AQA A-level Biology: Nerve Impulses and Synaptic Transmission (7402) – Revision Notes

These are condensed notes for AQA A-level Biology (7402) sections 3.6.2.1 and 3.6.2.2, both A-level only, from the specification for first teaching 2015. Read the study guide for full explanations and test yourself with the practice questions. The AQA A-level Biology hub, the printable checklist and the free 10-minute diagnostics show what to cover next. Earlier material is in Survival, Response and Receptors.

3.6.2.1 Nerve impulses

Key terms

Term	Meaning
Resting potential	Potential difference across the membrane of an inactive neurone, inside negative (about −70 mV)
Differential permeability	Membrane much more permeable to K⁺ than Na⁺ at rest
Electrochemical gradient	Combined concentration gradient and electrical gradient for an ion
Depolarisation	Inside becomes less negative as Na⁺ enters
Threshold	Potential (about −55 mV) at which many more sodium channels open
Repolarisation	Inside becomes negative again as K⁺ leaves
Hyperpolarisation	Potential falls below the resting value
Refractory period	Time after an action potential when sodium channels cannot open
Saltatory conduction	Action potential jumping between nodes of Ranvier

Myelinated motor neurone: parts to label

Cell body (nucleus), dendrons, axon, Schwann cells, myelin sheath, nodes of Ranvier, axon terminals with synaptic knobs.

Resting potential in steps

1. Sodium-potassium pump: 3 Na⁺ out, 2 K⁺ in, using ATP.
2. Membrane more permeable to K⁺ (open potassium channels) than to Na⁺.
3. K⁺ diffuses out down its gradient; Na⁺ cannot diffuse in as fast.
4. Inside is negative relative to outside.

Action potential in steps

1. Stimulus opens some voltage-gated sodium channels; Na⁺ diffuses in.
2. Threshold reached: positive feedback opens many more sodium channels.
3. Depolarisation to about +40 mV.
4. Sodium channels close; voltage-gated potassium channels open; K⁺ diffuses out (repolarisation).
5. Potassium channels close slowly, giving hyperpolarisation.
6. Resting potential restored by the pump and open K⁺ channels.

Quick trace summary:

Phase	Potential	Main ion movement
Resting	About −70 mV	Pump active; K⁺ leaks out
Depolarisation	Rises past −55 mV to about +40 mV	Na⁺ in
Repolarisation	Falls back through 0 to resting	K⁺ out
Hyperpolarisation	Below −70 mV	K⁺ still leaving
Recovery	Returns to −70 mV	Pump and K⁺ leak

All-or-nothing

Below threshold: no action potential. At or above threshold: an action potential of the same size. Stimulus size is signalled by the frequency of impulses and by how many neurones fire, not by the size of each action potential.

Refractory period: three jobs

• Keeps impulses discrete (separate).
• Makes impulses travel one way only, away from the region just used.
• Limits the maximum frequency of impulses.

Method: maximum frequency = 1 / refractory period (in seconds).

Worked reminder. Refractory period 2.0 ms = 0.0020 s, so maximum frequency = 1 / 0.0020 = 500 impulses per s.

Passage along an axon

	Non-myelinated	Myelinated
Where channels act	Along the whole membrane	Only at nodes of Ranvier
How it spreads	Local currents depolarise the next region	Local currents between nodes
Speed	Slower	Faster (saltatory conduction)

Speed of conduction

• Myelination: action potential jumps between nodes, so fewer depolarisations.
• Larger axon diameter: less resistance to ion flow and less leakage, so faster.
• Higher temperature: faster diffusion of ions and faster ATP supply, so faster up to the point where proteins denature.

Method: speed = distance / time, with time in seconds.

Worked reminder. 0.80 m in 13 ms: 0.80 / 0.013 = 62 m per s (2 significant figures).

3.6.2.2 Synaptic transmission

Structure to know

Presynaptic knob: mitochondria, vesicles of acetylcholine, voltage-gated Ca²⁺ channels. Synaptic cleft (about 20 nm). Postsynaptic membrane: acetylcholine receptors linked to Na⁺ channels. Acetylcholinesterase in the cleft.

Cholinergic transmission in steps

1. Action potential arrives at the knob.
2. Ca²⁺ channels open; Ca²⁺ enters.
3. Vesicles fuse with the membrane; acetylcholine released by exocytosis.
4. Acetylcholine diffuses across the cleft and binds to receptors.
5. Na⁺ channels open; Na⁺ enters; postsynaptic membrane depolarises.
6. If threshold is reached, an action potential starts.
7. Acetylcholinesterase breaks down acetylcholine to choline and ethanoate.
8. Choline and ethanoate are taken up and acetylcholine is resynthesised using ATP.

Four explanations to give in full

• Unidirectional: vesicles and transmitter only in the presynaptic knob; receptors only on the postsynaptic membrane.
• Spatial summation: several presynaptic neurones release transmitter at one postsynaptic neurone at the same time.
• Temporal summation: one presynaptic neurone releases transmitter repeatedly in quick succession.
• Inhibition: transmitter opens Cl⁻ and K⁺ channels; Cl⁻ enters and K⁺ leaves; hyperpolarisation makes threshold harder to reach.

Worked reminder. Resting potential −70 mV, threshold −55 mV, and each excitatory input adds 2.5 mV with no decay. The change needed is 15 mV and 15 / 2.5 = 6 inputs. If one inhibitory input removes 5 mV, the same cell needs 15 + 5 = 20 mV, so 20 / 2.5 = 8 excitatory inputs.

Neuromuscular junction compared with a synapse between neurones

Feature	Neurone to neurone	Neuromuscular junction
Postsynaptic cell	Neurone	Skeletal muscle fibre
Postsynaptic membrane	Not folded	Folded, with more receptors and more acetylcholinesterase
Effect of transmitter	Excitatory or inhibitory	Excitatory
End result	Action potential in next neurone, or none	Action potential in muscle fibre and contraction
Shared features	Calcium channels, vesicles, acetylcholine, receptors, acetylcholinesterase	Same

Drug prediction in three steps

1. Identify the step the drug affects: calcium entry, vesicle release, receptor binding, enzyme action, or reuptake.
2. State what happens to the amount or duration of acetylcholine, or to the postsynaptic response.
3. State the final effect on the postsynaptic potential and on the muscle or next neurone.

If the drug…	Then…
Blocks voltage-gated Ca²⁺ channels	Less acetylcholine released; weaker or no postsynaptic response
Blocks acetylcholine receptors	No depolarisation even with normal release
Inhibits acetylcholinesterase	Acetylcholine stays in the cleft; response prolonged
Mimics acetylcholine and is not broken down	Prolonged depolarisation
Stops reuptake of choline	Less acetylcholine resynthesised; transmission falls over time

The specification says you need not recall drug names. Use the information given in the question.

Must-know distinctions

• Depolarisation and repolarisation: the first is Na⁺ entering, the second is K⁺ leaving. Never swap the ions.
• Resting potential and threshold: the resting potential is the steady value of about −70 mV. Threshold is the less negative value at which the positive feedback starts.
• Hyperpolarisation in an action potential and at an inhibitory synapse: the first is a brief overshoot caused by slow closing of K⁺ channels. The second is caused by transmitter opening Cl⁻ and K⁺ channels in the postsynaptic membrane.
• Spatial and temporal summation: spatial means many neurones at one time, temporal means one neurone many times.
• Refractory period and threshold: one is a delay after an impulse, the other is the level a stimulus must reach. Neither changes the size of an action potential.
• Calcium and sodium at a synapse: Ca²⁺ enters the presynaptic knob and triggers release, whereas Na⁺ enters the postsynaptic cell and causes depolarisation.

Quick self-test

1. What is the sodium-potassium pump’s ratio of ions moved?
2. Which ion mainly causes depolarisation, and which mainly causes repolarisation?
3. A neurone has a refractory period of 1.25 ms. What is its maximum frequency?
4. State two effects of the refractory period other than limiting frequency.
5. An impulse covers 0.72 m in 8.0 ms. Calculate its speed in m per s.
6. Why is conduction faster in a myelinated axon?
7. A stimulus of twice threshold strength is applied. What changes in the neurone’s response?
8. Which ion entering the presynaptic knob triggers release of acetylcholine?
9. Explain why a postsynaptic neurone may need summation to fire.
10. A drug blocks acetylcholinesterase. Predict the effect at a neuromuscular junction.

Answers

1. 3 Na⁺ out and 2 K⁺ in.
2. Na⁺ entering causes depolarisation; K⁺ leaving causes repolarisation.
3. 1.25 ms = 0.00125 s; 1 / 0.00125 = 800 impulses per s.
4. The impulse cannot travel backwards, and impulses stay separate.
5. 8.0 ms = 0.0080 s; 0.72 / 0.0080 = 90 m per s.
6. The action potential jumps between nodes of Ranvier because myelin insulates the rest of the axon, so depolarisation is needed at fewer points.
7. The action potential is the same size; the frequency of action potentials is higher.
8. Ca²⁺.
9. One impulse may release too little acetylcholine to depolarise the membrane to threshold, so releases from several neurones or repeated releases must add together.
10. Acetylcholine is not broken down, so it keeps binding, the muscle fibre stays depolarised and contraction is prolonged.

Where marks are usually lost

• Describing the pump as causing depolarisation.
• Writing “sodium moves in” with no mention of diffusion through channels.
• Leaving out the potassium channels when explaining hyperpolarisation.
• Saying the refractory period stops the next impulse “being sent” instead of saying sodium channels cannot open.
• Forgetting to convert milliseconds into seconds.
• Saying calcium causes depolarisation of the postsynaptic membrane. It causes vesicle fusion.
• Saying acetylcholine is actively transported across the cleft.
• Describing summation without saying which kind it is, or confusing the two.
• Predicting a drug’s effect with no explanation of the step it changes.

Official syllabus

AQA AS and A-level Biology (7401/7402) specification, for first teaching 2015, published by AQA. These notes follow sections 3.6.2.1 and 3.6.2.2. Check the current document on the AQA website for the latest version.