Skip to main content

Post 6

My initials thoughts when reading Ayhan et al. 2011 is that modelling schizophrenia based on a single gene mutation seemed like an oversimplification of a complex disorder. However, I do realize how difficult it is to even attempt to model this disorder. I thought it was really interesting to see that the gene expression has to happen at particular critical periods in order to cause changes in behavior.  This is something we have been talking about a lot in the class Brain, Behavior, and Immunity (BBI). Something else we have been talking about a lot in BBI is that these critical periods are usually very different in females and males. This paper used both females and males and there are differences in behaviors between genders with the forced swim test (FST) and tail suspension task (TST) but the paper never offers a thorough explanation as to what they might think this means. I would have like their thoughts on the differences in critical period between females and males with schizophrenia for this gene.

The second paper, Burrows et al. 2015, was my favorite of the two and takes a very different approach to modelling schizophrenia. I was actually unaware that environmental factors needed to be taken into consideration with schizophrenia; I was under the misconception that it is a purely genetic disease. I had seen the environmental enrichment (EE) paradigm used in studies of depression but to see it implemented in this context was very cool.  I was a little confused as to why this paper did not also use an environment derived paradigm (small cage without standard bedding maybe?) as additional comparison for the differences between the knockouts, as I feel like this would have provided even more support to idea that EE is responsible for altering behavioral impairments.

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...