Week 1: Bessa and Santarelli

I started reading the paper by Bessa et al. first, and I thought that it was helpful to get a preview of the Santarelli et al. paper from the first group’s perspective and to predict their main results in the context of Bessa et al.’s findings. It was interesting to see, in one hand, how Bessa et al. not only highlighted the potential contribution of neuronal plasticity in depression, but also emphasized the results from Santarelli et al. on the role of neurogenesis in studying the pathogenesis of this mental illness. On the other hand, Santarelli et al. briefly presented in their introduction the uncertainty of the contribution of different factors, including dendritic shrinkage and decrease in neurotrophins, but quickly moved on to focus solely on the role of neurogenesis. In other words, the wider context provided by Bessa et al. seemed to be more inclusive and convincing from the beginning.

Apart from the contexts provided, the fact that Santarelli et al. based all of their behavioral assessment only on the NSF model makes their results restricted compared to the different paradigms used by Bessa et al. Although both authors found that neurogenesis is involved in the modulation of depression when using the NSF model, Santarelli et al didn’t fully present a clear picture of its mechanism. At the same time, Bessa et al talked about how it could be implicated in the integration of new neurons impacting emotional behavior, but still considered that to be a non-critical event. To me, it seemed to be more of a difference in perspective between the two groups.

Overall, I thought that the specific approach taken by Santarelli et al. was less convincing than the general wider perspective of Bessa et al. Neurogenesis seems to be involved in one way or another, but the idea of considering neuroplasticity factors seemed more promising given all the findings on volumetric and dendritic changes presented. That being said, I think it might be important for future studies to still consider the role of neurogenesis but going beyond the role of only the 5-HTA1 receptor. Other adrenergic receptors could possibly have a specific contribution in neurogenesis that ties back to the changes in neuroplasticity. Furthermore, exploring any possible interaction between neurogenesis and neuronal remodeling could be more helpful in the future than just considering one to be more critical than the other.