Skip to main content

Final paper proposal

The mental illness I’d like to focus on for my final paper is bipolar disorder. It’s one that we haven’t fully touched on in class. We spent a few weeks discussing depression but haven’t discussed mania yet. Learning about mania after learning about depression would be interesting because then I could think about how they might relate and be two different extremes of the same neurological processes. I would like to learn more about the biological basis of mania and also how it combines with depression to create the cycles of depressive and manic episodes.

It’s also a mental disorder that I’ve seen portrayed in several shows that I’ve watched lately like Modern Love and Spinning Out. I’d like to take this opportunity to learn more about the mental illness in general to see if the popular culture portrayals of the illness are accurate.

Behavioural sensitization to repeated sleep deprivation in a mice model of mania. (2008)


Lateral hypothalamic kindling induces manic-like behavior in rats: a novel animal model (2014)


Evaluation of the effects of lamotrigine, valproate and carbamazepine in a rodent model of mania.


Animal Models of Bipolar Disorder and Mood Stabilizer Efficacy: a Critical Need for Improvement


Genomic variants in an inbred mouse model predict mania-like behaviors


Comments

Popular posts from this blog

Gut-Brain Interactions: Buffington et al, Reber et al 2016

April 13 Papers (Buffington et. al, Reber et. al) I found this week’s papers to be quite novel in that they both proposed potential treatments for neurodevelopmental or psychiatric disorders that target bacterial or microbial abnormalities and how these give rise to certain behavioral and physical symptoms associated with the disorders. I thought this was a very unusual yet interesting approach, and as I have not previously studied the gut-brain axis, these papers offered me a fresh perspective on researching psychiatric and neurodevelopmental disorders. They were also unconventional in their focus of the physical symptoms that often accompany mental disorders, as this is not something that I have seen many other papers touch upon very much. Particularly, I was surprised by the Reber et al paper’s focus on the link between psychiatric disorders and inflammation in organs other than the brain, such as the colon, and the Buffington et al paper’s description of a relationship between ...

Gut-brain axis

This weeks papers Reber et al. 2016 and Buffington et al. 2016 present a super interesting look into the gut-brain axis. Regarding both of these papers, it was amazing to see how potent favorable or unfavorable gut microbiome compositions are in affecting neuronal signaling and overall behavior. Reber et al. shows how immunoregulatory immunization with specifically heat killed M.vaccae can serve as a protective factor against chronic subordinate stress induce colotis as well as behavioral symptoms due to chronic stress as such. Interestringly, this paper depleted regulatory T cell activity via the anti CD25 antibody in order to show that the antiinflammatory mechanism induced by m vaccae immunization is depented on the secondary regulatory mechanisms offered by Treg proliferation and signaling. But, when T reg signaling was removed, this did not seem to cause a significant change in behavior . Therefore, this begs the consideration of what othe rmechanisms may be at play in order ...

Ramirez et al.: 2013 and 2015 Papers

In these papers, Ramirez et al. strive to understand how memory encoding via optogenetic manipulation of engram-bearing cells in the hippocampus, specifically the dentate gyrus, can affect an animal’s response to a stressful context.  The first paper, published in 2013, was crucial to the field as it introduced this very exciting technique; in this paper, Ramirez et al. use tet-tag to manipulate brain circuity and establish associations between two contexts. Throughout the paper, this is referred to as “false memories.” Using these artificial memories, the investigators are able to manipulate the animal’s fear response in a specific context. Specifically, after the animals are conditioned to a repeated fearful stimulus (a foot shock, in context B), activation of the involved DG cells in a different context (context A’) will also initiate a fear response (in absence of any foot shock). In this experiment, the false memory is used to create an unnatural fear association in a given...