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

This guide covers AQA A-level Biology (7402) sections 3.6.2.1 (Nerve impulses) and 3.6.2.2 (Synaptic transmission), from the AQA AS and A-level Biology specification for first teaching 2015. Both sections are marked A-level only. Topic 6 is part of the content of the A-level papers that list topics 5 to 8 and topics 1 to 8. It follows on from Survival, Response and Receptors and leads into skeletal muscle in 3.6.3.

Use the revision notes for quick recall and the practice questions to test yourself. The AQA A-level Biology hub and the printable checklist show where this unit sits, and the free 10-minute diagnostics help you find weak spots first.

What the specification asks for

Section	What you must be able to do
3.6.2.1	Describe the structure of a myelinated motor neurone
3.6.2.1	Explain how a resting potential is established using differential membrane permeability, electrochemical gradients and the movement of sodium and potassium ions
3.6.2.1	Explain how changes in permeability cause depolarisation and an action potential; state the all-or-nothing principle
3.6.2.1	Describe passage of an action potential along non-myelinated and myelinated axons
3.6.2.1	Explain the refractory period: discrete impulses and a limit on frequency
3.6.2.1	Explain how myelination and saltatory conduction, axon diameter and temperature affect speed
3.6.2.2	Describe the detailed structure of a synapse and a neuromuscular junction
3.6.2.2	Explain transmission across a cholinergic synapse: unidirectionality, temporal and spatial summation, inhibition
3.6.2.2	Compare a cholinergic synapse with a neuromuscular junction
3.6.2.2	Use information provided to predict and explain the effects of specific drugs on a synapse

The specification says you do not need to recall the names or modes of action of individual drugs. Any drug in an exam question is described for you.

The myelinated motor neurone

A motor neurone carries impulses from the central nervous system to an effector. Know these parts:

• The cell body, which contains the nucleus and most of the organelles.
• Dendrons, which carry impulses towards the cell body.
• A long axon, which carries impulses away from it.
• Schwann cells wrapped around the axon. They make the fatty myelin sheath, which acts as an electrical insulator.
• Nodes of Ranvier, the short gaps in the myelin where the axon membrane is bare.
• Axon terminals ending in synaptic knobs.

The resting potential

A neurone that is not carrying an impulse has a potential difference across its membrane, with the inside negative compared with the outside. This is the resting potential, often about −70 mV. It comes from two things.

1. The sodium-potassium pump, driven by ATP, exports 3 Na⁺ from the axon and imports 2 K⁺. This builds a concentration gradient for each ion and makes the inside slightly more negative.
2. The membrane is differentially permeable. At rest it is much more permeable to K⁺ than to Na⁺, because many potassium channels are open and most voltage-gated sodium channels are closed. K⁺ diffuses out down its gradient. Na⁺ cannot diffuse back in quickly.

Because positive charge leaves faster than it enters, the inside becomes negative. Each ion then experiences both a concentration gradient and an electrical gradient, which together are its electrochemical gradient. The resting potential is held steady where these gradients balance.

The action potential

An action potential is a rapid, temporary reversal of the potential difference across the membrane. The sequence:

1. Stimulus. Some voltage-gated sodium channels open. Na⁺ diffuses in down its electrochemical gradient and the inside becomes less negative.
2. Threshold. If depolarisation reaches the threshold (about −55 mV), many more sodium channels open. This is positive feedback: more depolarisation opens more channels.
3. Depolarisation. Na⁺ floods in and the potential rises to about +40 mV.
4. Repolarisation. Sodium channels close. Voltage-gated potassium channels open and K⁺ diffuses out, so the inside becomes negative again.
5. Hyperpolarisation. Potassium channels are slow to close, so too much K⁺ leaves and the potential dips below resting level.
6. Recovery. The potassium channels close. The sodium-potassium pump and the open K⁺ channels restore the resting potential.

The all-or-nothing principle. A stimulus below threshold produces no action potential. A stimulus at or above threshold produces one of the same size. A bigger stimulus does not give a bigger action potential. It gives more frequent action potentials, and can start impulses in more neurones that have a higher threshold. This is how the brain reads the size of a stimulus.

The refractory period

After an action potential the sodium channels cannot open again for a short time, and the membrane is hyperpolarised. This period is the refractory period. It matters for two reasons.

• Discrete impulses. Each action potential is separate from the next one.
• One direction. The region behind the impulse is refractory, so the impulse travels forwards only.

It also limits the frequency of impulses, because a second one cannot start until the refractory period ends.

Worked example 1. A neurone has a refractory period of 5.0 ms. Find the maximum frequency of impulses.

5.0 ms = 0.0050 s
maximum frequency = 1 / 0.0050 s = 200 impulses per s

The unit matters. Convert milliseconds to seconds before dividing.

Passage of an action potential

Non-myelinated axon. The action potential at one point makes Na⁺ diffuse sideways along the inside of the axon. This local current depolarises the next region to threshold, so sodium channels open there. The wave moves along the whole membrane, one small region at a time.

Myelinated axon. Myelin insulates the axon: no ions can flow through the membrane under it. Channels are concentrated at the nodes of Ranvier. Depolarisation at one node sets up local currents that reach the next node, and the action potential appears to jump from node to node. This is saltatory conduction.

Factors affecting speed

Factor	Effect	Reason
Myelination	Faster	The action potential jumps between nodes, so fewer points need to depolarise
Axon diameter	Larger is faster	Less resistance to ion flow in the cytoplasm and less leakage of ions out of the axon
Temperature	Higher is faster, up to a point	Ions diffuse faster and enzymes make ATP faster for the pump; very high temperatures denature proteins

Worked example 2. An impulse travels 0.28 m along a myelinated axon in 4.0 ms. Another impulse travels 0.036 m along a non-myelinated axon in 18 ms. Compare the speeds.

myelinated:      0.28 m / 0.0040 s = 70 m per s
non-myelinated:  0.036 m / 0.018 s = 2.0 m per s
70 / 2.0 = 35

The myelinated axon conducts 35 times faster. Always state the unit and the conversion from ms.

Synapse structure

A synapse is a junction between two neurones. The detailed structure:

• The presynaptic neurone ends in a synaptic knob. It contains many mitochondria (ATP for making and releasing transmitter), vesicles of the transmitter acetylcholine, and voltage-gated calcium channels in its membrane.
• The synaptic cleft is the gap, about 20 nm wide, between the membranes.
• The postsynaptic membrane has specific receptors for acetylcholine, linked to sodium channels. The cleft contains the enzyme acetylcholinesterase.

A synapse that uses acetylcholine is called cholinergic.

Transmission across a cholinergic synapse

1. An action potential reaches the presynaptic knob and depolarises it.
2. Voltage-gated Ca²⁺ channels open and Ca²⁺ diffuses in.
3. Calcium ions make vesicles merge with the knob’s membrane, and acetylcholine leaves by exocytosis.
4. Acetylcholine diffuses across the cleft and binds to receptors on the postsynaptic membrane.
5. Sodium channels open and Na⁺ diffuses in and the postsynaptic membrane depolarises. Reaching threshold starts a new action potential.
6. Acetylcholinesterase hydrolyses acetylcholine into choline and ethanoate. The receptors are cleared and the response stops.
7. Choline is taken back into the presynaptic knob and joined to ethanoate (as acetylcoenzyme A) to remake acetylcholine, using ATP from mitochondria.

Unidirectionality

Only the presynaptic knob has vesicles of transmitter, and only the postsynaptic membrane has receptors. The impulse can therefore pass in one direction only.

Summation

One impulse often releases too little transmitter to reach threshold.

• Spatial summation: impulses from several presynaptic neurones release transmitter at the same postsynaptic neurone together, and their effects add up.
• Temporal summation: one presynaptic neurone fires many times in quick succession, so the effects of repeated releases add up before the depolarisation fades.

Worked example 3. Resting potential is −70 mV and threshold is −55 mV. Assume each excitatory impulse depolarises the postsynaptic membrane by 3 mV and the effect of each is the same. How many are needed?

change needed = −55 − (−70) = 15 mV
15 / 3 = 5

Five simultaneous impulses from five neurones is spatial summation. Five rapid impulses from one neurone is temporal summation.

Inhibitory synapses

At an inhibitory synapse the transmitter opens chloride ion channels and potassium ion channels in the postsynaptic membrane. Cl⁻ moves in and K⁺ moves out, so the inside becomes more negative: hyperpolarisation. A larger depolarisation is now needed to reach threshold, so an action potential is less likely. Inhibition lets the nervous system balance and refine its responses.

The neuromuscular junction

This is a synapse between a motor neurone and a skeletal muscle fibre. It uses acetylcholine and follows the same sequence. The differences are:

Feature	Cholinergic synapse between neurones	Neuromuscular junction
Postsynaptic cell	A neurone	A muscle fibre
Postsynaptic membrane	Smooth	Folded into clefts, with more receptors and more acetylcholinesterase
Effect	Excitatory or inhibitory	Always excitatory
Result	A new action potential in a neurone, or none	Action potential in the muscle fibre, which leads to contraction

Predicting the effects of drugs

You are given what a drug does and must work out the consequence. Find the step it changes, then follow the effect forward.

Worked example 4. A drug binds to the acetylcholine receptors on a postsynaptic membrane. It opens chloride channels but does not open sodium channels. Predict and explain the effect.

• Cl⁻ diffuses into the postsynaptic cell, so the membrane hyperpolarises.
• Na⁺ does not enter, so there is no depolarisation.
• An action potential is much less likely, so transmission is reduced even though presynaptic impulses and acetylcholine release carry on as normal.

Other useful cases: blocking calcium channels reduces transmitter release; blocking receptors stops depolarisation; blocking acetylcholinesterase keeps acetylcholine in the cleft and prolongs the response.

Common errors

• Saying the sodium-potassium pump alone causes the action potential. The pump restores gradients; channels cause the rapid changes.
• Writing that Na⁺ “moves” without saying it is by diffusion through channels.
• Saying a stronger stimulus gives a larger action potential.
• Forgetting to convert ms to s when finding frequency or speed.
• Saying the impulse “jumps” over myelin with no mention of local circuits between nodes.
• Claiming acetylcholine crosses the synapse by active transport. It diffuses.
• Saying acetylcholinesterase destroys the receptors.

Official syllabus

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