The 2011 paper by Ayhan and colleagues used mice models to examine the effect of DISC1 expression during different neurodevelopmental periods on behavioral and mood disorders. Specifically, Ayhan et al. were interested in evaluating components of the neurodevelopmental hypothesis of schizophrenia.
On the other hand, the research by Burrows and colleagues (2015) relied on the glutamatergic hypothesis of schizophrenia to evaluate the role that environmental enrichment has on behaviors while manipulating metabotropic glutamate receptors. This paper had a lot going on, so it was tricky to follow their train of thought. I think this paper strived to make a connection between clinical interventions for schizophrenia and the molecular biology that impacts how a treatment works (or doesn't work). My knowledge of metabotropic receptors, particularly NMDA receptors, is mostly centered around LTP and learning/memory. I don't think any of my classes have really covered the role these receptors play in psychiatric disease, but it makes sense to me that glutamate, which is generally excitatory, could play a role in a hyperactive, hyper locomotive disorder like schizophrenia. Although difficult to follow and often questionable, I thought this paper did a really good job highlighting the need to understand epigenetic effects to truly understand and treat mental illnesses, which are not necessarily controlled by one gene being completely "on" or "off".
The results of the Ayhan paper were more interesting to me—that postnatal Disc1 expression resulted in behavioral and psychiatric dysfunction (schizophrenia-like behaviors in males; depressive-like behaviors in females). After reading the Burrows paper, I went back and re-read the conclusions from the Ayhan paper because I started to think about combining the two seemingly-opposing hypotheses of schizophrenia. Is there some reason why schizophrenia couldn't be controlled by both neurodevelopment and glutamatergic signalling? With our understanding of psychiatric disorders, it seems pretty clear that there is no single thing that determines whether you end up "normal" or abnormal. This led me to think more about other hypotheses of schizophrenia, and I saw that both articles actually cited previous works that examined the dopamine hypothesis of schizophrenia. I didn't read those papers, but I did wonder why neither Burrows or Ayhan mentioned the role of dopamine as a prominent hypothesis—not even to provide evidence against that theory.
On the other hand, the research by Burrows and colleagues (2015) relied on the glutamatergic hypothesis of schizophrenia to evaluate the role that environmental enrichment has on behaviors while manipulating metabotropic glutamate receptors. This paper had a lot going on, so it was tricky to follow their train of thought. I think this paper strived to make a connection between clinical interventions for schizophrenia and the molecular biology that impacts how a treatment works (or doesn't work). My knowledge of metabotropic receptors, particularly NMDA receptors, is mostly centered around LTP and learning/memory. I don't think any of my classes have really covered the role these receptors play in psychiatric disease, but it makes sense to me that glutamate, which is generally excitatory, could play a role in a hyperactive, hyper locomotive disorder like schizophrenia. Although difficult to follow and often questionable, I thought this paper did a really good job highlighting the need to understand epigenetic effects to truly understand and treat mental illnesses, which are not necessarily controlled by one gene being completely "on" or "off".
The results of the Ayhan paper were more interesting to me—that postnatal Disc1 expression resulted in behavioral and psychiatric dysfunction (schizophrenia-like behaviors in males; depressive-like behaviors in females). After reading the Burrows paper, I went back and re-read the conclusions from the Ayhan paper because I started to think about combining the two seemingly-opposing hypotheses of schizophrenia. Is there some reason why schizophrenia couldn't be controlled by both neurodevelopment and glutamatergic signalling? With our understanding of psychiatric disorders, it seems pretty clear that there is no single thing that determines whether you end up "normal" or abnormal. This led me to think more about other hypotheses of schizophrenia, and I saw that both articles actually cited previous works that examined the dopamine hypothesis of schizophrenia. I didn't read those papers, but I did wonder why neither Burrows or Ayhan mentioned the role of dopamine as a prominent hypothesis—not even to provide evidence against that theory.
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