Skip to main content

Post 6

I was really interested to read the papers on schizophrenia animal models because schizophrenia seems to be a much more complex, internal mental illness than some of the other ones we’ve seen and its symptoms sound like they would be harder to cause and also observe in animals, especially in rodents. Some of the big symptoms that come to mind when I think of schizophrenia are hallucinations, delusions, and changes in speaking. From the little that I know about rodent research, I would imagine that these would be hard to observe in mice or rats. The Burrows (2015) paper focused on three symptoms, prepulse inhibition, long term spatial learning, and spontaneous hyperactivity. These few symptoms put together do not seem like a comprehensive representation of schizophrenia. I think this combined with my lack of background knowledge on the role NMDA plays in schizophrenia made it hard for me to fully understand how the Burrows (2015) paper really related to schizophrenia. The use of the mGLU5 receptor built off the assumption that the NMDA receptor is involved in schizophrenia. Does the NMDA receptor research that this mGLU5 receptor built off of also only use a few, unrepresentative symptoms to model schizophrenia? I could see this snowballing into a problem where research builds off of research that doesn’t fully and accurately model the illness it is supposed to model. How can scientists and journals stop this kind of domino effect?

We’ve discussed several times in class about how research has been using only male mice in experiments and leaving out female mice and we finally have a paper that uses both male and female mice in their research. It’s especially interesting that this particular research uses both male and female mice because it deals with prenatal development versus postnatal development. Male and female brains develop differently during prenatal periods and as a result are also different during postnatal development so it’s interesting to see here that there are actually differences in male and female behavior and phenotypes which support the stance that females should not be left out of research and that males are not representative of the entire species.

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...