Skip to main content

Brain-gut microbiome interactions

Buffington (2016)
In the figures for experiments that measure interaction time, the authors included a graph for contact duration in addition to interaction time but they don’t mention contact duration in the text. What’s the relevance of contact duration here/what does it add? The results appear relatively consistent with the results of interaction time. I don’t think that the authors would waste previous figure space on graphs that don’t add any value.
I thought the sociability vs. social novelty tests were interesting. I don’t know much about mice so I was a bit surprised that they prefer a new mouse over a familiar mouse. I would have expected them to prefer spending time with a familiar mouse but I guess it makes sense if they want to explore and investigate this novel mouse that has just entered their space. In the experiment examining the effect of social interaction on long-term potentiation in VTA DA neurons, the results show that interaction with an unfamiliar mouse triggered LTP in the VTA (in MRD offspring) but not interaction with a familiar mouse. Along the same lines, this isn’t what I would have expected. I would have expected the opposite results. I would expect interacting with a familiar mouse to be rewarding since the mice would already have a shared bond. Why is social novelty rewarding? I could see exploring a new mouse to reduce anxiety and fear about it but I was surprised that it was actually rewarding to mice.
What is the relationship between sociability and social avoidance? In the sociability test, the MHFD spend similar amounts of time in the empty chamber and the Mouse 1 chamber so while they don’t prefer the Mouse 1 chamber like the MRD mice, they also don’t prefer the empty chamber and from the one activity diagram included, they don’t appear to prefer the middle chamber either. If the mice were to avoid Mouse 1, I would expect to see them spending more time in the empty chamber than in the Mouse 1 chamber. I would expect sociability and social avoidance to have an inverse relationship but here we see decreased sociability without seeing increased social avoidance.
A doubt I still have is that in the co-housing experiment, how can we know how much of the rescue is from shared microbiota and how much is from social learning? The results show that co-housing is effective in rescuing social behaviors and that microbiota individually also rescues social behaviors (from germ-free mice experiment) but I’m interested in knowing how just social learning compares to shared microbiota in rescuing social deficits.
I was confused by the weighted and unweighted UniFrac measures and don’t understand what either of them means so I’m not sure if one of them being significant while the other one isn’t is a bad thing.
I thought it was so fascinating that this one bacteria being present in the gut made such a big impact on social behaviors. I didn’t realize that the brain and social behaviors were so closely linked and that bacteria in the gut could influence neuropeptide levels in the brain. Overall I really enjoyed reading this paper and thought that it flowed really well. The questions and ideas I had about what they should also investigate after each section were answered in the next one and each experiment clearly builds on the results from the last to really strengthen their points and conclusions.

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...