that make rapid, coordinated responses possible.