Drugs and synaptic transmissionEdexcel International A Level Biology: Revision notes

Many drugs and toxins work by interfering with synaptic transmission or with the conduction of impulses. A drug may:

• Mimic a neurotransmitter and stimulate the receptors
• Block receptors or ion channels, preventing transmission
• Increase the amount of neurotransmitter in the cleft, by stimulating its release or inhibiting its removal
• Supply a precursor to make more neurotransmitter

You must be able to explain the effect of five examples: nicotine, lidocaine, cobra venom alpha toxin, L-DOPA and MDMA.

Nicotine has a shape similar to acetylcholine, so it binds to acetylcholine receptors on the postsynaptic membrane and opens sodium ion channels. The postsynaptic membrane is depolarised, so nicotine stimulates the postsynaptic neurone. Unlike acetylcholine it is not broken down by acetylcholinesterase, so the stimulation is prolonged.

Alpha toxin in cobra venom also binds to acetylcholine receptors, but at neuromuscular junctions it blocks them. Acetylcholine cannot bind, sodium ion channels stay closed and the muscle membrane is not depolarised. The muscles are paralysed, including the diaphragm and intercostal muscles, so the victim may die from respiratory failure.

Lidocaine is a local anaesthetic. It blocks voltage-gated sodium ion channels in the membrane of sensory neurones.

• Sodium ions cannot enter the axon
• The membrane is not depolarised to threshold
• No action potentials are generated, so pain impulses do not reach the brain

The numbness is local, because the drug is injected where it is needed, and it fades as the drug is removed.

In Parkinson's disease, dopamine-secreting neurones in the brain degenerate. Less dopamine is released at synapses that control movement, causing tremor, stiff muscles and slow movement.

Dopamine cannot cross the blood-brain barrier, but its precursor L-DOPA can. In the brain, L-DOPA is converted into dopamine, which is released into synapses and binds to dopamine receptors, restoring transmission and reducing symptoms.

L-DOPA treats the symptoms only. As more neurones die, fewer can release dopamine, so the drug becomes less effective and the dose may need to rise.

MDMA acts at synapses that use serotonin, and also affects dopamine. It:

• Causes release of serotonin from presynaptic neurones into the cleft
• Inhibits reuptake of serotonin into the presynaptic knob

Serotonin stays in the cleft longer, so postsynaptic neurones are stimulated more, giving raised mood and euphoria.

Afterwards the serotonin stores of the presynaptic neurones are depleted, so less is released and stimulation falls below normal. This can cause low mood and, with regular use, long-term damage to neurones.