Week 4: PTSD Animal Models (Reznikov et. al and Herry et. al)

I really enjoyed the Herry et. al (2008) paper, because it effectively distinguishes between fear and extinction neurons. These neurons are both co-existing in an intermingled fashion in the BA. This study does a great job at showing how specific each of these particular neurons can be, as it shows them distinguishing between tones and contexts. This study also went into connecting these fear and extinction neurons to other parts of the brain, which sets this up for the future to more closely look at how these interactions are working. It would be really interesting in the future to see how these neurons are working in a human brain, and potentially if this firing of the fear neurons could be inhibited to prevent a fearful/anxious behavior. Although, I do think that quite a lot of research needs to be done before something like this could ever be implemented. It was extremely interested that these neurons differentiate due to the same fear conditioning. There is specificity of the neurons located in the BA to only respond to certain factors and then illicit a behavioral response to follow that information.

I enjoyed Reznikov et. al (2015) study because it is finally doing a more longitudinal study and examining the effects of the fear conditioning over time. I think that fear conditioning is an excellent model for PTSD, because an aversive stimuli is giving a differential behavioral response after a significant amount of time. In humans, PTSD occurs and then after a certain amount of time passes they will start having anxiety in particular situations and flashbacks. However, I personally believe that there were some flaws in this study. First, I think that there distinction of the "weak phenotype" and "strong phenotype" were kind of arbitrary. I know that they were trying to connect this to clinical populations where only about 20% of people exposed to a traumatic event will develop PTSD, but I wish that they had some more reasoning behind those particular numbers for distinction of the two groups. Secondly, the plasma corticosterone data to me isn't particularly striking. In my previous coursework, I have learned to correlate corticosterone with a stress hormone in the hypothalmic-pituitary gland. If I had to reason, I would hypothesize that the baseline corticosterone would be higher in the patients that are more anxious. This was discussed in the conclusions and their reasoning behind it was that the weak extinction phenotype mice have to overcompensate for having a lower corticosterone value, which then produces an end result of higher anxiety. With such a big baseline stress hormone difference, I would imagine that there would be more significant differences in the behavioral tests performed in experiment 2 (before the Fear conditioning). I think in the future they should use a much bigger sample size and their data may be more compelling, especially with the correlational data. The middle of the rue in the spectrum of weak/strong extinction animals were included in the correlational data, so that may be accounting for the differences in the correlational graph. I do think that this model is good for PTSD especially because it is looking at a smaller subpopulation and over a greater amount of time, which is highly translatable to clinical research.