1. What is the central idea of this paper (or the central ideas)?2. A hallmark of clinical depression is atrophy of the hippocampus. What are some observable behaviors associated with depression? What role(s) does the hippocampus play normally? How do you think this lines up with the clinical presentation of depression? What does the HPA axis mean?3. Describe the method used for inducing depression in mice. How do the authors show that the mice are actually showing signs of depression? What is the tail suspension test? In the analysis of the tail suspension test, why do they use a two-tailed test when mice only have one tail (this is sort of a dumb dad joke but really, what is a two-tailed test)?4. How do the authors attempt to depress other mice, without using the “standard” method of question 3?5. What is the difference (most relevant to what they’re studying) between using a pathogen-free mouse and a mouse that has been treated with antibiotics?6. The authors observe no difference in the baseline corticosterone level. Why mention this? What is corticosterone known for (relevant to what they’re studying)?7. What specific findings do you think caused the authors to consider a role for eCB metabolism in this gut-associated depression?8. What is mTOR and what does its phosophorylation mean (both literally, “what is phopshorylation?” and what is the expected result of mTOR phosphorylation in the hippocampus?) I should probably talk about Western blots and phosphospecific antibodies9. What dietary or microbial interventions were able to reduce or reverse the depression-inducing effects in mice? There was a specific species of bacterium — why did they think to try adding that one (not a trick question)?10. How do the authors explain the beneficial effect of [the bacterium from question 9] on depression and anxiety? What evidence do they present to back this claim up? Would you say it’s convincing? Why or why not?
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