Skip to main content

Paper Response #5: Sial 2016 and Allsop 2018


WEEK 7: Feb. 24 Papers (Sial et. al, Allsop et. al)

Sial et al’s 2016 paper describes a new experimental paradigm that can be used to induce stress in mice in a laboratory setting in order to study the neurobiological intricacies of stress and stress-related disorders such as PTSD. Importantly, this new Vicarious Social Defeat Stress (VSDS) paradigm includes a witness component where one mouse witnesses another mouse go through a traumatic event (physical stress) but does not experience physical stress itself. The study found that witness mice will still become emotionally stressed and express symptoms such as social avoidance and other anxiety-like behaviors after watching another mouse be physically attacked The VSDS paradigm is used to differentiate between physical and emotional stress and is a key development in the study of PTSD, as this disorder can be developed after simply witnessing a traumatic event without the need to have been directly involved in it. I think this new paradigm is a very interesting and necessary experimental development, as many of the other papers we have read throughout the semester have not made much of an effort to differentiate between several mental illnesses such as depression, anxiety, and PTSD that are distinct from one another despite having overlapping symptoms. Increasing specificity in the study of mental illnesses can only be beneficial in furthering our understanding of them, and crucial information regarding the neurobiological mechanisms behind these disorders may be uncovered by paying greater attention to the details that differentiate their respective symptomologies. 

Allsop et al’s 2018 paper examines the neuronal connections that underlie observational learning and socially derived information. The study shows that innervation from the Anterior Cingulate Cortex (ACC) to the Basolateral Amygdala (BLA) is essential for encoding information learned from observing others, including observational fear conditioning. This paper ties really nicely into the Sial paper, as it provides more specific insight into the neurobiological mechanisms responsible for encoding fear information for the witness mice in Sial’s study. The Allsop paper compliments the Sial paper and provides some answers as to how witnessing a traumatic event leads to emotional stress on a neuronal level, or at least the very first steps in that process. It is not unreasonable to say that a gap remains to be bridged between the initial observational learning driven by ACC innervation to the BLA and this resulting in lasting emotional stress. What other brain regions and neuronal signalling pathways are involved in this process?

Furthermore, the Allsop paper discussed how prior experience leads to more robust observational learning, which was not something the Sial paper touched upon. It would be interesting to see if previous experience would also predict greater emotional stress in witness mice in the VSDS paradigm. However, this may complicate the mapping of these findings to real-life clinical cases in which a witness to a traumatic event develops PTSD despite not having any present or previous experience with the given trauma themselves. I’m unfamiliar with any research that may have been conducted into whether a person is more likely to develop PTSD after witnessing an event if they have previous experience with related trauma. 

Lastly, the results from Allsop’s study can also be more broadly applied to other psychiatric conditions beyond PTSD that involve social observation and learning, such as autism and social anxiety. Despite earlier praising the increased specificity of the VSDS paradigm in studying PTSD, there are also benefits to be reaped from uncovering basic neurobiological pathways like the one in Allsop’s study that can open many new avenues of research into a broader range of clinical disorders. 

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...