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Post 2- Dopamine Circuits and Recovery from Stress

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Tye et al and Chaudhury et al both elaborate on a mechanism available to indicate the relationship between depressive behaviour and dopamine neurons in the brain. Both papers use the methodology of optogenetics in the vental tegmental area (VTA) of the brain. However, the two research groups obtained contrasting conclusions. As this needs to be investigated with more scrutiny, it can primarily be agreed upon that the mechanism of depression is very complex. Depression affects individuals and animals differently, which needs to be taken with large consideration. 
Tye et al used behavioural, pharmacological, optogenetic and electrophysiological methods in mice to investigate the effect that dopamine has on depression, affected by chronic mild stress. They silenced VTA neurons which made normal mice behave as if they were stressed. They then stimulated the VTA with light and found that in this instance animals showed a reduction in time spent struggling and a reduction in anhedonia-like behaviour compared to when no light was present, thereby a sign of depression. This is potentially due to that dopamine neurons were turned off, decreasing the amount of dopamine available which is related to an increase in depressive behaviour. 
Moreover, Chaudhury et al, whose paper is published in the same journal, in the same year, exposed mice and rats to another more intense kind of stress known as social-defeat stress. This more severe kind of stress and depressive behaviour in mice resulted from an increase in VTA firing dopamine activity. It remains very questionable as to how these two papers could have similar procedures and technology and yet yield different results. However, it may be due to that there are many different routes of depression affecting areas of the brain. It may also be possible that the type of stressor affected the rodents’ response. It is also important to note that Chaudhury et al investigated mice only, and Tye et al used mice and rats in their experiment. This could potentially have an overall effect on the difference in results, and may be essential to consider when attempting to apply similar findings to depressive behaviour in humans. 
In a paper by Warden et al, A prefrontal cortex-brainstem neuronal projection that controls response to behavioural challenge, mPFC was stimulated in rats. The results presented a decrease in depressive behaviour. The study suggests that this is due to serotonin, but it may also be possible that there were circuits involved that relate to the dorsal raphae nucleus (which mPFC projects to). Adding this study to the considerations of Tye and Chaudhury’s findings, it is questionable as to whether serotonin or dopamine or both are the most influential in brain circuits and their relation to depression, again emphasising the complexity of the disorder. 
In summary, the two papers were comprehensive in the investigation of dopamine in depressive like behaviour; however, I yet wonder how they were able to reach such contrasting conclusions. It may potentially be due to the methodology, circuits of the brain, statistics or simply confounding variables, but is yet a large question that remains in the research of depressive behaviour and optogenetics. 

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