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Post 6- Ayhan et al (2011) & Burrows et al (2015)

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Ayhan et al (2011) investigated the effect that the DISC1 gene has on various stages of neural development, and the gene’s influence on major psychiatric mood disorders. The researchers mention the effect that the gene and its mutant has on schizophrenia, but also other disorders such as depression. As I read the paper, it becomes clear that through the substantial number of experiments, the effect that the mutant hDISC1 has differs depending on if it was expressed prenatally, postnatally or both. The researchers' findings support their hypothesis. However, from my understanding, each individual with a mood disorder such as schizophrenia exhibit differences in symptoms as well as brain composition- so how are the researchers able to generalise these findings to all mood related disorders and individuals? 
I would also be curious to know if the immune system plays a greater or smaller role than the mutant gene in neurodevelopment during perinatal periods. In one of my other classes (Brain, Behavior & Immunity), we discussed that there is strong evidence regarding early immune life challenges and their effect on neuropsychiatric disorders developing later in life. For example, maternal flu development during the second/third trimester prenatally has shown to increase the risk of schizophrenia and bipolar disorder in the offspring later in life. Additionally, maternal bacterial infection during pregnancy has indicated an increase in autism development in the offspring. Furthermore, I am happy to see that the researchers included both male and female mice, which is impressive considering that the study was published nine years ago. The findings throughout the paper clearly express that male and female mice exhibit different behaviours, brain volumes and spine density. It is therefore significant to include these variances in studies for more reliability. 

In the second paper, Burrows et al (2015) investigate the effect of glutamatergic signalling and the relationship between schizophrenia and genetic/environmental factors. When reading about glutamate receptors, the first thing that comes to mind is long term potentiation (LTP); the tetanus of EPSPs that occurs as a result of a prolonged glutamate activity involving both AMPA and NMDA receptors. As mentioned in the discussion, LTP appears to be an essential component of NMDA. Due to this, it would be interesting to read even further about the short and long term effects of environmentally enriched condition versus a standard condition have in regards to glutamate receptors.
Another component in the study that may need clarification are the concepts of dendritic spine and density. Firstly, it was mentioned that increased dendritic branching was evident in WT EE but KO mice both in EE and SH were resistant to this plasticity. Additionally, dendritic spine density should predict a significant difference between EE and SH since enrichment increases spine density in general cases. However, the study claims that dendritic spine density reveals no effect between KO and WT mice. What could these two differences depend on? Finally, what is the difference between dendritic spine density and dendritic complexity? Is there any overlap between these mechanisms? 
Overall, the two papers provide further insight and comprehension to the complexity of neuropsychiatric disorders. They also confer interesting perspectives of environmental and molecular levels of behavioural phenotypes in rodents and humans. 






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