Drugs and nerve impulse transmission

Coordination, Response and Gene Technology · Impulses, synapses and receptors · note 5 of 7

Spec 8.7

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Drugs and nerve impulse transmissionSpec 8.7

In short

Drugs affect the nervous system by changing nerve impulse transmission. Nicotine mimics acetylcholine, lidocaine blocks voltage-gated sodium channels, cobra venom alpha toxin blocks acetylcholine receptors, L-DOPA is converted to dopamine in Parkinson’s disease, and MDMA increases the amount of serotonin in synapses.

A drug can stimulate (an agonist), block (an antagonist) or alter the amount of neurotransmitter, so it changes transmission of impulses along axons or across synapses.

Drugs that affect nerve impulse transmission
Drug	Action	Effect
Nicotine	Binds to acetylcholine receptors and mimics ACh, so Na⁺ channels open and the postsynaptic neurone is depolarised. It is not broken down by acetylcholinesterase, so stimulation lasts longer.	Stimulates nerve impulses: raises heart rate and blood pressure; in the brain it also triggers release of dopamine, which contributes to addiction
Lidocaine	A local anaesthetic that blocks voltage-gated Na⁺ channels in the axon membrane, so no depolarisation occurs and action potentials are not conducted.	Impulses from pain receptors do not reach the brain: numbness
Cobra venom alpha toxin	Binds very tightly (almost irreversibly) to acetylcholine receptors on the postsynaptic membrane, so ACh cannot bind and Na⁺ channels do not open.	No depolarisation of the muscle: paralysis, including breathing muscles
L-DOPA	A precursor of dopamine that crosses the blood–brain barrier and is converted to dopamine in the brain. Dopamine itself cannot cross it.	Replaces dopamine lost in Parkinson’s disease, reducing tremor and rigidity
MDMA (ecstasy)	Causes release of serotonin from presynaptic neurones and prevents its reuptake, so more serotonin stays in the synaptic cleft and acts on the postsynaptic membrane for longer.	Raised mood and energy; can cause overheating; serotonin stores become depleted

Exam tip:

In a ‘suggest how’ question, name the target (receptor, channel or reuptake), say whether the drug mimics or blocks, and link it to the effect on depolarisation of the postsynaptic membrane.

Written and checked against the Edexcel International A Level Biology (YBI11) specification · Updated October 2026

Frequently asked questions

How does an action potential work?

An action potential is a brief reversal of the potential across an axon membrane. Voltage-gated sodium channels open at threshold, so Na⁺ enters and the membrane depolarises. The sodium channels then close and potassium channels open, so K⁺ leaves and the membrane repolarises. Local circuits depolarise the next region, so the impulse travels.

Why do myelinated axons conduct impulses faster?

Myelin insulates the axon so ions cross the membrane only at the nodes of Ranvier. The action potential jumps from node to node by local circuits, which is called saltatory conduction. Less of the membrane has to depolarise, so conduction reaches about 100 m s⁻¹, much faster than the 0.5 to 2 m s⁻¹ in an unmyelinated axon.

How does acetylcholine transmit a signal across a synapse?

An impulse opens calcium channels in the presynaptic knob, and calcium ions make vesicles release acetylcholine by exocytosis. Acetylcholine diffuses across the cleft and binds to receptors on the postsynaptic membrane, opening sodium channels. Sodium ions enter and depolarise it. Acetylcholinesterase then breaks the acetylcholine down.

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