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 :)