Week 1

My initial response to Santeralli et al.’s paper was, “Hmm... I’m fairly convinced”. The central question they aimed to address was whether or not an increase in neurogenesis is required for antidepressant action. I liked how they conducted multiple simplistic experiments to tease apart the role 5HT_IA receptors play for fluoxetine induced, but not imipramine induced neurogenesis. I also found their approach to narrow down the region of the hippocampus susceptible to irradiation to be quite clever. On a side note, (even though this may be a weird observation/question), I didn’t quite understand what the sucrose application on the snouts of the mice had anything to do with grooming behavior of the coat?

Having said that, my confidence in the paper quickly deteriorated when I began reading Bessa et al.’s paper. I immediately noticed that their approach was way more technical, descriptive and detail oriented, diving into further intricacies that Santeralli et al. did not attempt to highlight at all. Their methods employed for inducing and measuring stress (CMS model) were far more convincing than the first paper. I’m starting to see why comparing papers is insightful and beneficial, especially when it comes to believing scientific claims. I was super excited with the finding that “antidepressants not only reversed the anti-proliferative effects of CMS, but also stimulated neurogenesis to levels above those found in controls”. It further emphasized on the relation between neurogenesis and using antidepressants as treatments for depression and anxiety disorders. But I wonder, what would happen with chronic use of antidepressants? Could increased neurogenesis and the lack of simultaneous pruning potentially pose a problem? I know from previous classes that increased dependence on AD may lower baseline levels of those neurotransmitters (for example side effects of SSRI’s, etc.) but if simply increased neurogenesis leads to a permanent increase in the number of neurons, thereby reducing negative symptoms, is it safe to say that AD use can be discontinued once “normal” density is achieved?