What are the main features of a presynaptic knob?

Many mitochondria, vesicles of neurotransmitter and voltage-gated calcium ion channels.

What is found in the synaptic cleft of a cholinergic synapse?

Acetylcholinesterase, which hydrolyses acetylcholine.

Why does calcium ion entry matter at a synapse?

It causes vesicles containing acetylcholine to fuse with the presynaptic membrane and release their contents by exocytosis.

What happens when acetylcholine binds to postsynaptic receptors?

Sodium ion channels open, sodium ions enter and the postsynaptic membrane depolarises.

How is the effect of acetylcholine ended?

Acetylcholinesterase hydrolyses it into acetate and choline, which are reabsorbed by the presynaptic neurone and used to resynthesise acetylcholine.

Why is synaptic transmission unidirectional?

Vesicles of transmitter are only in the presynaptic knob and receptors are only on the postsynaptic membrane.

Define temporal summation.

Repeated releases of transmitter from one presynaptic neurone in quick succession whose depolarisations add up to reach threshold.

Define spatial summation.

Transmitter released at the same time from several presynaptic neurones onto one postsynaptic neurone, so their depolarisations add up to reach threshold.

How does an inhibitory synapse reduce the chance of an action potential?

It opens chloride (and potassium) ion channels, causing hyperpolarisation, so a larger depolarisation is needed to reach threshold.

Name two ways a neuromuscular junction differs from a cholinergic synapse between neurones.

The postsynaptic membrane is a folded muscle fibre membrane with more receptors, and it is always excitatory, ending in muscle contraction.

A drug inhibits acetylcholinesterase. What is the effect at a neuromuscular junction?

Acetylcholine is not broken down, so it keeps binding to receptors, sodium channels stay open, and the muscle contracts continuously.

A drug has a shape like acetylcholine and binds to the receptors without opening the channels. What is the effect?

It blocks acetylcholine binding, so there is no depolarisation of the postsynaptic membrane and no response (muscle paralysis at a neuromuscular junction).

Synaptic transmissionAQA A-Level Biology: Flashcards

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Why is a nerve impulse specific to its target cell?

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Why is a nerve impulse specific to its target cell?: Because the neurone releases a neurotransmitter directly onto the target cell; the response is rapid, short-lived and localised.
What are the main features of a presynaptic knob?: Many mitochondria, vesicles of neurotransmitter and voltage-gated calcium ion channels.
What is found in the synaptic cleft of a cholinergic synapse?: Acetylcholinesterase, which hydrolyses acetylcholine.
Why does calcium ion entry matter at a synapse?: It causes vesicles containing acetylcholine to fuse with the presynaptic membrane and release their contents by exocytosis.
What happens when acetylcholine binds to postsynaptic receptors?: Sodium ion channels open, sodium ions enter and the postsynaptic membrane depolarises.
How is the effect of acetylcholine ended?: Acetylcholinesterase hydrolyses it into acetate and choline, which are reabsorbed by the presynaptic neurone and used to resynthesise acetylcholine.
Why is synaptic transmission unidirectional?: Vesicles of transmitter are only in the presynaptic knob and receptors are only on the postsynaptic membrane.
Define temporal summation.: Repeated releases of transmitter from one presynaptic neurone in quick succession whose depolarisations add up to reach threshold.
Define spatial summation.: Transmitter released at the same time from several presynaptic neurones onto one postsynaptic neurone, so their depolarisations add up to reach threshold.
How does an inhibitory synapse reduce the chance of an action potential?: It opens chloride (and potassium) ion channels, causing hyperpolarisation, so a larger depolarisation is needed to reach threshold.
Name two ways a neuromuscular junction differs from a cholinergic synapse between neurones.: The postsynaptic membrane is a folded muscle fibre membrane with more receptors, and it is always excitatory, ending in muscle contraction.
A drug inhibits acetylcholinesterase. What is the effect at a neuromuscular junction?: Acetylcholine is not broken down, so it keeps binding to receptors, sodium channels stay open, and the muscle contracts continuously.
A drug has a shape like acetylcholine and binds to the receptors without opening the channels. What is the effect?: It blocks acetylcholine binding, so there is no depolarisation of the postsynaptic membrane and no response (muscle paralysis at a neuromuscular junction).

Exam questions on Synaptic transmission

A neurophysiologist is studying a cholinergic synapse between a presynaptic neurone and a postsynaptic neurone in an autonomic ganglion removed from a mammal. She stimulates the presynaptic neurone so that action potentials arrive at its synaptic knob, and records the response of the postsynaptic neurone.
Explain why transmission across the synapse can only occur in one direction.2 marks
A postsynaptic neurone in a spinal cord preparation has a resting potential of −70 mV and a threshold potential of −55 mV. Each time an excitatory presynaptic neurone releases neurotransmitter, it depolarises the postsynaptic membrane by about 5 mV; this depolarisation fades within a few milliseconds.
A different presynaptic neurone is inhibitory. Explain how it would reduce the chance of an action potential in the postsynaptic neurone.2 marks
A student prepares a frog nerve–muscle preparation in which a motor neurone is still attached to a skeletal muscle fibre. The motor neurone ends at a neuromuscular junction, which uses the same neurotransmitter as the cholinergic synapse in an autonomic ganglion.
Compare transmission across a cholinergic synapse between two neurones with transmission across a neuromuscular junction.3 marks

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Written by the Exaim team, led by Shaun Daswani (Head of Upper Secondary, Improve ME Institute; MSc Financial Mathematics, Imperial College London; BSc, UCL) and Jason Daswani (operational lead, Improve ME Institute; LSE).