Lesson 8.6.2
8.6.2 Drugs acting on synaptic transmission Quiz: Pearson Edexcel Biology A (Salters-Nuffield), Unit 8
20 questions
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Lesson 8.6.2, Drugs acting on synaptic transmission: 20 multiple choice questions for the Pearson Edexcel Biology A (Salters-Nuffield) (9BI0), Unit 8: Grey Matter, written with Revision Ninja.
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The 20 questions
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What is an agonist drug at a synapse?
- A drug that stops calcium entering the presynaptic knob only, so that no vesicles fuse with the membrane
- A drug that digests the myelin sheath, which removes the insulation from the axon and slows impulses
- A drug that blocks the receptor so the neurotransmitter cannot bind and produce any response
- A drug that binds to the receptor and mimics the effect of the natural neurotransmitter
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What is an antagonist drug at a synapse?
- A drug that increases the release of dopamine only, which raises the level of the neurotransmitter in the cleft
- A drug that converts L-Dopa into dopamine, which increases the amount of neurotransmitter in the brain
- A drug that is a copy of acetylcholine, which activates the receptor just as the natural transmitter does
- A drug that binds the receptor and prevents the natural neurotransmitter from binding and acting
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How does a reuptake inhibitor affect synaptic transmission?
- It increases the speed of the action potential, which shortens the time that neurotransmitter spends in the cleft
- It stops neurotransmitter being taken back into the presynaptic neurone, so it stays in the cleft longer
- It stops neurotransmitter from being released into the cleft, which removes the signal before it is sent
- It breaks down the receptor on the postsynaptic membrane, which prevents the neurotransmitter from binding
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How does an acetylcholinesterase inhibitor affect synaptic transmission?
- It makes acetylcholine bind to dopamine receptors, which switches the signal to a different pathway in the brain
- It prevents acetylcholine from being released, so the postsynaptic neurone receives no signal at all
- It prevents sodium channels from opening, which stops the postsynaptic membrane from depolarising
- It stops acetylcholine being broken down, so it stays in the cleft and stimulates the postsynaptic membrane for longer
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Which drug acts on synapses by increasing the release of serotonin and blocking its reuptake?
- Insulin, a hormone which lowers blood glucose by promoting the uptake of glucose into cells
- Penicillin, an antibiotic which kills bacteria by stopping the synthesis of their cell walls
- MDMA (Ecstasy), which increases serotonin release and blocks the serotonin transporter
- Paracetamol, a pain reliever which acts mainly by reducing the production of prostaglandins
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How does L-Dopa act to help people with Parkinson's disease?
- It blocks dopamine receptors, which reduces the overactive signalling that causes the tremor
- It is converted to dopamine, increasing the dopamine available to act on postsynaptic receptors
- It destroys the substantia nigra to stop tremor, which removes the source of the abnormal electrical activity
- It stops all neurotransmitters from being released, which quietens the uncontrolled activity of the brain
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A drug is found to block the postsynaptic receptor for acetylcholine. What would be expected at a neuromuscular junction?
- Calcium channels in the axon open continuously, which keeps the motor neurone firing at a high rate
- Muscle contraction is reduced or prevented, because the signal cannot be transmitted to the muscle fibre
- Acetylcholine release is increased, since the blocked receptors cause the motor neurone to release more of the transmitter
- Muscle contraction is increased, because the blocked receptors allow more acetylcholine to reach the fibre
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Which feature of a synaptic drug determines whether it acts as an agonist or an antagonist?
- Its storage temperature, which affects whether the drug remains in its active form when it reaches the cleft
- Its molecular weight alone, since heavier molecules always act as agonists and lighter ones always act as antagonists
- Its colour, which determines whether the drug binds to the receptor or passes straight through the synapse
- Its ability to change the shape of the receptor in a way that activates or blocks it
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What is the expected effect of a drug that increases the amount of neurotransmitter released from a presynaptic neurone?
- No change to the postsynaptic membrane, since the number of receptors limits the response and not the amount released
- Increased myelin formation on the postsynaptic neurone, which is caused by a rise in neurotransmitter levels
- Increased postsynaptic stimulation, if the receptors are available to bind the extra neurotransmitter
- Decreased postsynaptic response, since more neurotransmitter causes the receptors to become less sensitive
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A patient takes an antagonist drug for a condition involving excess acetylcholine action. Which effect would be expected?
- Increased stimulation of the postsynaptic neurone, since the antagonist makes the receptor more sensitive
- Increased release of acetylcholine, since the antagonist causes the presynaptic neurone to release more transmitter
- Reduced stimulation of the postsynaptic neurone, since the antagonist blocks the receptor from binding acetylcholine
- Fewer receptors on the postsynaptic membrane permanently, since the antagonist destroys the receptor protein
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Which drug would most likely cause an increase in heart rate by acting on synaptic transmission?
- A reuptake inhibitor for acetylcholine only, which slows the heart by keeping acetylcholine in the cleft longer
- An agonist for adrenergic receptors that mimics adrenaline, which stimulates the receptors that speed up the heart
- A drug that prevents calcium entry into the nucleus, which blocks the release of neurotransmitter at the heart
- An antagonist for serotonin receptors only, which blocks the receptors that control the rate of the heart beat
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A researcher finds a drug increases dopamine activity by blocking its reuptake. Which statement is correct?
- Dopamine is converted into acetylcholine, which changes the type of signal sent to the postsynaptic cell
- Dopamine stays in the synaptic cleft for longer, increasing postsynaptic stimulation
- Dopamine can no longer be released, since the drug blocks the vesicles that carry it to the membrane
- Dopamine is destroyed in the cleft, which reduces the amount of neurotransmitter that can act on the receptors
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Why might an agonist that is not broken down cause a stronger or longer-lasting effect than the natural neurotransmitter?
- It stays bound to receptors for longer, because it is not removed by enzymes or reuptake
- It makes the myelin thicker, which increases the insulation and so prolongs the signal along the axon
- It stops calcium from entering the knob, which means the receptor stays open for longer after each impulse
- It is more quickly converted into hormones, which are then released into the blood and act on other organs
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A student compares the effects of an SSRI and MDMA on serotonin. Which statement is the best comparison?
- Both decrease serotonin activity, since each drug acts by blocking the serotonin receptors in the brain
- Neither drug has any effect on serotonin, since both act only on dopamine receptors in the brain
- SSRIs increase release and MDMA blocks receptors, which is the opposite of what the two drugs do
- Both increase serotonin activity, but MDMA also increases serotonin release
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Which statement describes a risk of using drugs that raise serotonin activity?
- They increase the number of neurones permanently, which can lead to excess tissue in the brain
- They always produce no side effects, since serotonin is a natural chemical that the body already makes
- They can cause side effects by affecting many synapses, and misuse can cause serious harm
- They cannot affect the heart, since serotonin acts only on the neurones of the brain and spinal cord
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Which statement best describes a neuromuscular blocking drug?
- It converts acetylcholine into dopamine, which changes the signal sent to the muscle fibres
- It increases the speed of action potentials in motor neurones, which speeds up the contraction of muscles
- It prevents acetylcholine from activating receptors at the neuromuscular junction, causing muscle relaxation
- It stimulates muscle contraction continuously, since it acts as an agonist for acetylcholine receptors
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Which pair correctly matches a drug type with its action at the synapse?
- Agonist: blocks the receptor so the natural transmitter cannot bind
- Antagonist: mimics neurotransmitter and stimulates the receptor in the postsynaptic membrane
- Reuptake inhibitor: blocks transporter that removes neurotransmitter from the cleft
- Enzyme inhibitor: increases release of neurotransmitter from the presynaptic knob
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A drug that increases neurotransmitter release has an effect on the frequency of action potentials in the postsynaptic neurone. Which statement is most consistent?
- Frequency is unaffected, since the action potential always has the same size and timing regardless of stimulus
- Frequency falls because release is increased, since more transmitter shuts down the postsynaptic neurone
- Frequency is independent of neurotransmitter, since the frequency is set entirely by the myelin sheath
- Frequency may rise if the postsynaptic neurone reaches threshold more often
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Which evaluation is most appropriate for the claim that a drug that blocks reuptake is always safe because it only uses the body's natural chemicals?
- Incorrect, because raising a natural chemical above normal levels can still cause harm
- Correct, because drugs never affect synapses, so any drug is safe provided the chemical is natural
- Correct, because natural chemicals are always safe in any amount, so no monitoring is needed for these drugs
- Incorrect, because drugs cannot be natural, so the claim has no meaning for any drug used in medicine
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A postsynaptic response measures 6 mV with the natural neurotransmitter and 9 mV with a drug agonist. By what percentage is the response greater with the drug?
- 50 per cent, found by taking the increase of 3 mV as a share of the natural response of 6 mV
- 33 per cent, found by taking the increase of 3 mV as a share of the drug response of 9 mV
- 3 per cent, found by taking the increase of 3 mV as a share of 100 mV
- 9 per cent, found by taking the drug response of 9 mV as a share of 100 mV
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