This week’s papers both Ramirez et
al and Yiu et al were focused on memory in relation to fear as to model PTSD. Ramirez et al focused on creating false
memories and activating such with light while
Yiu et al focused on the excitation of LA neurons and their role in memory
recall.
Even though I understood the
overall picture of Ramirez et al paper some figures were really confusing,
mainly because it was confusing to keep track what were the context in which
they were originally fear trained and where they were tested etc. It would be
rather helpful for it to be split up into more concrete sections including a
discussion section. They were probably
constrained by the journal to a specific amount of pages and thus it makes it
harder to understand the study in such few pages.
However, I found the material studied incredibly interesting and understand this can definitely be applied to humans. It is very typical for people to suffer pains that aren't really vivid and believe in the occurrence of false events. Treatment could be based on replacing memories of real events by creating artificial memories. Based on the methods used in this experiment, then it might seem invasive and confusing on how to activate these genes in order to create or erase these false memories, however I believe it can be further developed into something such as TMS.
I preferred Yiu et al paper’s structure to Ramirez et al. I like the fact that Yiu et al provides a background of what has been studied and then states what they did in order to then provide the results. Yiu et al used three different methods to determine whether higher excitability of neurons specifically before training demonstrated an advantage for neuronal allocation to fear memory.
I really like the use of expressing
dnKCNQ2 in order to compare its effect exciting th neurons with that of the
known CREB. Moreover, I also liked the addition
of the use of Kir2.1 to observe the counteracting of the effects of CREB. These are used as controls as to assure the
hypothesis of CREB and its effects on LA are as expected. I really liked all of the measures used as to
control and make their point on the excitability of the LA neurons and
CREB. For example, Yiu et al also
studied the time frame on which they administered the overexpression and in
fact also studied the overexpression on regions such as the BA and the CeA. This
being the latter work, I believe they could further their studies by including
the overexpression of the genes in other areas that are not the amygdala such
as the hippocampus which was studied by Ramirez et al.
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