Sunday, February 12, 2017

Week 4

I enjoyed reading this week’s papers; these two papers were intricately related, with Yiu et. al’s paper elaborating on the research described in the paper by Han et. al. While the paper by Han et. al sufficiently established a causal relationship between activated over-expressed CREB neurons and memory expression, Yiu et. al clearly provided a greater amount of detail and support to their findings. My biggest complaint involved the Han et. al paper. While I was convinced by the data Han et. al provided, I found myself asking several questions such as “why CREB is so important to activating neurons involved in fear memory” and “what is the difference between strong and weak training.” While some of these questions could have been answered had the paper included more details (I realize this may be a difference between the journals of publication), I appreciated how Han et. al were able to answer these questions and provide adequate details without overwhelming the reader. However, in general I found it difficult to find ways the researchers could have improved their experimental designs. Both papers eliminated every other possibility to verify that their results could not be explained by some other factor and clearly linked each experiment back to their original hypothesis. These papers also used very concise and clear language despite the complexity of their experiments.

In terms of future directions, it is intriguing to consider if there any other transcription factors that could be play a similar role in memory consolidation, or if this is strictly the role of CREB and other excitatory factors. Furthermore, I believe these findings have potential therapeutic value – selectively inhibiting fear memories could eventually be a novel tactic in treating a variety of mental disorders, specifically PTSD. I also find the concept of another neuron being able to selectively disinhibit its neighbors in the process of memory consolidation to be fascinating; I believe this could also hold therapeutic value in discouraging a population of neurons from forming a memory.


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