Skip to main content

Post 3: Ramirez et al. (2013 & 2015)

            In the first paper published by Ramirez and collaborators, the researchers outlined how they created false memories in mice using fear conditioning. In brief summary, mice were taken off Dox and allowed to explore context A so that their cells could be labeled with ChR2-mCherry. After, the mice were put back on Dox and fear conditioned via shocks in context B while the cells labeled in context A were activated. When placed in either context A or a novel context C, it was shown that the mice froze significantly more in context A, not C, than background levels. This discovery of creating false memories artificially could give us insight into how humans form false memories. I’ve watched several videos of people falsely recalling what a criminal looks like based on external input. I’m also very curious about the psychological phenomenon of rosy retrospection – looking back at past experiences in a disproportionally positive manner. Does this same population of DG cells play a role in that? How do these false memories occur naturally?
            In Ramirez’s second paper, researchers explored an application of these memory circuits to try to suppress depression-like behavior. One of the main findings was that activating dentate gyrus cells that were labeled by a positive experience was able to reverse the effects of stress in the tail suspension test, sucrose preference test, and novelty-suppressed feeding test. The experiment that I found the most interesting was when the researchers explored the long-term rescue of depression-like behaviors. The five days of stimulation of positive memories lead to an increase in struggling in the tail suspension test and an increase in sucrose preference. However, the chronic activation did not ameliorate anxiety-related behaviors as measured by the open field test and elevated plus maze test. The paper speculates that this is due to the fact that the circuitry for these anxiety-related behaviors must be different. As discussed in class, everyone experiences depression differently, and there are many ways in which it can manifest. This difference in circuitry could explain why last week’s papers came to differing conclusions and why people do experience depression differently.

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...