Introduction: The neuromuscular junction (NMJ) is the specialized synapse where motor neurons communicate with skeletal muscle fibers to produce contraction. Key elements include the motor end plate, synaptic cleft, synaptic vesicles containing acetylcholine (ACh), nicotinic acetylcholine receptors (nAChRs), and acetylcholinesterase (AChE). Understanding quantal release, end-plate potentials (EPPs), the safety factor for neuromuscular transmission, and presynaptic machinery such as SNARE proteins is essential for B.Pharm students. Clinical and pharmacological relevance spans myasthenia gravis, Lambert–Eaton syndrome, neuromuscular blockers (curare, succinylcholine), botulinum toxin, and cholinesterase inhibitors. This foundation links molecular structure to drug actions and disease mechanisms. Now let’s test your knowledge with 30 MCQs on this topic.
Q1. What is the primary neurotransmitter released at the neuromuscular junction?
- Glutamate
- GABA
- Acetylcholine
- Dopamine
Correct Answer: Acetylcholine
Q2. Which receptor subtype predominates on the postsynaptic motor end plate of skeletal muscle?
- Muscarinic M2 receptor
- Nicotinic muscle-type (Nm) receptor
- N-methyl-D-aspartate (NMDA) receptor
- GABA-A receptor
Correct Answer: Nicotinic muscle-type (Nm) receptor
Q3. Which enzyme rapidly hydrolyzes acetylcholine in the synaptic cleft at the NMJ?
- Monoamine oxidase
- Butyrylcholinesterase
- Acetylcholinesterase
- Choline acetyltransferase
Correct Answer: Acetylcholinesterase
Q4. Entry of which ion into the presynaptic terminal triggers synaptic vesicle fusion and ACh release?
- Na+
- K+
- Cl−
- Ca2+
Correct Answer: Ca2+
Q5. The concept of “quantal release” at the NMJ refers to:
- The release of a continuous stream of ACh molecules
- Release of neurotransmitter in fixed, discrete packets (vesicles)
- Single ion movements across the postsynaptic membrane
- Random diffusion of ACh without vesicles
Correct Answer: Release of neurotransmitter in fixed, discrete packets (vesicles)
Q6. Miniature end-plate potentials (MEPPs) are caused by:
- Action potentials arriving at the motor neuron
- Spontaneous, single-vesicle ACh release
- Postsynaptic receptor upregulation
- Blocking of acetylcholinesterase
Correct Answer: Spontaneous, single-vesicle ACh release
Q7. Which protein complex is essential for synaptic vesicle docking and fusion and is targeted by botulinum toxin?
- Sodium–potassium ATPase
- SNARE proteins
- Ryanodine receptor
- G-protein coupled receptor complex
Correct Answer: SNARE proteins
Q8. Botulinum toxin causes paralysis primarily by:
- Blocking postsynaptic nAChRs competitively
- Inhibiting choline uptake into the presynaptic terminal
- Cleaving SNARE proteins and preventing ACh release
- Inhibiting acetylcholinesterase activity
Correct Answer: Cleaving SNARE proteins and preventing ACh release
Q9. Curare and α-bungarotoxin produce muscle paralysis by which mechanism?
- Enhancing ACh release presynaptically
- Competitive antagonism of postsynaptic nAChRs
- Irreversible inhibition of acetylcholinesterase
- Blocking voltage-gated calcium channels
Correct Answer: Competitive antagonism of postsynaptic nAChRs
Q10. Succinylcholine acts as a neuromuscular blocker by:
- Depolarizing the motor end plate and causing sustained activation
- Binding and sequestering ACh in the synaptic cleft
- Inhibiting presynaptic calcium channels
- Cleaving the acetylcholinesterase enzyme
Correct Answer: Depolarizing the motor end plate and causing sustained activation
Q11. The “safety factor” at the NMJ refers to:
- The ratio of acetylcholine molecules to receptors
- The margin by which EPP amplitude exceeds threshold for muscle action potential
- The speed of acetylcholinesterase-mediated ACh breakdown
- The number of motor units innervating a fiber
Correct Answer: The margin by which EPP amplitude exceeds threshold for muscle action potential
Q12. Hemicholinium produces which effect relevant to NMJ function?
- Inhibits vesicle fusion by cleaving SNAREs
- Blocks high-affinity choline transporter, decreasing ACh synthesis
- Directly blocks postsynaptic nAChRs
- Enhances AChE activity
Correct Answer: Blocks high-affinity choline transporter, decreasing ACh synthesis
Q13. Which enzyme synthesizes acetylcholine in the presynaptic terminal?
- Acetylcholinesterase
- Choline acetyltransferase
- Butyrylcholinesterase
- Choline kinase
Correct Answer: Choline acetyltransferase
Q14. Myasthenia gravis is characterized by:
- Autoantibodies against presynaptic P/Q-type calcium channels
- Autoantibodies against postsynaptic nAChRs causing receptor loss
- Excessive acetylcholine release from the motor neuron
- Mutation in acetylcholinesterase producing hyperactivity
Correct Answer: Autoantibodies against postsynaptic nAChRs causing receptor loss
Q15. The edrophonium (Tensilon) test transiently improves muscle strength in myasthenia gravis by:
- Blocking presynaptic calcium channels
- Reversibly inhibiting acetylcholinesterase
- Directly activating nAChRs as an agonist
- Stimulating choline uptake into terminals
Correct Answer: Reversibly inhibiting acetylcholinesterase
Q16. Lambert–Eaton myasthenic syndrome (LEMS) differs from MG primarily because LEMS:
- Is due to postsynaptic receptor antibodies
- Is caused by autoantibodies to presynaptic voltage-gated Ca2+ channels reducing ACh release
- Results from acetylcholinesterase hyperactivity
- Is treated only with nAChR agonists
Correct Answer: Is caused by autoantibodies to presynaptic voltage-gated Ca2+ channels reducing ACh release
Q17. Aminoglycoside antibiotics can potentiate neuromuscular blockade by:
- Enhancing acetylcholine synthesis
- Blocking presynaptic calcium channels and reducing ACh release
- Acting as direct nAChR agonists
- Increasing acetylcholinesterase activity
Correct Answer: Blocking presynaptic calcium channels and reducing ACh release
Q18. Which structural feature anchors acetylcholinesterase within the synaptic basal lamina at the NMJ?
- SNARE motif
- ColQ collagen tail
- Muscle ryanodine receptor
- Neuregulin domain
Correct Answer: ColQ collagen tail
Q19. The muscle-type nicotinic receptor at adult human NMJ contains which subunit composition?
- α1, α1, β1, δ, ε
- α3, β4, β2, γ, δ
- α7 homopentamer
- α4, β2 heteromer
Correct Answer: α1, α1, β1, δ, ε
Q20. Repetitive nerve stimulation in myasthenia gravis typically shows which pattern?
- Incremental response of compound muscle action potential (CMAP)
- Decremental response of CMAP amplitude with low-frequency stimulation
- No change with repetitive stimulation
- Transient complete block of transmission on the first stimulus only
Correct Answer: Decremental response of CMAP amplitude with low-frequency stimulation
Q21. End-plate potential (EPP) differs from an action potential in that EPP is:
- An all-or-none event propagating along muscle fiber
- A local graded depolarization of the motor end plate due to ACh
- Generated only by voltage-gated sodium channels
- Unaffected by acetylcholinesterase activity
Correct Answer: A local graded depolarization of the motor end plate due to ACh
Q22. Which statement best explains “quantal content” at the NMJ?
- It is the number of ACh molecules per vesicle
- It is the average number of vesicles released per nerve impulse
- It is the amplitude of a single MEPP
- It is the number of postsynaptic receptors available
Correct Answer: It is the average number of vesicles released per nerve impulse
Q23. Inhibition of acetylcholinesterase leads to which immediate effect at the NMJ?
- Reduced EPP amplitude due to decreased ACh
- Prolonged presence of ACh in cleft and enhanced EPPs
- Block of vesicle docking and reduced quantal release
- Permanent desensitization of presynaptic calcium channels
Correct Answer: Prolonged presence of ACh in cleft and enhanced EPPs
Q24. Which pharmacological agent reverses rocuronium-induced neuromuscular blockade by encapsulation of the drug?
- Neostigmine
- Edrophonium
- Sugammadex
- Physostigmine
Correct Answer: Sugammadex
Q25. Which phase describes succinylcholine’s prolonged blockade when plasma cholinesterase is deficient?
- Phase III block
- Phase I block with prolonged depolarization
- Phase II rapid recovery
- Complete resistance to depolarization
Correct Answer: Phase I block with prolonged depolarization
Q26. A decremental CMAP with low-frequency stimulation that improves with brief exercise suggests which disorder?
- Botulism
- Myasthenia gravis
- Lambert–Eaton myasthenic syndrome
- Muscular dystrophy
Correct Answer: Lambert–Eaton myasthenic syndrome
Q27. Which of the following alters the size of MEPPs by changing postsynaptic receptor sensitivity?
- Changing vesicle ACh content only
- Modulation of postsynaptic receptor number or conductance
- Altering presynaptic choline uptake exclusively
- Changing extracellular Na+ concentration only
Correct Answer: Modulation of postsynaptic receptor number or conductance
Q28. The synaptic delay at the NMJ (time between presynaptic AP and postsynaptic response) is largely due to:
- Diffusion of ACh across the synaptic cleft and vesicle fusion processes
- Slow propagation of the muscle action potential
- Postsynaptic transcriptional changes
- Electrical resistance of the basal lamina only
Correct Answer: Diffusion of ACh across the synaptic cleft and vesicle fusion processes
Q29. Which change would reduce the safety factor at the NMJ and predispose to transmission failure?
- Increased quantal release of ACh
- Upregulation of postsynaptic nAChRs
- Loss of postsynaptic receptors or decreased EPP amplitude
- Enhanced acetylcholinesterase inhibition
Correct Answer: Loss of postsynaptic receptors or decreased EPP amplitude
Q30. Which clinical toxin causes flaccid paralysis by blocking presynaptic ACh release and is associated with canned food outbreaks?
- Tetanus toxin
- Botulinum toxin
- Alpha-bungarotoxin
- Organophosphate insecticide
Correct Answer: Botulinum toxin
I am a Registered Pharmacist under the Pharmacy Act, 1948, and the founder of PharmacyFreak.com. I hold a Bachelor of Pharmacy degree from Rungta College of Pharmaceutical Science and Research. With a strong academic foundation and practical knowledge, I am committed to providing accurate, easy-to-understand content to support pharmacy students and professionals. My aim is to make complex pharmaceutical concepts accessible and useful for real-world application.
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