Membrane depolarization

[663697]

If an inhibitor of acetylcholinesterase is added to a neuromuscular junction, then the postsynaptic membrane will:

A) be depolarized by action potentials more frequently
B) be depolarized longer with each action potential
C) be resistant to depolarization
D) spontaneously depolarize

Can anyone help me differentiate between A and B? I chose A but the TPR book says B is the correct answer. Wouldn't more depolarization = higher frequency of action potentials?

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[desperadoflakes]

This is weird, I would've picked A too. I think I can reason why they picked B.

The important thing here is that it is asking what will happen to the post-synaptic membrane. The post-synaptic membrane is on the dendrites of the soma. It is for sure a fact that the axon can not remain depolarized longer than the duration of an action potential, being that the AP is an all or none event with a set refractory period. However, the post-synaptic membrane is depolarized by EPSPs, NOT action potentials.

I think this question is operating under the premise that inhibiting AChase WILL increase the frequency of action potentials, but those action potentials will NOT depolarize the post-synaptic membrane, because the action potential flows through the axon and not through the soma. So when you inhibit AChase, than ACh will remain bound to the ligand-gated receptors on the post-synaptic membrane. This will cause the constant induction of EPSPs, which will keep the dendritic membrane depolarized for a longer period of time. However, even if the dendritic membrane is constantly depolarized, the axon can not receive action potentials more frequently than what is allowed by its refractory period.

So the answer is that adding an inhibitor of AChase will cause longer (and a higher magnitude, due to more ACh being available to bind to more receptors) depolarization of the dendritic membrane, and increase the frequency of action potentials. But those action potentials don't depolarize the post-synaptic membrane.