Skip to main content

Post 5: Observational fear learning and its underlying neural circuitry



Animals can learn and experience fear by observation in their environments. Especially in humans, not all situations of trauma have to do with a direct physical stress but also an emotional component, which might stem from observation. Sial et al. aims to establish a model that untangles direct physical fear experience from emotional fear by placing mice in an observational position to fear. It is seen that even in this emotional stress model that corticosterone levels and anxiety-related behaviors are upregulated even in re-exposure after one month. It is interesting to consider the reason for this observational fear to have such a profound effect on the mice as it might be an evolutionary mechanism in which either is a feeling of helplessness in being able to help out a fellow specie or an interoceptive pain response or conditioning that happens through observation. If the true underpinnings of such response could be further parsed out, this could have far-reaching implications in formulating studies to assist those with human PTSD by understanding the mechanisms behind the root of their trauma. Both situations are very real scenarios in which can cause significant trauma. 
            Allsop et al., examines the neural circuitry underlying observational fear learning to find that ACC neurons that project to the baso-lateral amygdala preferentially encode these situations and are necessary to respond only to observed fear but not direct physical fear. Interestingly, when these ACC->BLA neurons were inhibited only during the observational conditioning did the freezing response decrease when cued. Therefore, this truly reinforces that this circuit is responsible and could definitely become a therapeutic target for subtypes of trauma-related conditions. A very interesting observation made was that prior experience with the stressor was needed in this study in order for the observational learning to be affective. It would be good to study other types of stressors such as restraint or forced swimming in order to see if prior experience is still needed. If so, this is intriguing as then observational learning does require a mechanism including memory feedback to recognize another mouse’s fear or pain.

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 ...

Buffington et al. and Reber et al.: Gut-Brain Interactions

While I have not encountered a lot of gut-brain interaction literature yet. I found each paper unique and fascinating. Reber et al felt inaccessible for me. I felt like I didn’t understand what the goal of the paper really was and why they did the tests that they did. It seems like most of their relevant information got shoved into numerous supplementary figures and their behavior was quite difficult to follow. Multiple sections of their paper were supported with data found entirely in supplementary figures, which makes it difficult to follow the same conclusions. I have a few issues with the behavior they chose and because of this, I struggle to find driving conclusions from their work. I don’t understand why the CSC was not only the prior stressor but was also the acute stress condition both groups faced. To me, I feel like it would have made more sense to have the CSC be the prior stressor and then judge the effect on social behavior with maybe a three choice chamber test or te...

Buffington et al (2016) and Reber et al. (2016)

This week's articles were about the role of the gut-brain axis in neurodevelopment and stress. Reber and colleagues used a heat-killed version of the bacteria, M. vaccae, as a type of vaccine and found that administration to mouse models resulted in decreased response to chronic stress, prevented colitis related to stress, and reduced measures of anxiety. Reber et al. also used the inactivated M. vaccae in a mouse model of IBD and found that the bacteria prevented stress-induce flare-ups of colitis, but that this could be reversed by removing T cells. Buffington and colleagues instead examined the role of gut microbiota in maternal high-fat diets (MHFD) in the neurodevelopment and social behaviors of their offspring. Buffington et al. found that housing MHFD rats with the offspring of regular diet (MRD) rats prevented social deficits in their offspring. They also found that this co-housing arrangement prevented an imbalance in the gut bacteria Reber and colleagues' findings w...