Drugs and the nervous systemEdexcel A-Level Biology B: Revision notes

Many drugs and toxins act on the nervous system by changing synaptic transmission or the conduction of action potentials. To explain any one you need to say:

• Where it acts: the presynaptic knob, the synaptic cleft, the postsynaptic receptors or the axon membrane
• What it does: mimics the transmitter, blocks a receptor, or blocks an ion channel
• The consequence: the postsynaptic membrane depolarises more or less, so action potentials are more or less likely

At a cholinergic synapse, acetylcholine binds to receptors, Na⁺ channels open, and the postsynaptic membrane depolarises.

Nicotine has a shape similar to acetylcholine, so it binds to acetylcholine receptors on postsynaptic membranes, in the brain and at neuromuscular junctions.

Binding opens Na⁺ channels and depolarises the postsynaptic membrane, so it can start action potentials even when no acetylcholine has been released. Unlike acetylcholine, nicotine is not broken down by acetylcholinesterase, so its effect is prolonged.

Nicotine is described as an agonist: it mimics the transmitter.

Lidocaine is a local anaesthetic. It enters sensory neurones and blocks voltage-gated Na⁺ channels in the axon membrane.

When a pain receptor is stimulated the membrane may depolarise slightly, but Na⁺ cannot flood in, so the potential does not reach threshold. No action potential is generated or conducted, so no impulses reach the brain and pain is not felt.

Lidocaine acts on the axon, not the synapse, so the receptors and transmitter are unaffected.

Cobra venom contains a toxin that binds to acetylcholine receptors on the postsynaptic membrane without opening the channel. It acts as an antagonist.

Acetylcholine released from the presynaptic neurone cannot bind, so Na⁺ channels do not open and the muscle membrane is not depolarised. The muscle cannot contract, causing paralysis. If breathing muscles fail, the victim can die from respiratory failure.

Compared with nicotine: both act at the same receptors, but nicotine activates them and the toxin blocks them.

Compare the drugs by site and effect:

• Nicotine: postsynaptic receptor; mimics acetylcholine; depolarises
• Lidocaine: axon membrane; blocks voltage-gated Na⁺ channels; no action potentials
• Cobra venom: postsynaptic receptor; blocks acetylcholine binding; no depolarisation

A useful experiment: stimulate a nerve, then add acetylcholine directly to the junction. Contraction shows the receptors work (lidocaine acts earlier); no contraction shows they are blocked (cobra venom).