Chaudhary et al. (2012) and Tye et al. (2012)

Chaudhury et al. (2012) and Tye et al. (2012) wrote very different papers. One difference is that the focus of their papers were slightly varied. Chaudhury et al. (2012) focused on what type of dopamine firing in the VTA that can cause a susceptible phenotype. This paper also examined both the VTA-NAc pathway and the VTA-mPFC pathway. On the other hand, Tye et al. (2012) focused on the mechanism behind dopamine’s involvement in depression.

 

What I found most interesting about the reading was how the two papers had very contradictory findings about the role of VTA dopamine neurons and depression. Tye et al. (2012) found that the inhibition of VTA dopamine neurons induces a depression-like phenotype, while phasic activation of these neurons relieves these symptoms. Contrary to this, Chaudhury et al. (2012) found that enhanced phasic activation of VTA neurons caused mice to exhibit an increase in the depression-like phenotype.

 

I think that the difference in findings is likely due to the differences in their methods. Tye et al. (2012) used a chronic mild stress paradigm that is very similar to the one that we read about last week. Chaudhury et al. (2012) used a social-defeat stress paradigm in which the mouse was placed in a breeder cage and physically attacked for two minutes. These two paradigms obviously induce very different kinds of stress. One is chronic, while the other is acute. I have learned in many of my classes that chronic stress and acute stress have very different effects on the body. Also, while the chronic mild stress paradigm is merely an annoyance to the mice, the social-defeat stress paradigm seems as if it could actually put the mice in danger of being harmed. To me, this seems almost traumatizing to the mice. If you take a college student who has been chronically stressed due to homework and job demands, they are going to show clear symptomatic differences from someone who was placed in a room with a stranger who threatens to attack them. It is definitely possible that the brain chemistry is also reflective of these differences, and perhaps in chronic stress VTA dopamine neurons fire less, while in acute stress they have increased activation. I believe that some of the differences seen in these papers could definitely be a result of the paradigm used.