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Neuromuscular junctions (NMJ) are synapses between skeletal muscles and axonal terminals that innervate them. Synaptic transmission at the neuromuscular junction is mediated by nictotinc acetylcholine receptors (nAChR).

Alpha-bungarotoxin is a component of snake venom that irreversibly binds to nAChRs causing muscle paralysis, respiratory failure and ultimately death in the victim.

Which of the following can we observe at the NMJ inhibited by alpha-bungarotoxin?

Select ALL that apply.


Direct electrical stimulation of the muscle will not cause a contractile response.


Increasing levels of acetylcholine by inhibiting acetylcholinesterase will restore synaptic transmission at the NMJ.


Electrical stimulation of the efferent axons will cause acetylcholine release, but there will not be any $Na^+$ currents and membrane depolarization on the post-synaptic side.


Intracellular calcium will still rise in a muscle affected by alpha-bungarotoxin upon direct electric stimulation.

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