Week Five: Ramirez (2013) and Yiu (2014)

The two papers this week focused on the creation of memories and the neurons that are involved in this process. Ramirez et. al (2013) explored the creation of false memories in the dentate gyrus. Ramirez et. al (2013) found that by activating specifically labeled neurons they could manipulate the animal's memory so that they exhibited an increased freezing in a context that never was fear conditioned. Thus inducing a false memory. I thought this study was extremely interesting; however, relatively difficult to follow. The methods were pretty complex with introducing new contexts, so it took me a bit to grasp what they were doing in each paradigm and the implications of seeing changes. The figures descriptions were also grouped together throughout the paper, which made it more difficult for me to interpret the figures. However, after accepting the methods and the implications of the data, I found this paper fairly convincing. Ramirez et. al (2013) also showed that the creation of false memories was specific to the dentate gyrus area of the hippocampus. Although fairly complex and difficult to understand, I could see the translatability of Ramirez et. al (2013) research to human clinical populations as a potential treatment option. This could be a valuable treatment if we could find a way to create false memories and change aversive memories in humans suffering from PTSD.

Yiu et al (2014) determines that dnKCNQ2 and CREB vectors in the lateral amygdala are preferentially recruited into a memory trace pathway due to their high levels of excitability. Yiu et. al (2014) showed that there is a very small portion (~10%) of pyramidal/principal neurons in the lateral amygdala that actually are recruited into the trace pathway. This study also shows that the neurons that are highly excitable prevent their neighboring neurons from joining the memory trace. Although, I found this paper much easier to understand and follow compared with Ramirez et. al (2013), I had more difficulty finding a way to translate this research to humans as a treatment option for PTSD. I think a lot more further research would have to be done before there would be a way to translate this to clinical populations. Ramirez et. al (2013) shows that you can tap into specific neurons to alter memories and potentially in the future could change humans' aversive memories into positive ones using these same principles. However, Yiu et. al (2014) explores a very small percentage of neurons that are involved in specific memory traces. Perhaps in the future, Yiu et. al (2014) research could be used to identify neurons in the dentate gyrus that are responsible for certain aversive memories, but I think it would be difficult to change the specific excitability of those neurons in humans to diminish aversive memories. Yiu et. al (2014) found that doing training before the microinjection of the CREB and dnKCNQ2 vectors doesn't have an effect on the expression of the fear memory. In human populations, the person has to experience a traumatic event before developing PTSD, so this made it difficult for me to think about translating this research to humans.