Aamc 6 bs 128

[letaps]

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Hey,

Can anyone explain why A is wrong? An cholinesterase blocker would increase the acetylcholine, so how would that interfere with muscle contraction?


Which of the following changes would NOT interfere with the repeated transmission of an impulse at the vertebrate neuromuscular junction?
A) Addition of a cholinesterase blocker

B) Addition of a toxin that blocks the release of acetylcholine

C) An increase in acetylcholine receptor sites on the motor end plate

The question asks what process would not interrupt the repeated transmission of a nerve impulse to a muscle cell. The impulse is transmitted by release of the neurotransmitter acetylcholine from the presynaptic membrane and its reception by membrane-bound proteins on the postsynaptic membrane. Answers B and D are incorrect, because they involve substances that would interfere with the presynaptic release or postsynaptic reception of neurotransmitter. Addition of a cholinesterase blocker would produce a buildup of acetylcholine in the synapse and prevent receptors from responding to impulses, so option A is incorrect. The only change that would not result in blockage of the impulse transmission is option C, which is the correct answer. An increase in acetylcholine receptors on the postsynaptic membrane would enhance transmission, not interfere with it.

D) Addition of a substance that binds to acetylcholine receptor sites

 

[rotatedline]

Hey,

Can anyone explain why A is wrong? An cholinesterase blocker would increase the acetylcholine, so how would that interfere with muscle contraction?


Which of the following changes would NOT interfere with the repeated transmission of an impulse at the vertebrate neuromuscular junction?
A) Addition of a cholinesterase blocker

B) Addition of a toxin that blocks the release of acetylcholine

C) An increase in acetylcholine receptor sites on the motor end plate

The question asks what process would not interrupt the repeated transmission of a nerve impulse to a muscle cell. The impulse is transmitted by release of the neurotransmitter acetylcholine from the presynaptic membrane and its reception by membrane-bound proteins on the postsynaptic membrane. Answers B and D are incorrect, because they involve substances that would interfere with the presynaptic release or postsynaptic reception of neurotransmitter. Addition of a cholinesterase blocker would produce a buildup of acetylcholine in the synapse and prevent receptors from responding to impulses, so option A is incorrect. The only change that would not result in blockage of the impulse transmission is option C, which is the correct answer. An increase in acetylcholine receptors on the postsynaptic membrane would enhance transmission, not interfere with it.

D) Addition of a substance that binds to acetylcholine receptor sites

Here's the only answer I can come up with (I got the right answer when I took it, so I think its the right explanation).

If you think of what happens when the postsynaptic region experiences a large amount of nicotine or other nicotinic activators, there is at first a stimulation and then a huge desensitization on the postsynaptic side, which causes a decrease (in this case) in muscle excitability. I'll agree, it's kind of a convoluted question. This explanation also explains the odd physical symptoms of nicotine overdose associated with a desensitization of nicotinic receptors. I just remembered; nicotine is a partial agonist. I hope that's the reason.

 

[muhali3]

It's easy to narrow this down to A and C. I would eliminate A just based on knowledge that when receptors are exposed to a constant and unchanging stimulus they can become desensitized to it. Like if you walk into a room that smells really weird, after a few minutes you'll get used to it and won't smell it anymore. Or let's say someone wants to get wet and jumps into a pool; after he jumps in, putting more water on him won't make him wetter, since every part of his body is already wet...but if you could hypothetically add more areas of dry skin to him (extra receptors) then you could make him wetter by putting water on those extra dry spots. Idk, maybe that was a bad analogy.

I would say that if you have more receptors, then the acetylcholine has a greater chance of binding. If you add more acetylcholine to bind to a limited amount of receptors, there really won't be any change in transmission because the receptors are probably close to their Vmax anyways (can you use Vmax in terms of receptor-ligand complexes?). Anyways, I would say C is the better answer, even if you can't eliminate A, just think which one would make transmission better.

 

[MediumDef]

It's easy to narrow this down to A and C. I would eliminate A just based on knowledge that when receptors are exposed to a constant and unchanging stimulus they can become desensitized to it. Like if you walk into a room that smells really weird, after a few minutes you'll get used to it and won't smell it anymore. Or let's say someone wants to get wet and jumps into a pool; after he jumps in, putting more water on him won't make him wetter, since every part of his body is already wet...but if you could hypothetically add more areas of dry skin to him (extra receptors) then you could make him wetter by putting water on those extra dry spots. Idk, maybe that was a bad analogy.

I would say that if you have more receptors, then the acetylcholine has a greater chance of binding. If you add more acetylcholine to bind to a limited amount of receptors, there really won't be any change in transmission because the receptors are probably close to their Vmax anyways (can you use Vmax in terms of receptor-ligand complexes?). Anyways, I would say C is the better answer, even if you can't eliminate A, just think which one would make transmission better.

Essentially correct. Inhibiting cholinesterase is actually the way nerve agents work and this makes it impossible for physiological function since the saturation of the synaptic cleft and the post-synaptic receptor just shuts the whole thing down.

 

[inthebay]

key word: repeated

 

[rotatedline]

Essentially correct. Inhibiting cholinesterase is actually the way nerve agents work and this makes it impossible for physiological function since the saturation of the synaptic cleft and the post-synaptic receptor just shuts the whole thing down.

Right. I was trying to use nicotine as an analogue to a cholinesterase inhibitor even though they are not similar, I just don't think it came across correctly. The important thing is desensitization and receptor shut-down.