How does inhibiting acetylcholinesterase at neuromuscular junctions prevent breathing in the described toxin?

• A. Acetylcholine not broken down / stays bound to receptor; Na+ ions continue to enter / depolarisation occurs; intercostal muscles stay contracted.
• B. Acetylcholine is rapidly degraded, preventing receptor activation.
• C. The toxin blocks Na+ channels, preventing action potentials.
• D. The toxin prevents acetylcholine release from the neuron.

Answer: (A)

The key idea is that stopping acetylcholinesterase leaves acetylcholine in the neuromuscular junction, so it keeps binding to nicotinic receptors and continuously activating them. That ongoing receptor activity keeps sodium channels open, causing ongoing depolarization of the muscle end plate. For respiratory muscles, this sustained depolarization means the muscles stay in a contracted state and can’t properly relax or coordinate breathing, leading to paralysis of the intercostal muscles and diaphragm and, ultimately, failure to breathe. The other scenarios describe removing acetylcholine, blocking sodium channels, or stopping acetylcholine release, which would prevent contraction rather than cause the dangerous, sustained contraction that blocks breathing.