At the NMJ, DFP causes ACh action to ____, so the muscle fiber experiences _____.

Question

BlackTom AI · Accepted Answer

DFP irreversibly inhibits acetylcholinesterase (AChE) at the motor endplate, so acetylcholine (ACh) remains in the synaptic cleft and continues to activate nicotinic receptors. This prolongation of ACh action causes persistent depolarization of the muscle endplate and continuous contraction — clinically producing spastic (tetanic) paralysis.

1) Relevant knowledge points and concepts
- At the neuromuscular junction (NMJ), ACh released from the motor neuron binds nicotinic ACh receptors (nAChRs) on the muscle motor endplate to produce end-plate potentials and trigger action potentials.
- Acetylcholinesterase rapidly hydrolyzes ACh, terminating its action and allowing the muscle membrane to repolarize between stimuli.
- Diisopropyl fluorophosphate (DFP) is an organophosphate that phosphorylates the serine hydroxyl in AChE’s active site, irreversibly inhibiting the enzyme and preventing ACh breakdown.

2) Step-by-step reasoning
- Step 1: DFP binds and irreversibly inhibits AChE at the NMJ.
- Step 2: ACh released during nerve impulses is no longer efficiently hydrolyzed.
- Step 3: ACh accumulates in the synaptic cleft and continuously stimulates nAChRs.
- Step 4: Continuous receptor activation causes prolonged depolarization and repetitive muscle fiber contractions.
- Step 5: Clinically, this manifests as sustained contraction (spasm, tetany) and eventually a depolarization block if channels/inactivation gates become dysfunctional — overall described as spastic paralysis.

3) Intermediate/calculation steps
- No numeric calculations apply; mechanism and sequence of events are the critical steps shown above.

4) Why the correct answer is correct
- Because DFP prevents ACh breakdown, ACh “lasts longer” in the cleft. Prolonged receptor activation produces continuous muscle contraction and hyperactivity (spasticity/tetany), hence “spastic paralysis.”

5) Why other possible answers are incorrect
- “ACh action shortened” is incorrect because DFP inhibits the enzyme that shortens ACh action; it does the opposite.
- “Flaccid paralysis” (loss of muscle tone) is characteristic of agents that block ACh release (botulinum toxin) or block nAChRs (curare), not of AChE inhibitors which cause overstimulation and spasm.

Conclusion: DFP causes ACh action to last longer, producing spastic paralysis — matching the provided answer: "Last longer, spastic paralysis."

At the NMJ, DFP causes ACh action to , so the muscle fiber experiences _.单项选择题

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At the NMJ, DFP causes ACh action to ____, so the muscle fiber experiences _____.单项选择题