WorksheetsNeuromuscular Junction Quiz
Total questions: 20
Worksheet time: 10mins
Neuromuscular junction is a synapse between
Two neurons
Motor neuron and skeletal muscle
Sensory neuron and muscle
Autonomic neuron and smooth muscle
Neurotransmitter released at NMJ is
GABA
Glutamate
Acetylcholine
Noradrenaline
Type of receptor present at NMJ is
Muscarinic
Nicotinic Nm
Alpha adrenergic
Beta adrenergic
Width of synaptic cleft at NMJ is about
2 nm
5 nm
20–30 nm
100 nm
NMJ transmission is
Electrical
Chemical
Both electrical and chemical
Inhibitory
Calcium is required at NMJ for
Muscle contraction
ACh synthesis
ACh release
Na⁺ influx
End plate potential is due to influx of
Calcium ions
Potassium ions
Sodium ions
Chloride ions
Enzyme present in synaptic cleft is
Choline acetyltransferase
Acetylcholinesterase
Monoamine oxidase
COMT
Myasthenia gravis is caused by antibodies against
ACh
Nm receptors
Muscle actin
Calcium channels
Characteristic feature of myasthenia gravis is
Muscle rigidity
Muscle wasting
Fatigability of muscles
Spastic paralysis
Drug of choice for myasthenia gravis is
Atropine
Neostigmine
Curare
Adrenaline
Curare acts by
Blocking ACh release
Blocking Nm receptors
Inhibiting AChE
Stimulating muscle fiber
Botulinum toxin causes paralysis by
Blocking ACh synthesis
Blocking ACh release
Destroying receptors
Inhibiting AChE
Acetylcholine is synthesized in nerve terminal from
Choline + Acetate
Choline + Acetyl CoA
Acetate + CoA
Choline alone
Safety factor at NMJ refers to
Amount of Ca²⁺ present
Excess ACh released
Width of synaptic cleft
Number of receptors
NMJ is always
Inhibitory
Excitatory
Both
Electrical
Junctional folds are present on
Presynaptic membrane
Postsynaptic membrane
Synaptic vesicles
Axon hillock
Hemicholinium blocks
Choline uptake
ACh release
ACh receptors
ACh breakdown
Organophosphates act by
Blocking receptors
Inhibiting AChE
Blocking Na⁺ channels
Blocking Ca²⁺ channels
Lambert-Eaton syndrome involves antibodies against
ACh receptors
Na⁺ channels
Ca²⁺ channels on nerve terminal
Muscle fibers
