The two papers being discussed this week, Tye et al and Chaundhury et al, both explore the effects of controlling midbrain dopamine neurons on depression-related behaviors. However, they bring about differences in results, which can be attributed to the models used. Tye et al showed that chronic mild stressors (CMS) decreased firing of dopamine neurons in the VTA, whereas Chaundhury et al showed that social defeat (analogous to more severe stressors) increased the firing of dopamine neurons in the VTA. I found this to be an interesting observation because it shows the complexity of the dopaminergic system in the midbrain and how multiple experiments showing different stressors are needed to show the varying effects of dopamine on depression. Thus, you cannot read Tye et al, for example, and simply say that increased dopamine produces anti-depressant-like behaviors because it differs based on the type of stress. The study of depression can be very problematic in this sense and requires immense time, care and research.
Last week’s discussion on the effects of serotonin and norepinephrine in the hippocampus on depression and this week’s discussion on the effects of dopamine in the midbrain on depression further show the complexity of the mechanisms of depression and make me want to learn more about these different processes and if they are at all related. In this week’s papers, the effects of modulating dopamine firing on depressive behavior occurred rather quickly, as compared to last week’s slow-acting antidepressant effects on neurogenesis and neural plasticity. Since current antidepressant use on humans is slower acting and can take weeks, researchers should develop more experiments on altering the dopamine system (such as this week’s papers) so that effects can occur swifter in humans. Further exploration in this subject is extremely important because of the complexity of depression and the fact that millions of people are affected by it.