Contrasting Santarelli et al. and Bessa et al.

     Published six years apart, both the Bessa et al. and Santarelli et al. papers took a look at what happens in regards to the structure changes of the hippocampus in rats when placed under chronic stress and treated with antidepressants. Santarelli et al. hypothesized that neurogenesis was required for antidepressants to be effective, yet Bessa et al. showed that this is not the whole story. Santarelli et al. were on the right track in that antidepressants do indeed stimulate neurogenesis, but neurogenesis is not necessary for mood-alteration during the treatment. Bessa et al. concluded that antidepressants stimulate “neuronal remodeling and synaptic plasticity” which do seem to be relevant to overall mood changes in the lack of neurogenesis. 

     I think it was smart of Bessa et al. to focus on a very specific aspect of the question “how does depression work?” It is extremely important to avoid researching too broad of a topic, and therefore to perform a thorough experiment. Santarelli et al. may have had good intentions, but I feel that they may have been looking at too broad of a topic and at the same time did not delve deep enough into it. The novelty-suppressed feeding paradigm was exclusively used, and a better picture may have been painted if more varying types of data were collected. Bessa et al., on the other hand did just this. They looked at a few more facets of depression as seen in humans. They assessed anhedonia via the sucrose preference test, learned helplessness via the forced swimming test, and anxiety-like behaviors via the novelty-suppressed feeding test as well. An overall clearer picture was visualized via the results of these experiments and there were fewer lingering questions.

     One thing which will always stand out in animal studies is the relevancy of these results to the human situation. With a common goal to better understand the mechanisms and causes of human illnesses and disease, rats are a commonly used as subjects. One has to wonder, however, if they are an appropriate model for the human brain. Both articles tackled the task of mimicking this human illness pretty well (via the use of knockout mice and the use of methylazoxymethanol), but we may not know for a long time if these models are good enough.