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The action potentialThe brief electrical signal a nerve cell fires to pass information along its length.Read more → matters because it is the basic electrical signal every neuron uses, and several psychiatric drugs work by altering the ion channels that generate it. A neuron at rest sits at about -70mV (millivolts), held there by ion (charged particle) gradients across its membrane. For example, imagine a stimulus depolarising the membrane past a threshold: a chain of channel openings fires an all-or-nothing electrical spike that travels down the axon (the neuron's signal-sending fibre). In practice, several anticonvulsant and mood-stabilising drugs work by blocking the sodium channels that generate this very spike.

At rest, the neuron sits at about -70mV, maintained by ion gradients across the membrane. When a stimulus depolarises the membrane past a threshold, voltage-gated sodium (Na+) channels open. Na+ rushes in, driving rapid depolarisation, a sharp rise in membrane potential. These sodium channels then inactivate, and voltage-gated potassium (K+) channels open, letting K+ flow out and repolarising the membrane. This typically overshoots slightly into a brief hyperpolarisation, an undershoot below resting potential, before settling back to rest. During the refractory period that follows, the neuron cannot fire again, or can only fire with a stronger stimulus. MyelinThe fatty insulating sheath around nerve fibres that speeds up electrical signals.Read more →, the fatty insulating sheath around some axons, lets the signal jump between gaps called nodes of Ranvier, called saltatory conduction, which speeds transmission considerably. Picture a demyelinated axon, as in multiple sclerosis: saltatory conduction is lost, and signal transmission slows or fails. Local anaesthetics and the anticonvulsants carbamazepine, lamotrigine, and phenytoin all block voltage-gated sodium channels, stopping the rapid depolarisation that pain signals or seizures depend on.

• Shortly after a nerve impulse, a stronger than usual stimulus can trigger a further impulse, though a normal one cannot. Which phase does this describe?
• A student asks how a neuron signals that a stimulus was very intense, given that every impulse it fires has the same size. What is the usual answer?
• Immediately after an impulse, the membrane briefly becomes more negative than its usual baseline before settling. Which mechanism best explains this brief overshoot?
• Carbamazepine suppresses rapidly repeating discharges far more than normal firing. Which pharmacological property best explains that selectivity for overactive cells?

• Depolarisation, driven by sodium (Na+) influx, unlike repolarisation's potassium (K+) efflux.
• Refractory period, neuron cannot fire, or needs a stronger stimulus, whereas resting potential is a stable, excitable baseline.
• Saltatory conduction, signal jumps between nodes of Ranvier in myelinated axons, unlike the slower continuous conduction of unmyelinated axons.
• Sodium-channel blockers (carbamazepine, lamotrigine, phenytoin, local anaesthetics): stop depolarisation at its source, rather than acting on neurotransmitterA chemical messenger that nerve cells release to signal to the next cell.Read more → receptors.

• That is the voltage at which firing begins, not a recovery phase.
• That is the stable baseline state between impulses, not a recovery phase.
• During that phase no stimulus of any size can trigger a further impulse.
• That is the rapid rising portion of the impulse itself.
• Impulse height is fixed by the all-or-none principle and cannot grow.

• Localise the clue to the relevant anatomical level, cell type, pathway or molecular process.
• Map that structure or process to its normal function.
• Predict the deficit or clinical sign produced when it is disrupted.
• Reject options that belong to a neighbouring structure, pathway or level of explanation.