Synaptic transmission (A-level only)
AQA
A-Level
A synapse is the junction between the synaptic knob at the end of one neurone and the membrane of the next cell. The presynaptic knob contains many mitochondria, supplying ATP for making and packaging neurotransmitter, a large amount of smooth endoplasmic reticulum, and vesicles filled with acetylcholine. Its membrane holds voltage-gated calcium ion channels. The synaptic cleft is a gap of about 20 nm. The postsynaptic membrane carries specific receptor proteins whose binding sites are complementary in shape to acetylcholine and which form part of sodium ion channels, and acetylcholinesterase in the cleft hydrolyses acetylcholine into choline and ethanoic acid. A neuromuscular junction has the same basic components but its postsynaptic membrane is the folded sarcolemma of a muscle fibre, forming the motor end plate, and it is the muscle fibre that is excited to contract.
13
Objectives
11
Exam Tips
19
Pitfalls
22
Key Terms
20
Mark Points
Subtopics in this area
The detailed structure of a synapse and of a neuromuscular junction.
The sequence of events involved in transmission across a cholinergic synapse in sufficient detail to explain: unidirectionality temporal and spatial summation inhibition by inhibitory synapses.
A comparison of transmission across a cholinergic synapse and across a neuromuscular junction.
Students should be able to use information provided to predict and explain the effects of specific drugs on a synapse.
Synaptic transmission (A-level only) Revision Guide
Learning Objectives
What you need to know and understand
- Label a synapse and a neuromuscular junction, identifying the knob, vesicles, cleft, receptors and sarcolemma.
- Explain why the synaptic knob contains many mitochondria, linking this to the resynthesis of acetylcholine.
- Explain how the arrangement of vesicles and receptors makes transmission at both junctions one-way.
- Sequence the events at a cholinergic synapse from the arrival of an action potential to its generation in the postsynaptic neurone.
- Explain why transmission across a cholinergic synapse is unidirectional.
- Distinguish temporal from spatial summation and explain how each allows sub-threshold inputs to trigger an action potential.
- Explain the mechanism of inhibition by inhibitory synapses, including the roles of chloride and potassium ions in hyperpolarisation.
- Give three differences between transmission at a cholinergic synapse and at a neuromuscular junction.
- Explain why summation is normally needed at a synapse between neurones but not at a neuromuscular junction.
- Explain why there is no inhibitory equivalent of a neuromuscular junction.
- Predict the effect on postsynaptic action potentials of a drug that blocks calcium ion channels, justifying each step of the chain.
- Explain how inhibiting acetylcholinesterase can strengthen a weak muscle contraction.
- Distinguish, from information given, between a drug that mimics a neurotransmitter and one that blocks its receptor.
Marking Points
Key points examiners look for in your answers
- one mark for vesicles containing acetylcholine and numerous mitochondria in the presynaptic knob
- one mark for calcium ion channels in the presynaptic membrane
- one mark for the synaptic cleft as a gap of about 20 nm between the two membranes
- one mark for receptors on the postsynaptic membrane that are specific or complementary to the neurotransmitter and linked to sodium ion channels
- one mark for the neuromuscular junction having a folded sarcolemma, the motor end plate, with acetylcholinesterase present in the cleft
- Depolarisation of the presynaptic membrane opens voltage-gated Ca²⁺ channels, allowing Ca²⁺ to diffuse into the synaptic knob.
- Vesicles fuse with the presynaptic membrane, releasing acetylcholine into the synaptic cleft by exocytosis.
- Acetylcholine diffuses across the cleft and binds to specific receptors on the postsynaptic membrane, opening Na⁺ channels.
- In spatial summation, neurotransmitter released simultaneously from multiple presynaptic neurones combines to exceed the threshold.
- Inhibitory synapses cause hyperpolarisation of the postsynaptic membrane by opening Cl⁻ and K⁺ channels, preventing threshold from being reached.
- one mark for a shared feature, such as acetylcholine released by exocytosis and hydrolysed by acetylcholinesterase at both
- one mark for the neuromuscular junction occurring only between a motor neurone and a muscle fibre, whereas a cholinergic synapse joins two neurones
- one mark for the neuromuscular junction being only excitatory, whereas a cholinergic synapse may be excitatory or inhibitory
- one mark for the motor end plate carrying more receptors, so one action potential is usually enough without summation
- one mark for the different end points: contraction of a muscle fibre against an action potential in the next neurone
- change in calcium ions entering the synaptic knob through its calcium ion channels, stated as no or fewer where the drug blocks them
- matching change in synaptic vesicles moving to and fusing with the presynaptic membrane, and so in the neurotransmitter released
- change in the amount of neurotransmitter diffusing across the synaptic cleft
- change in the amount of neurotransmitter attaching to receptors on the postsynaptic membrane
- change in sodium ions entering the postsynaptic neurone, and so in the number of impulses produced, with threshold not being reached accepted for fewer impulses
Examiner Tips
Expert advice for maximising your marks
- 💡Learn the structure as a checklist that maps onto the transmission sequence; every structure you label has a job in the next question.
- 💡Synaptic transmission takes time, so if a question asks why a measured response was slower than predicted, synaptic transmission or transmission at a neuromuscular junction earns a mark.
- 💡State that receptors are only on the postsynaptic membrane; that single fact answers most unidirectionality questions.
- 💡Learn the sequence of synaptic transmission as a numbered list; questions often ask you to apply this sequence to a novel drug or toxin by stating which specific step is disrupted.
- 💡When explaining how a drug reduces synaptic transmission, explicitly state the comparative change, such as 'fewer Na⁺ channels open' or 'less depolarisation occurs'.
- 💡Use comparative language in every line: whereas, but, compared with.
- 💡If a table is provided, fill in both columns of every row; a row with one side blank scores nothing.
- 💡Keep similarities and differences in separate paragraphs so the examiner can find each one.
- 💡Sketch the five-step sequence in the margin and mark more or less against each step before you begin writing.
- 💡Quote line numbers or details from the passage; these are application marks, not recall marks.
- 💡If the drug relieves a symptom, finish by saying what the patient experiences, not only what the neurone does.
Common Mistakes
Pitfalls to avoid in your exam answers
- drawing the two membranes in contact, leaving no cleft for the neurotransmitter to diffuse across
- putting receptors on the presynaptic membrane as well, which would destroy unidirectionality
- describing the neurotransmitter as crossing the cleft by active transport rather than by diffusion
- calling a synapse a gap between two nerves instead of between two neurones, or between a neurone and a muscle fibre
- omitting the mitochondria, and so being unable to explain where the ATP for resynthesising acetylcholine comes from
- Writing 'signals' or 'messages' instead of 'action potentials' or 'impulses'; always use the correct neurobiological terminology.
- Confusing temporal and spatial summation; remember temporal is one neurone firing rapidly over time, whereas spatial is multiple neurones firing simultaneously in space.
- Stating that inhibitory synapses 'block' the impulse; correct this by explaining they cause hyperpolarisation (making the membrane potential more negative) via Cl⁻ influx or K⁺ efflux, so threshold is not reached.
- Claiming acetylcholine is destroyed by the postsynaptic membrane; it is actually hydrolysed by the enzyme acetylcholinesterase in the synaptic cleft.
- listing as differences features that are in fact the same at both, such as the use of acetylcholine
- saying an impulse passes into the muscle, when what crosses is neurotransmitter and what follows is depolarisation of the sarcolemma
- claiming a neuromuscular junction can be inhibitory
- comparing structures without naming the sarcolemma or the motor end plate
- answering a comparison question with two separate descriptions and no comparative words
- describing normal synaptic transmission without ever writing more, less, fewer or no, which caps the answer below full marks
- calling a receptor an active site and the drug a competitive inhibitor of it, since active site is rejected in this context
- stopping at less neurotransmitter is released without carrying the chain through to action potentials
- assuming every drug must be inhibitory, when agonists and acetylcholinesterase inhibitors increase transmission
- recalling a real drug from memory instead of using the information supplied in the question