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Post 3- Ramirez et al (2013 & 2015)

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At a first glance, the two papers appear to build upon each other, primarily since they are by the same researchers and published two years apart. With more insight, it becomes clear that one paper investigates the negative, fear emotions involved in memory whist the later aims to investigate behavioural effect on positive memories. These are two separate paths in the brain brain that may relate to depressive behaviour. Thus, the latter includes information and findings from their previous research for further support, strengthening the understanding of brain regions relation to behaviour.
The paper published in 2013, overall aims to investigate the dentate gyrus and CA1 neurons as well as the amygdala in relation to channelrhodopsin-2 and the effect that these have on false memory creation. The research was conducted on multiple brain areas, which became beneficial as it created an understanding to that optical reactivation of cells was contributing to false memories in different circumstances. We know that humans (in addition to mice) have false memories, seen through fMRI data. However, contrary to mice findings, it is yet unclear about the full pathway of the human hippocampus involved in false memories. Therefore, it becomes questionable as to what extent these mouse model findings can be applied to humans. The hypotheses of the researchers are supported through different experimental manipulations, but since the experiment was conducted in a strict lab setting, the effect that the findings have on natural settings may be taken with caution. Thus, the researchers suggest that their observations are consistent with the Rescorla-Wagner model for two independent conditioned stimuli, a model that is prevalent in both humans and animals. 
Furthermore, in their 2015 paper, Ramirez et al elaborate on brain mechanisms, specifically the hippocampus that involves an expansion to more behavioural and positive memories. They emphasize that animal models exhibit “limited but not quantifiable” behaviours. In addition, the researchers investigate even more brain regions in addition to DG, such as the nucleus accumbens (NAcc) and the basolateral amygdala (BLA), all in the attempt to see whether either region exhibited a reduction in depressive behaviours. Their positive memory involved female mouse interactions and the findings also suggested an increase in neurogenesis. Ramirez et al overall claim that depressive behaviours can be reduced by the activation of positive memories in the hippocampus. Thus, they mention that further research is needed to understand why that is. I also believe that other potential scenarios that may yield positive memories in mice, in addition to female mice exposure, could be included in the study for more comprehensive findings. 
Overall, the two papers go hand in hand as the researchers reactivated and stimulated different brain regions in to see if these could alter depressive behaviour of mice. The papers are similar in style and clarity of conveying ideas (since they are written by the same primary authors). However, published in two distinct journals, they differ in section lengths as well as supplementary information.

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