8.1.7Unit 6: Practical Skills in Biology II
The Effects of Drugs on Nervous Transmission — IAL Edexcel Linear Revision Notes & Topical Questions
5 min read 4 parts Lesson 41 of 48 Unit quiz
Section 1 of 4How Drugs Alter Synaptic Transmission

Most drugs that affect the nervous system act at synapses, either boosting or reducing the signal.
How Drugs Alter Synaptic Transmission
More transmitter
- A drug can increase production or release of neurotransmitter, so the postsynaptic cell is stimulated more often.
Mimics transmitter
- Some drugs have a shape similar to the neurotransmitter and bind to and activate its receptors.
Blocks breakdown
- Inhibiting the enzyme that destroys neurotransmitter leaves it active in the cleft for longer.
Blocks reuptake
- Preventing neurotransmitter from being taken back into the presynaptic cell keeps its concentration high.
Blocks receptors
- A drug that binds to receptors without activating them stops the real neurotransmitter from binding.
Less transmitter
- Preventing synthesis or release of neurotransmitter lowers the chance of an action potential in the next cell.
Section 2 of 4Nicotine and MDMA
Both drugs increase activity at some synapses but through different mechanisms.
Nicotine mimics ACh
- It binds to nicotinic acetylcholine receptors on the postsynaptic membrane and can start an action potential.
Receptor desensitising
- After nicotine stimulates them, the receptors stay unresponsive for a prolonged time to other stimulation.
Dopamine release
- Nicotine stimulates release of dopamine in reward areas of the brain, which reinforces the habit of smoking.
Body effects
- Nicotine raises heart rate and blood pressure, adding to the health risks of tobacco use.
MDMA and serotonin
- It binds to the reuptake proteins on the presynaptic membrane, so less serotonin is recycled back.
Extra release
- MDMA also triggers further release of serotonin, so levels in the synapse rise, affecting mood and sensation.
Section 3 of 4Blocking Drugs and a Replacement Drug
Lidocaine
- This local anaesthetic blocks voltage-gated sodium channels, so sodium ions cannot enter and no action potential forms.
Use of lidocaine
- Dentists inject it to numb a small area, and it can also help regulate an irregular heartbeat.
Cobra venom
- α-cobratoxin binds to acetylcholine receptors, so sodium ions cannot enter and no action potential is generated.
Paralysis
- At neuromuscular junctions this causes muscle paralysis, and failure of the breathing muscles can be fatal.
L-dopa
- It is taken up into the brain, where dopa-decarboxylase converts it to dopamine, relieving Parkinson's disease symptoms.
Why not dopamine
- Dopamine itself cannot cross the barrier between the blood and the brain, so the precursor is given instead.
| Drug | Main action | Effect on transmission |
|---|---|---|
| Nicotine | Mimics acetylcholine | Increases, then desensitises receptors |
| MDMA | Blocks serotonin reuptake and increases release | Increases |
| Lidocaine | Blocks voltage-gated sodium channels | Decreases |
| Cobra venom | Blocks acetylcholine receptors | Decreases |
| L-dopa | Converted to dopamine | Increases |
Section 4 of 4Exam Checklist & Tips
8.1.7 – Key Points for the Exam
- Reuptake The absorption of neurotransmitter back into the presynaptic neurone so it can be recycled.
- Nicotinic receptor A type of acetylcholine receptor on the postsynaptic membrane that nicotine can bind to.
- Neuromuscular junction The synapse between a motor neurone and a muscle fibre.
- Local anaesthetic A drug such as lidocaine that blocks nerve impulses in a small area of the body.
- L-dopa A drug converted to dopamine in the brain, used to treat Parkinson's disease.
Common Mistakes
- Stating that lidocaine and cobra toxin act in the same way;
- one blocks sodium channels and the other blocks receptors.
- Saying dopamine is given to Parkinson's patients; it cannot cross from blood to brain, so L-dopa is used.
- Describing nicotine as only blocking receptors; it first mimics acetylcholine and activates them.
- Not stating the effect on the action potential; always link the drug action to whether threshold is reached.
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