Biology - Neuro Passage Question

[sciencebooks]

*From TPR Online Passages

Passage/information:

The first two paragraphs of the passage describe the process of starting an action potential from the pre-synaptic cell (Ca+ release, etc.) to the post-synpatic cell (neurotransmitter release, AP, etc.) as we should understand.

The third paragraph adds new information:

"Even when the synaptic terminal is not electrically stimulated, spontaneous depolarizations of about 1 mV can be detected with microelectrodes at the postsynaptic membrane. These miniature endplate potentials (MEPPs) result from the fusion of a single synaptic vesicle with the terminal membrane. They occur randomly and at a typical frequency of about once per second. The study of these MEPPs has yielded important information about the quantal nature of transmitter release, because the voltage of each MEPP is equal to a whole number times a certain minimum voltage. This minimum voltage is thought to represent the postsynaptic depolarization resulting from exocytosis of a single vesicle."

Question:

The addition of curare, an ACh receptor blocker, to the synapse should affect spontaneous MEPPs by:

I. decreasing their amplitude.
II. decreasing their frequency.
III. increasing their frequency.

A. I only
B. II only
C. III only
D. I and II only


Answer (highlight):
A

Can anybody explain how they worked through this?

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[Singhp03]

well i cant say if they used the same logic as me, but can state my thought process in arriving at an answer. first I concluded that MEPP is an activated by product of an excited neuron, then I asked by myself how would a neuron get excited?answer was simple, ACh is a major exciter neurotransmitter. Then I connected the question with my understanding of what was happening, an ACh blocker would decrease the tendency of the neuron to get activated and thus result in decreased MEPP by product. this led me cancel III and look at I and II. To cancel I, i thought if MEPP is an activated by product of an exciteory input, its magitude should not be effect by amount of excitation it receives(its either produced or not). Conclusion left only II as a possible answer.

 

[sciencebooks]

well i cant say if they used the same logic as me, but can state my thought process in arriving at an answer. first I concluded that MEPP is an activated by product of an excited neuron, then I asked by myself how would a neuron get excited?answer was simple, ACh is a major exciter neurotransmitter. Then I connected the question with my understanding of what was happening, an ACh blocker would decrease the tendency of the neuron to get activated and thus result in decreased MEPP by product. this led me cancel III and look at I and II. To cancel I, i thought if MEPP is an activated by product of an exciteory input, its magitude should not be effect by amount of excitation it receives(its either produced or not). Conclusion left only II as a possible answer.

Wow, I'm so sorry, I accidentally put the wrong answer. I also reasoned it just as you did and am curious as to why this is incorrect.

 

[Singhp03]

Wow, I'm so sorry, I accidentally put the wrong answer. I also reasoned it just as you did and am curious as to why this is incorrect.

lol flawed reasoning in that case, maybe the spontaneous part had something to do with it?

 

[lunalight]

It would decrease the amplitude of the MEPPs because there are less receptors able to bind Ach but not less Ach being released into the synaptic cleft. So if all of the Ach reached the postsynaptic membrane then you would have an MEPP of 1mV. In this case, you have the same amount of Ach (because adding curare does not change how often the spontaneous vesicles are released), but less places for it to bind so now you may only achieve an MEPP of 0.5mV. Hopefully that makes sense.

 

[sciencebooks]

It would decrease the amplitude of the MEPPs because there are less receptors able to bind Ach but not less Ach being released into the synaptic cleft. So if all of the Ach reached the postsynaptic membrane then you would have an MEPP of 1mV. In this case, you have the same amount of Ach (because adding curare does not change how often the spontaneous vesicles are released), but less places for it to bind so now you may only achieve an MEPP of 0.5mV. Hopefully that makes sense.

Okay, that does make sense. But why does it not affect the frequency? It says a MEPP is caused by the fusion of one vesicle so if less vesicles attached, the frequency wouldn't go down?

 

[lunalight]

Okay, that does make sense. But why does it not affect the frequency? It says a MEPP is caused by the fusion of one vesicle so if less vesicles attached, the frequency wouldn't go down?

No, remember that the vesicles fuse with the presynaptic terminal membrane from inside the neuron. The curare has no effect on the presynaptic neuron, so the same number of vesicles will fuse and release their Ach into the synapse. Thus the frequency remains the same. Only the amplitude changes because less Ach is allowed to bind to the postsynaptic terminal due to the receptors being blocked by curare.

It sounds weird, I know, but if you look at how neurotransmitters are released I think it will make more sense.

 

[sciencebooks]

No, remember that the vesicles fuse with the presynaptic terminal membrane from inside the neuron. The curare has no effect on the presynaptic neuron, so the same number of vesicles will fuse and release their Ach into the synapse. Thus the frequency remains the same. Only the amplitude changes because less Ach is allowed to bind to the postsynaptic terminal due to the receptors being blocked by curare.

It sounds weird, I know, but if you look at how neurotransmitters are released I think it will make more sense.

Aaah, okay, that's what I was confusing in this passage! I don't know what I was thinking. The vesicles bind at the pre-synaptic and then release their neurotransmitters into the synapse. Lol, so much confusion over such a basic concept, lol. Got it, . Thank you.

 

[circulus vitios]

No, remember that the vesicles fuse with the presynaptic terminal membrane from inside the neuron. The curare has no effect on the presynaptic neuron, so the same number of vesicles will fuse and release their Ach into the synapse. Thus the frequency remains the same. Only the amplitude changes because less Ach is allowed to bind to the postsynaptic terminal due to the receptors being blocked by curare.

It sounds weird, I know, but if you look at how neurotransmitters are released I think it will make more sense.

But doesn't the question ask about the frequency of MEPPs, not the frequency of Ach being released into the synapse?

 

[sciencebooks]

But doesn't the question ask about the frequency of MEPPs, not the frequency of Ach being released into the synapse?

I think this line helped me understand a little: These miniature endplate potentials (MEPPs) result from the fusion of a single synaptic vesicle with the terminal membrane.

Because the vesicles with Ach still attached to the terminal membrane on the pre-synaptic side of the membrane, this still occurs, the MEPPs still occur at the same rate (apparently one vesicle = one MEPP). If Ach attaches, then the action potential as we know it occurs in addition to the spontaneous depolarization and increases it's amplitude.

 

[Raiden2012]

I think this line helped me understand a little: These miniature endplate potentials (MEPPs) result from the fusion of a single synaptic vesicle with the terminal membrane.

Because the vesicles with Ach still attached to the terminal membrane on the pre-synaptic side of the membrane, this still occurs, the MEPPs still occur at the same rate (apparently one vesicle = one MEPP). If Ach attaches, then the action potential as we know it occurs in addition to the spontaneous depolarization and increases it's amplitude.

Yea, I remember scratching my head for this question when I first encountered it myself. I reasoned that the influx of ions from the attachment was greater and thus resulted in a larger amplitude and not necessarily the frequency

 

[sciencebooks]

Yea, I remember scratching my head for this question when I first encountered it myself. I reasoned that the influx of ions from the attachment was greater and thus resulted in a larger amplitude and not necessarily the frequency

Yeah, makes much more sense once I reasoned it out. Almost like summation in a way... But not really, lol, because it doesn't quite fit under spatial or frequency summation.

 

[shouldvestudied]

This is a a very poorly conceived question.

I see what the writer is getting at, now that I have seen the answer, but his/her reasoning is specious. Answer D is a much more reasonable answer given the role that Curare plays at nicotinic ACh synapses.

The question clearly defines a MEPP as being the mini-depolarization of the endplate. Thus, if no endpolate depolarization occurs, there can be no MEPP.

The only way that you can arrive at answer A is if you assume that these transient vesicle releases are still causing some kind of post-synaptic mini-depolarization even in the presence of Curare.

Since it is possible to completely silence a nicotinic ACh synapse (which neuromuscular junctions are) using curare, there will be no endplate depolarizations (even mini ones). Therefore there will be no MEPPs and thus both the frequency and the amplitude will decrease.

Of course, the spontaneous single vesicle release will continue to occur at the same frequency, but it won't be producing MEPPs anymore.