Skip to main content

Week 5: PTSD and Vicarious Fear Condtioning

I’ve been interested in vicarious/social fear learning since I first took the Neuropsychology of Fear in Spring 2017. I’ve been interested in how fear can be passed down through observational learning and the things that influence it. As each of the papers this week build on one another, I want to consider the role of other sensory stimuli in the ACC -> BLA circuit. Ana Pereira from Marta Moita’s lab published a paper a few years ago about the role of silence in the social transmission of fear. They did a similar behavioral paradigm as the Allsop and had an experienced observer watch another rat undergo fear conditioning. They concluded that the rats relied on auditory cues in the environment, namely the silence resulting from the absence of movement in the conditioned rat.  Given the necessity of ACC cells in the social transmission of fear as Allsop concluded, I’m wondering if these two notions relate to one another.  The cingulate cortex is related to many autonomic and cognitive functions, one being hearing and attention. I’d be interested to see if there could be a way to study the connection of the role of auditory cues and the ACC -> BLA pathway.  Perhaps one could replicate the Pereira methodology of conducting observed conditioning in the dark and playing/stopping recorded sounded of rat movements at various times while stimulating or inhibiting the ACC -> BLA pathway in both conditions. This could determine if and what role auditory cues play in the transmission of fear. If the cingulate to BLA pathway is modulated in some part by auditory cues, then freezing would be affected in the absence of silence but not in the absence of visual cues. I’d be interested to see if there is a way to understand how the transference and recognition of other sensory stimuli affect this particular pathway.

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...