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Week 3: Dopamine circuits and recovery from stress

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Chaudhury et al. and Tye et al. present two opposing viewpoints in regards to the mechanisms behind depression and depressive-like behavior. I was surprised to find that both these papers were published in the same issue of Nature in 2012. Whereas Chaudhury et al. establishes two links—one between the excitation of VTA dopaminergic neuron phasic firing patterns and a susceptibility to a depression-like phenotype as well as one between the inhibition of the same VTA neuronal projections to the nucleus accumbens (validated by a social defeat behavioral paradigm and sucrose preference test)—Tye et al. utilizes a tail-suspension test as a CMS paradigm as well as a sucrose preference test to claim that a reduced modulation of dopamine cell firing in the VTA causes depressive-like symptoms whereas the inhibition of VTA dopaminergic projection neurons to the nucleus accumbens increases depressive phenotypes. I would assert that both arguments are backed with adequate research models and extensive methodology sections, (using similar optogenetic, chemogenetic, and electrophysiology techniques to derive their conclusions), and hence both are sound and demonstrate validity. That being said, the question isn’t which paper is “right”, but rather, how can we use the combination of the two to further develop a model for how depression works. It’s a well known fact that depression is one of the most complex psychological phenomena, as it manifests itself in such a multitude of ways across the board. Furthermore, it’s often accompanied with various forms of anxiety—whether it be social, GAD, PTSD, etc.—and each individual prognosis expresses different symptomatic behavior. After reading the two review articles on Scientific American as well, it becomes clear that the Chaudhury et al. repeated social defeat paradigm attempts to induce a stress model that is objectively more severe than the chronic mild stress model used by Tye et al. It brought me to thinking about how although we often assume the mesolimbic dopamine system is modulated by more or less the same pathway, every different type of stress model causes varied downstream pathway effects, and we still have ways to go in the field before we truly understand depression in the brain. 

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