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Bio Class 5 - Systems Chapter 2 ICE
Victoria_5738
#1 Posted : Friday, July 30, 2021 3:14:16 AM
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Hi! I have a few questions about the Biology (Systems) ICE 2 (Nervous System) from today, specifically Passage 3. I was quite confused about the passage overall, as well as a few details in the answer choices & answer explanations.

Passage:

1. Since stimulation of the Na+/K+ pump results in *hyperpolarization*, does this mean that hyperpolarization is also what triggers an action potential in this case? Or is it that hyperpolarization still inhibits an action potential, but it's the *lack of an action potential* that acts as a "positive" signal?

For question 34:

2. How do you know that ouabain does not affect E(Nernst)? What factors *do* affect E(Nernst)?

3. What are the general implications for poisons binding to receptors in the body? Do they act as competitive antagonists for the intended ligands, thus preventing the mechanisms usually triggered by ligand:receptor binding?

For question 35:

4. The answer key for this question states that the Figure 1 "results indicate depolarization." Is this referring to the fact that nicotine causes the RMP to be higher -> less negative -> more depolarized?

5. What passage information leads to the conclusion that nicotine exposure desensitizes the nicotinic ACh receptor? The answer key's justification for this being correct was that repeated binding would logically/naturally desensitize the receptor, but I had trouble making this assumption because I thought it could be a case where repeated exposure results in increased sensitization.

6. What exactly is protein expression? My understanding was that it refers to the extent to which a protein is active and functioning, and that expression is usually modified at a genetic level (designation of introns/exons, methylation, etc). So, for example, overexpression would mean that the cell is creating and activating too many proteins, leading to excessive function.
a. Is this understanding correct?
b. Which other mechanisms might cause protein expression to change?

7. In the answer key, it states that "stimulation by nicotine must cause the isoform to be underexpressed," which was a conclusion made from the fact that "the results indicate depolarization" (which I'm assuming refers to the fact that nicotine lowers the RMP).
a. Does this mean that nicotine is *inactivating/lowering the activity* of alpha-2 Na+/K+ pumps?
b. My understanding was that nicotine could inhibit protein function through competitive antagonism, possibly by binding to the ligand-gated pumps - is this correct? If so, I'm having trouble seeing how this counts as "underexpressing" the protein itself, since (as mentioned above) I thought this required a genetic change. If incorrect, through what mechanism would nicotine affect the Na+/K+ pump expression itself?

Thank you so much in advance!
INSTR_Shinthujah_131
#2 Posted : Friday, August 06, 2021 6:49:06 PM
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Hi Victoria,

1) My approach to mcat passages is to understand it as given and try not to make assumptions. So what we can tell from that section of the passage is that when Ach binds to the receptor it stimulates Na,K-ATPase activity causing membrane hyperpolarization which changes Na+ channels into their available active state.

2) The passage indicates that "Na,K-ATPase is the only known receptor for the poison ouabain". This suggests that any effects of ouabain have to do something with the ATPase. We also know from the paragraph below that the ATPase generates a potential known as Vpump that contributes to the resting membrane potential (RMP). So as per the question, if we're seeing equivalent RMPs between the experimental and control groups (unlike what we saw in the experiment), its probably something to do with changes in Vpump.

You believe you have the Nerst equation in your neuro notes, I would just be familiar with what the variables of the equation are. The variables of any equation are typically the main factors that affect it.

3) Poisons can have varying effects on our bodies depending on the poison and what/where it targets....they can be competitive antagonists/agonists or allosteric effects. Any information you need will be provided in the passage.

4) Yes, so if you look at Figure 1, you can see that the dotted line (nicotine; representing the grey bars/nicotine treated rats) is more positive than the control group. A more positive resting membrane potential suggests depolarization.

5) I don't believe there is anything in the passage that speaks to the desensitization of the receptor. Typically when we're thinking about external drugs, like nicotine, repeated exposure results in desensitization. This is why people need more of a drug to get the same level of high/effect. If repeated exposure lead to increased sensitization, addiction of drugs wouldn't be an issue, since you would take less drugs to initiate the same degree of effect.

6) Yes, protein expression refers to how much protein is being "expressed". So anything that effects the production (e.g. MRNA degradation factors), modification (e.g. post-translational modifications) , or regulation (regulation by transcription factors or proteins) of a protein would affect how much of it is available for action.

7) A. I wouldn't say nicotine is "inactivating/lowering the activity" of the ATPase. We don't know from the passage or the question stem how exactly things are happening. All we know from our data is that with nicotine, we find a higher membrane potential and we know that the ATPase (which is regulated by the nAChR) causes hyperpolarization. So the answer choices that are given to you for this question are hypotheses of what could be happening....so maybe one mechanism is that nicotine results in underexpression of the ATPase (even with underexpression, we don't know at what level this is happening at...gene, mRNA etc). In order to know, we'd have to do more experiments so we can't make those assumptions.

B. Remember that nicotine is not directly binding to the ATPase. It binds to the nicotinic acetylcholine receptor (nAChR) which regulates the ATPase. So there are numerous secondary messenger-initiated events that can happen. This ties in with my response above (for A) of how we don't know the exact mechanism of what is happening...which is obviously not in the scope of the MCAT.

I hope this helps :)
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