Effect of Drugs on Synapses
Laura Armstrong
Teacher

Recall Questions
This topic requires prior knowledge of synaptic transmission. You can test your knowledge on this below.
What is the role of calcium ions in synaptic transmission?
They enter the presynaptic knob and trigger synaptic vesicle fusion with the pre-synaptic membrane, releasing neurotransmitter.
What is a neurotransmitter and where is it released?
A chemical that transmits signals across the synaptic cleft from the presynaptic neurone.
How is a signal stopped after transmission at a synapse?
Neurotransmitter is broken down by enzymes (such as acetylcholinesterase which breaks down ACh) and reabsorbed into the presynaptic neurone.
Topic Explainer Video
Check out this @JoeDoesBiology video that explains effect of drugs on synapses or read the full notes below. Once you've gone through the whole note, try out the practice questions!
How Synapses Work: Quick Recap
- An action potential arrives at the presynaptic knob.
- Calcium ions (Ca²⁺) diffuse into the presynaptic neurone when calcium ion channels open.
- Synaptic vesicles fuse with the pre-synaptic membrane, releasing neurotransmitter (e.g., acetylcholine) into the synaptic cleft via exocytosis.
- Neurotransmitter diffuses across the cleft.
- Neurotransmitter binds to receptors on the postsynaptic membrane.
- This opens sodium ion (Na⁺) channels and sodium ions diffuse into the post-synaptic neurone, causing depolarisation.
- If the threshold is reached, an action potential is generated in the post-synaptic neurone.
- Neurotransmitter is broken down and reabsorbed, stopping the signal.
How Drugs Affect Synapses
Drugs can affect any stage of synaptic transmission. Their effects can be:
Agonistic (Stimulating)
These enhance transmission by increasing the amount of neurotransmitter or mimicking its action.
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Example: Nicotine
- Mimics acetylcholine and binds to its receptors.
- Causing sodium ion channels to open and the post-synaptic membrane to be depolarised.
- Triggers more action potentials in the postsynaptic neurone.
Antagonistic (Inhibiting)
These reduce or block transmission by preventing neurotransmitter action.
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Example: Curare
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Blocks acetylcholine receptors on muscle cells → prevents depolarisation → prevents muscle contraction → leads to paralysis.
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Example: Benzodiazepines (e.g., Valium)
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Increase activity of inhibitory neurotransmitter GABA → causes negatively charged chloride ions to enter the post-synaptic neurone → leads to hyperpolarisation → threshold less likely to be reached → reduced chance of action potential.
Key Terms
- Agonist: A drug that mimics or enhances neurotransmitter action.
- Antagonist: A drug that blocks or inhibits neurotransmitter action.
- Cholinergic synapse: A synapse that uses acetylcholine as its neurotransmitter.
Exam Tips
You don’t have to learn specific examples of drugs, but be prepared to apply your knowledge of what happens at a synapse to a question where they tell you what the drug does.
Many students forget to link the drug’s action to the effect on the postsynaptic membrane (e.g., whether depolarisation is increased or reduced). Don’t just say ‘it blocks receptors’—always say what happens as a result.
Explain how a drug that inhibits the enzyme acetylcholinesterase affects synaptic transmission at a cholinergic synapse. (4 marks)
- Acetylcholinesterase breaks down acetylcholine in the synaptic cleft. The drug prevents this breakdown.
- Acetylcholine remains in the cleft for longer and continues to bind to receptors.
- Sodium ions continue to diffuse into the post-synaptic neurone. This results in continued depolarisation of the postsynaptic membrane.
- Action potentials will continue to be generated.
Practice Question
Try to answer the practice question from the TikTok on your own, then watch the video to see how well you did!