OxfordAQA International AS and A-level Biology: Nerve impulses and synapses (9610)

This guide covers sections 3.4.3.1 (Nerve impulses) and 3.4.3.2 (Synaptic transmission) of the OxfordAQA International AS and A-level Biology (9610) specification, Version 5.1, for International A-level exams May/June 2018 onwards. These sections sit in Unit 4, Control, which the specification lists as International A-level only. Typical values are given for teaching. If a question supplies values, use those.

Use the revision notes for quick recall and the practice questions to test yourself. For the course overview see the OxfordAQA A-level Biology hub and the printable checklist. The free diagnostics show which sections need work first.

What the specification asks for

Section	What you must be able to do
3.4.3.1	Describe the structure of a myelinated motor neurone
3.4.3.1	Explain how a resting potential is established: differential membrane permeability, electrochemical gradients, movement of Na⁺ and K⁺
3.4.3.1	Explain how permeability changes cause depolarisation then repolarisation; generation of an action potential; the all-or-nothing principle
3.4.3.1	Explain the refractory period: discrete impulses and a limit on frequency
3.4.3.1	Explain the role of ATP and sodium-potassium pumps in re-establishing the resting potential
3.4.3.1	Explain how myelination (saltatory conduction), axon diameter and temperature affect speed of conduction
3.4.3.2	Describe a cholinergic synapse and a neuromuscular junction in enough detail to explain unidirectionality, temporal and spatial summation, and inhibition
3.4.3.2	Use information provided to predict and explain the effects of drugs and toxins on synaptic transmission

The myelinated motor neurone

A motor neurone carries impulses from the central nervous system to an effector such as a muscle. Its parts, in order of travel:

dendrites -> CELL BODY (nucleus) -> axon, wrapped in myelin ... -> axon terminal
                                    |gap| = node of Ranvier

• The cell body holds the nucleus and most organelles.
• The long axon carries the impulse away.
• Schwann cells wind round the axon many times. Their membranes, rich in lipid, form the myelin sheath, an electrical insulator.
• Between neighbouring Schwann cells the axon membrane is bare. These short gaps are the nodes of Ranvier.
• The axon terminal forms a synapse, or a neuromuscular junction, with the next cell.

The resting potential

A neurone not carrying an impulse has a potential difference across its membrane. The inside is negative compared with the outside, typically about −70 mV. This is the resting potential. Two things create it.

1. Active transport. Each cycle of the sodium-potassium pump, powered by ATP, exports 3 Na⁺ from the axon and imports 2 K⁺. This builds a concentration gradient for each ion, and it leaves the inside slightly more negative.
2. Differential permeability. The resting membrane has many open K⁺ channels and very few open Na⁺ channels. K⁺ therefore diffuses out much faster than Na⁺ diffuses in. Net positive charge leaves, and the inside becomes negative.

Each ion feels a concentration gradient and an electrical gradient. Together these form its electrochemical gradient.

Worked example 1. The data supplied give these concentrations in mmol dm⁻³.

Ion	Inside axon	Outside axon
K⁺	140	5
Na⁺	12	145

K+  inside : outside = 140 / 5   = 28 : 1   -> diffuses OUT through open channels
Na+ outside : inside = 145 / 12  = 12.1 : 1 -> would diffuse IN, but few channels are open

K⁺ is far more free to move at rest, so the potential is set mainly by K⁺ leaving.

The action potential

An action potential is a brief reversal of the potential difference. It is produced by changes in membrane permeability, caused by voltage-gated channels. Typical values: threshold about −55 mV, peak about +40 mV.

1. Stimulus. A depolarising stimulus opens a few voltage-gated Na⁺ channels. Na⁺ diffuses in and the inside becomes less negative.
2. Threshold. If the potential reaches threshold, many more Na⁺ channels open. This is positive feedback.
3. Depolarisation. Na⁺ rushes in and the inside becomes positive.
4. Repolarisation. Near the peak, the Na⁺ channels close and voltage-gated K⁺ channels open. K⁺ diffuses out and the inside becomes negative again.
5. Hyperpolarisation. The K⁺ channels close slowly, so the potential briefly falls below the resting value.
6. Recovery. K⁺ channels shut. K⁺ leakage and the sodium-potassium pump return the membrane to rest.

The all-or-nothing principle. A stimulus below threshold produces no action potential. A stimulus at or above threshold produces one of fixed size. A stronger stimulus does not make a taller action potential. It makes impulses more frequent.

Worked example 2. A recording from an axon gives these values.

Time / ms	0	0.5	1.0	1.5	2.0	2.5	3.0	3.5	4.0	5.0
Potential / mV	−70	−69	−55	+10	+38	+5	−52	−78	−74	−70

amplitude         = 38 - (-70)  = 108 mV
below resting at 3.5 ms: -70 - (-78) = 8 mV  (hyperpolarisation)

The rise from −55 to +38 mV is depolarisation by Na⁺ influx. The fall to −78 mV is repolarisation, and the overshoot is K⁺ channels closing late.

The role of ATP and the pump

One action potential moves only a small fraction of the ions, so an axon can fire several impulses before the gradients change much. The pump uses ATP to put Na⁺ back outside and K⁺ back inside, which re-establishes the ion distribution and so the resting potential. If ATP production stops, the pump stops. Gradients run down and the axon eventually cannot fire.

The refractory period

Straight after an action potential, the Na⁺ channels cannot be opened. No stimulus, however strong, will start another impulse. Later the membrane is still hyperpolarised, so only a stronger stimulus works. The whole period is the refractory period. It matters because:

• Discrete impulses. Each action potential is separate from the next one.
• One direction. The region just passed is refractory, so the impulse cannot travel backwards.
• Maximum frequency. A new impulse cannot start until the refractory period ends.

Worked example 3. A neurone has a refractory period of 1.25 ms. What is its maximum frequency?

1.25 ms = 0.00125 s
maximum frequency = 1 / 0.00125 s = 800 impulses per s

Speed of conduction

Non-myelinated axon. Na⁺ entering at one point spreads sideways inside the axon. These local circuits depolarise the next stretch to threshold, so the action potential moves as a wave along the whole membrane.

Myelinated axon. Myelin stops ions crossing the membrane. Channels are concentrated at the nodes. Local circuits carry the depolarisation from node to node, and the action potential appears to jump between them. This is saltatory conduction. Fewer points depolarise per metre, so it is faster. It also saves ATP, because fewer ions need pumping back.

Factor	Effect on speed	Reason
Myelination	Faster	Saltatory conduction
Axon diameter	Wider is faster	Less resistance to ion flow inside; less leakage out
Temperature	Higher is faster, to a point	Faster diffusion of ions; faster respiration and so ATP for the pump; above the optimum, channel and pump proteins denature

Worked example 4. Impulse A travels 0.60 m along a myelinated axon in 8.0 ms. Impulse B travels 0.021 m along a non-myelinated axon in 7.0 ms.

A: 0.60 m / 0.0080 s  = 75 m per s
B: 0.021 m / 0.0070 s = 3.0 m per s
75 / 3.0 = 25

The myelinated axon conducts 25 times faster.

Worked example 5. In an ectothermic animal a non-myelinated axon conducts at 18 m per s at 12 °C and 29 m per s at 22 °C.

percentage increase = (29 - 18) / 18 x 100 = 61.1 %

The cholinergic synapse

A synapse is a junction between two neurones. A cholinergic synapse uses acetylcholine (ACh).

• The presynaptic knob contains many mitochondria, vesicles of ACh and voltage-gated Ca²⁺ channels.
• The synaptic cleft is a gap of about 20 nm. It contains acetylcholinesterase.
• The postsynaptic membrane has receptors that bind ACh. Binding opens channels through which Na⁺ diffuses in.

Transmission

1. An action potential arrives and depolarises the presynaptic knob.
2. Voltage-gated Ca²⁺ channels open. Ca²⁺ diffuses in.
3. Ca²⁺ causes vesicles to fuse with the presynaptic membrane. ACh is released by exocytosis.
4. ACh diffuses across the cleft and binds to receptors.
5. Na⁺ channels open. Na⁺ diffuses in and the postsynaptic membrane depolarises. If threshold is reached, an action potential starts.
6. Acetylcholinesterase hydrolyses ACh to choline and ethanoate. The response stops.
7. Choline is taken back into the presynaptic knob and recombined with ethanoate, using ATP from mitochondria, to remake ACh for new vesicles.

Unidirectionality. Vesicles of transmitter and Ca²⁺ channels are only in the presynaptic knob. ACh receptors are only on the postsynaptic membrane. The signal cannot pass backwards.

Summation

One impulse often releases too little ACh to reach threshold.

• Spatial summation: several presynaptic neurones release ACh onto the same postsynaptic neurone together. The depolarisations add up.
• Temporal summation: one presynaptic neurone fires repeatedly. The depolarisations add up if they arrive before the earlier ones fade.

Worked example 6. Resting potential is −65 mV and threshold is −52 mV. Each excitatory impulse depolarises the membrane by 2.5 mV, and all arrive together.

needed  = -52 - (-65) = 13 mV
13 / 2.5 = 5.2  -> 6 impulses (round UP: 5 gives only 12.5 mV)

If an inhibitory synapse at the same time lowers the potential by 5 mV, 18 mV is needed: 18 / 2.5 = 7.2, so 8 impulses.

Worked example 7. One neurone adds 4.0 mV per impulse, and half of the existing depolarisation has faded by the next impulse.

after impulse 1: 4.0
after impulse 2: 4.0 + 0.5 x 4.0   = 6.0
after impulse 3: 4.0 + 0.5 x 6.0   = 7.0
after impulse 4: 4.0 + 0.5 x 7.0   = 7.5

The total approaches 8 mV and never reaches 13 mV. Add a second neurone firing in step and each volley adds 8.0 mV: 8.0, 12.0, 14.0. The third volley reaches threshold. Spatial and temporal summation work together.

Inhibitory synapses

An inhibitory transmitter binds to receptors that open Cl⁻ channels and K⁺ channels. Cl⁻ diffuses in and K⁺ diffuses out, so the inside becomes more negative: hyperpolarisation. More depolarisation is now needed to reach threshold, so an action potential is less likely.

The neuromuscular junction

This is a cholinergic synapse between a motor neurone and a skeletal muscle fibre. The sequence is the same, with differences:

Feature	Neurone-to-neurone cholinergic synapse	Neuromuscular junction
Postsynaptic cell	Neurone	Muscle fibre
Postsynaptic membrane	Relatively smooth	Deeply folded, with more receptors and more acetylcholinesterase
Effect	Excitatory or inhibitory	Always excitatory
Outcome	Action potential in the next neurone, or none	Action potential in the muscle fibre, then contraction

Predicting the effects of drugs and toxins

You are told what the substance does. Find the step it changes, then follow the consequences.

1. Name the step affected.
2. State whether it increases or decreases.
3. Follow it to the postsynaptic potential.
4. Conclude about the action potential or the muscle.

If the substance…	Then…
blocks presynaptic Ca²⁺ channels	less ACh released, smaller depolarisation, action potential less likely
stops vesicles fusing with the membrane	no ACh released, no response in the muscle
binds ACh receptors without opening them	ACh cannot bind, no depolarisation
inhibits acetylcholinesterase	ACh stays in the cleft and keeps stimulating the receptors
blocks voltage-gated Na⁺ channels in the axon	no action potential reaches the knob

Worked example 8. A toxin binds irreversibly to acetylcholinesterase. Predict the effect at a neuromuscular junction.

• ACh is no longer hydrolysed, so it stays in the cleft.
• It keeps binding to receptors and Na⁺ channels stay open.
• The muscle fibre is stimulated repeatedly, so contraction is prolonged and relaxation is delayed.

Common errors

• Saying the pump alone makes the action potential. Channels cause the rapid changes.
• Saying a bigger stimulus gives a bigger action potential.
• Rounding down in a summation count when the question asks how many are needed.

Official syllabus

OxfordAQA International AS and A-level Biology (9610), Version 5.1, for International A-level exams May/June 2018 onwards, published by OxfordAQA. This guide follows sections 3.4.3.1 and 3.4.3.2. Check the current specification on the OxfordAQA website.