Skip to main content

Post 5: Vicarious social defeat and observational learning

Our studies this week discussed two different aspects of fear learning and conditioning in the contexts of vicarious stress and observational learning. I thought both groups of researchers did a fantastic job setting up their experimental groups and establishing control parameters. For instance, Sial et al (2016) specified how the social defeats were performed in a separate room so as not to influence control animals and how aggressor mice that consistently wounded the stressed/control mice were removed and not included in the data set. As I’ve mentioned before, I do not have hands-on experience with mouse research and having these details specified makes comprehending the articles much clearer. 

A few questions that came up: Allsop et al (2018) noted how experienced and naive observers showed increase interaction with the demonstrator mice, possibly due to ‘empathic processes’ or the ‘social buffering of stress’. Although not a primary focus of the paper, this was the first time these terms have come up in our discussions. What research methods are currently in practice to study empathy? Do studies ever focus on empathic behaviors or is it usually only something noted in addition to the main study?  

I was also intrigued by the conclusions made about the necessity of the ACC —> BLA circuitry for certain memory pairings. The paper notes that the BLA receives social information specifically during the cue presentation and it is therefore what ultimately makes the pairing stick. So, could the ACC potentially play a similar role for other types of memories that are not socially motivated? In some response, the authors later mention how they performed reciprocal inhibition (i.e. BLA —> ACC) and it did not affect observational fear conditioning. Perhaps there is some credence then to the reverse pathway playing a role in encoding different types of memories and experiences that might not be socially derived. 

Lastly, I kept thinking about the role that mirror neurons might play in these types of experimental setups. It is known that these neurons fire when we perform an action but also when we observe someone else performing that same action. With the limited knowledge I have about the topic, I think it is reasonable to think they must be somehow involved in the pathways discussed here and I'd be interested to know if anyone has experience or insight on that hypothesis. 

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...