A student investigates the effect of a toxin on nerve impulse transmission. The toxin blocks voltage-gated sodium ion channels in the axon membrane. Explain why the affected neurone is unable to generate an action potential after exposure to this toxin.

OCR A-Level Biology A (H420) — 5.3 Neuronal communication · Explain · 4 marks · View as Markdown

Written & reviewed by James Millett — Biology (Imperial College London), PGCE Science (University of Cambridge).

Voltage-gated sodium ion channels open in response to a change in membrane potential. In a healthy neurone at rest, the membrane potential is approximately −70 mV.

Model answer (4 marks)

Voltage‑gated Na⁺ channels are essential for the rapid depolarisation that initiates an action potential.
1. Depolarisation requires Na⁺ to rush into the axon.
2. The toxin blocks these channels, so Na⁺ cannot enter.
3. Without Na⁺ influx the membrane potential cannot become less negative or reach the threshold.
4. The membrane therefore stays at or near the resting potential and no action potential is fired.

Examiner tips

  • Use the term ‘depolarisation’ and ‘threshold potential’. Show the causal chain: block → no Na⁺ influx → no depolarisation → no AP. Keep each point short and directly linked to the marks.

Common mistakes

  • Confusing resting potential with threshold potential. Failing to mention that Na⁺ influx is required for depolarisation. Using vague language such as ‘the neuron is damaged’ instead of the specific channel blockage mechanism.

Mark scheme (4 marks)

  1. Depolarisation requires sodium ions to rush into the axon
  2. The membrane potential cannot become less negative / cannot reach the threshold potential
  3. An action potential requires a sufficient change in membrane potential to trigger further channel opening
  4. The membrane remains at / close to resting potential so no action potential is fired

Key terms in this question

voltage-gated sodium ion channels · action potential

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