Week 2: Dopamine Neurons & Depression

Both of this week's papers focused on the effects of dopamine neurons on animal depression models. Specifically, the focus was on the dopamine neurons in the ventral tegmental area (VTA) - a main source of dopamine in the brain. Although both papers were released in the same year, used the same method of optogenetics, and even performed many of the same tests, these papers found opposite findings:
Tye et al found that selective inhibition of these VTA dopamine neurons will induce what they call a "depression-like phenotype" in the animal models, while stimulating the neurons will actually reverse that phenotype.
Chaudhury et al, on the other hand, found the reverse: that optical stimulation of the VTA dopamine neurons will induce the "depressive" or "susceptible" phenotype.
Of course, there were important differences among the studies including some of the tests, the amount of stress, etc. While at first it seems as though they are completely contradicting, I think this is actually a nice example of the complexities of stress, depression, and modeling them in animals, and that the two studies may actually work together. Tye et al used a chronic stress model (contrary to what we saw in last week's papers). I found this interesting because it is slightly more applicable to human depression, opposed to the short term stress induction in the other studies we saw. Chaudhury et al, however, used a social defeat model, which again represents a different aspect of depression/stress in humans. As I learned in previous classes, stress can manifest differently depending on duration, sex of the organism, and other factors, so I think it is perfectly reasonable for these two papers to have found opposite findings with such different models of stress. In addition, dopamine affects many brain processes and is involved in much more than just depression and stress, so there is clearly much more to learn. Just as in last week's articles, these two go to show that when modeling mental disorders in animals, there is a variety of ways to go about it, and we must be careful when interpreting those results. I find it fortunate that Tye et al and Chaudhury et al came out with opposite findings in the exact same year, showing this necessity of careful interpretation of results, as well as careful representation of human disease in animals.