(a) Fig. 1.1 is a diagram of part of a neurone membrane at resting potential. (i) With reference to Fig. 1.1, name A , B , and D . A \_\_\_\_\_\_ B \_\_\_\_\_\_ D \_\_\_\_\_\_ (ii) Substance C is required to make structure A function. Name substance C . (b) Some drugs can affect the functioning of neuromuscular junctions or cholinergic synapses. Table 1.1 lists three drugs and describes their action on neuromuscular junctions or cholinergic synapses. Table 1.1 drug action of…

(a)(i) A: sodium–potassium pump; B: potassium ions; D: sodium ions · (a)(ii) ATP · (b) See working

Biology 9700/42 — May/June 2021

Cambridge A-Level · worked solutions for every part, with the mark scheme

questions

100

marks

120

minutes

Topics Control and Coordination · Inheritance · Energy and Respiration · Photosynthesis · Homeostasis · Genetic Technology · +2 more

Q1Control and CoordinationFree sample

(a)

Fig. 1.1 is a diagram of part of a neurone membrane at resting potential.

Fig. 1.1

(i)

With reference to Fig. 1.1, name A, B, and D.

A ______

B ______

D ______

DifficultyMedium-Easy

Worked solution

Answer

A – sodium–potassium ( $\text{Na}^+\text{/K}^+$ ) pump
B – potassium ions ( $\text{K}^+$ )
D – sodium ions ( $\text{Na}^+$ )

Final answer

A: sodium–potassium pump; B: potassium ions; D: sodium ions

Detailed explanation

Background Concept

At the resting potential, a neurone membrane actively maintains steep ionic gradients using the sodium–potassium (Na⁺/K⁺) pump. This is an integral transport protein that spans the phospholipid bilayer. With each cycle it hydrolyses one molecule of ATP and moves 3 Na⁺ out of the axon into the tissue fluid and 2 K⁺ into the axon from the tissue fluid, both against their concentration gradients. As a result, at rest the tissue fluid is rich in Na⁺ and the axoplasm is rich in K⁺. The pump therefore both creates and maintains the electrochemical gradient on which action potentials depend.

Understanding the Question

Fig. 1.1 shows a small section of a neurone membrane at resting potential. The figure labels four things: a large structure (A) that crosses the bilayer, two triangular molecules in the tissue fluid (B), a small square molecule in the axoplasm entering the pump (C), and three circular molecules in the axoplasm (D). The question simply asks us to name each structure (apart from C, which is asked in (a)(ii)).

Approach

Identify each structure by what it physically is in the diagram and where it sits relative to the bilayer, then link this to the biology of the resting membrane.

Step-by-Step Reasoning

A crosses the entire bilayer and has a small molecule entering it from the axoplasm — this is consistent with the active-transport protein that uses ATP, i.e. the sodium–potassium pump (not a channel, which would have no use for ATP).
B is in the tissue fluid — at rest the tissue fluid is rich in K⁺ (the ions that, having been pumped in, leak back out through K⁺ leak channels).
D is in the axoplasm — at rest the axoplasm contains a high concentration of Na⁺ relative to the inside (although the absolute concentration inside is lower than outside, the pump has loaded the inside with Na⁺ that has not yet left).

Key Takeaways

The Na⁺/K⁺ pump is an active transport protein that uses ATP to move ions against their concentration gradients.
At resting potential, Na⁺ is high outside and K⁺ is high inside — these gradients are the energy store for future action potentials.
"Channel" is wrong for A; the Na⁺/K⁺ pump is a carrier protein (active transport), not a channel.

Common Mistakes

Writing "sodium channel" or "potassium channel" for A — the pump is active transport, not a channel. The mark scheme explicitly rejects this.
Writing "sodium" without specifying ions ("Na⁺"). The mark scheme caps at 2 marks if "ions" is omitted.
Confusing the locations of Na⁺ and K⁺ at resting potential.

Things to Be Careful About

Use the precise term sodium–potassium pump (or Na⁺/K⁺ pump), not just "transporter" or "protein".
Always say "ions" after Na⁺ or K⁺ if the structure is an ion species — the word "ions" is part of the marking point.
The "CON if channel mentioned" annotation in the mark scheme for A means writing "sodium–potassium channel" loses the mark for A entirely.

Techniques used

identify the sodium-potassium pump from its position spanning the bilayeridentify ion species on a diagram of a neurone membrane at resting potential

(ii)

Substance C is required to make structure A function.

Name substance C.

DifficultyEasy

Worked solution

Answer

ATP (adenosine triphosphate)

Final answer

ATP

Detailed explanation

Background Concept

The sodium–potassium pump moves ions against their concentration gradients. Movement against a gradient requires energy; in cells that energy is supplied by the hydrolysis of ATP to ADP + Pᵢ. Without ATP the pump stops, the Na⁺ and K⁺ gradients run down, and the membrane can no longer maintain its resting potential or fire repeated action potentials.

Understanding the Question

The stem tells us that substance C (the small square molecule shown in Fig. 1.1 entering the pump from the axoplasm) is required to make structure A function. The question is simply asking for the name of C.

Approach

A molecule that is consumed to power an active transport protein is, by definition, ATP.

Step-by-Step Reasoning

The pump is active transport. Active transport is fuelled by ATP. The molecule drawn entering the pump from the axoplasm is therefore ATP.

Key Takeaways

Active transport always requires ATP (or another energy source).
ATP is hydrolysed to ADP + Pᵢ during each pump cycle.
Without ATP, ion gradients — and therefore all nerve signalling — fail.

Common Mistakes

Writing "ADP" — this is the product, not the substrate.
Writing "glucose" — glucose is the long-term energy source, but the molecule entering the pump directly is ATP.

Things to Be Careful About

The mark scheme accepts "ATP" alone; do not pad the answer with extra text.

Techniques used

identify ATP as the energy source for the sodium-potassium pump

(b)

Some drugs can affect the functioning of neuromuscular junctions or cholinergic synapses.

Table 1.1 lists three drugs and describes their action on neuromuscular junctions or cholinergic synapses.

Table 1.1

drug	action of drug
curare	blocks muscle cell membrane receptors at neuromuscular junctions
nerve gas	inhibits acetylcholinesterase function in synapses
alcohol	inhibits exocytosis of neurotransmitters in synapses

Suggest and describe the immediate consequence of the action of each drug on a neuromuscular junction or cholinergic synapse.

DifficultyMedium-Hard

Worked solution

Answer

Curare

Less / no acetylcholine (ACh) binds to the receptors on the sarcolemma / post-synaptic membrane.
Fewer / no (ligand-gated) $\text{Na}^+$ channels open, so less / no $\text{Na}^+$ enters the sarcoplasm / post-synaptic neurone and there is no / less depolarisation of the sarcolemma / post-synaptic membrane.

Nerve gas
3. Less / no acetylcholine is broken down in the synaptic cleft; ACh remains bound to the receptors on the post-synaptic membrane.
4. (Ligand-gated) $\text{Na}^+$ channels remain open / $\text{Na}^+$ continues to enter the post-synaptic neurone, giving permanent depolarisation of the post-synaptic membrane.

Alcohol
5. Less / no neurotransmitter (acetylcholine) is released because exocytosis is inhibited; therefore less / no acetylcholine binds to receptors.
6. Fewer / no (ligand-gated) $\text{Na}^+$ channels open, so less / no $\text{Na}^+$ enters the post-synaptic neurone and there is no / less depolarisation.

Final answer

See working

Detailed explanation

Background Concept

A cholinergic synapse (and the neuromuscular junction, which is also cholinergic) transmits a signal in this fixed sequence:

An action potential arrives at the presynaptic terminal.
Voltage-gated Ca²⁺ channels open; Ca²⁺ flows in.
Ca²⁺ triggers exocytosis of vesicles, releasing acetylcholine (ACh) into the synaptic cleft.
ACh diffuses across the cleft and binds to specific receptors on the postsynaptic membrane (or sarcolemma at the neuromuscular junction).
Binding opens ligand-gated Na⁺ channels; Na⁺ flows in down its electrochemical gradient and depolarises the postsynaptic membrane.
ACh is then hydrolysed by the enzyme acetylcholinesterase in the cleft, terminating the signal.

Any drug that interrupts steps 3, 4 or 6 will distort this sequence in a predictable way.

Understanding the Question

Table 1.1 lists three drugs and the step each one blocks:

Curare — blocks the postsynaptic receptors themselves (step 4).
Nerve gas — inhibits acetylcholinesterase (step 6).
Alcohol — inhibits exocytosis of neurotransmitter (step 3).

For each drug we must describe the immediate consequence on the synapse or neuromuscular junction. The mark scheme rewards six points (any 5 needed for full marks) covering both halves of the cause-and-effect chain for each drug: what fails to happen at the synapse, and the downstream consequence for Na⁺ entry and depolarisation.

Approach

For each drug, walk forward through the sequence above and ask: "because this step is blocked, what does ACh fail to do next, and what does that mean for Na⁺ entry and depolarisation?" Two linked points are credited for each drug.

Step-by-Step Reasoning

Curare (receptor blocker)

ACh is still released normally into the cleft, but less / no ACh can bind to the receptors on the sarcolemma / postsynaptic membrane.
With no (or fewer) receptors occupied, fewer / no ligand-gated Na⁺ channels open, less / no Na⁺ enters the sarcoplasm and there is no / less depolarisation. The muscle therefore cannot contract (neuromuscular block).

Nerve gas (acetylcholinesterase inhibitor)

ACh is still released and binds normally, but it is not broken down in the cleft — ACh remains bound to the receptors.
Because ACh is not removed, the Na⁺ channels stay open and Na⁺ continues to enter, producing permanent depolarisation of the postsynaptic membrane. Continuous firing of muscle (or neuronal) activity follows.

Alcohol (exocytosis inhibitor)

Fewer / no vesicles fuse with the presynaptic membrane, so less / no ACh is released into the cleft. Consequently less / no ACh binds to receptors.
With no ACh bound, fewer / no Na⁺ channels open, less / no Na⁺ enters and there is no / less depolarisation of the postsynaptic membrane.

Key Takeaways

Receptor blockade and exocytosis inhibition both produce the same visible outcome — no depolarisation — but for different upstream reasons.
Enzyme inhibition has the opposite outcome — permanent depolarisation — because the neurotransmitter accumulates.
Each answer must carry two linked points: the immediate biochemical consequence (binding / breakdown / release) and the downstream consequence (Na⁺ entry and depolarisation). One without the other does not score full marks.

Common Mistakes

Writing only "the synapse cannot function" or "signalling stops" — too vague. You must specify which step fails and what then happens to Na⁺ entry / depolarisation.
Saying "neurotransmitter" instead of acetylcholine (ACh). The mark scheme ignores "neurotransmitter" in the curare and alcohol points; only "acetylcholine" scores.
For curare, writing that Na⁺ channels "close" — they were never opened because no ACh bound.
For nerve gas, writing "no depolarisation" — the opposite happens; the depolarisation is permanent / sustained.
For alcohol, omitting the link to exocytosis — you must state that exocytosis is inhibited and therefore less / no ACh is released.

Things to Be Careful About

Use "acetylcholine" (or ACh), not "neurotransmitter", in curare and alcohol points — the mark scheme explicitly ignores "neurotransmitter".
The mark scheme accepts "sarcolemma" in place of "post-synaptic membrane" when discussing curare (because it acts at a neuromuscular junction), so either wording is acceptable in that context.
"Permanent depolarisation" is the specific wording credited for nerve gas; "continuous depolarisation" or "sustained depolarisation" is also accepted by the marker.
The mark scheme allows either "fewer / no Na⁺ channels open" or "less / no Na⁺ enters" or "less / no depolarisation" as alternatives within a single numbered point — any one of these three is enough to score that mark.

Techniques used

apply knowledge of synaptic transmission to predict drug effectstrace cause-and-effect through a cholinergic synapsedistinguish receptor blockade, enzyme inhibition and exocytosis inhibitionlink receptor occupancy to ligand-gated Na+ channel opening and depolarisation

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