Week 3

I found this week’s two papers to be very interesting to read. Both papers explored how optigenetics can be used to alter memory formation, but the 2015 paper seemed to expand dramatically on this concept in just the two years between publication dates. Of the two papers, I preferred the 2015 Ramirez et. al review. I was not entirely convinced of the results of the 2013 paper; I find it difficult to prove whether a false memory does or does not exist in an animal model, as this the mechanisms behind this concept are unclear even in humans. Furthermore, as my peers have mentioned, a false memory is defined as recalling an event that never happened. However, the mice that froze when exposed to a new context were recalling a shock received in context B; this arguably does not meet the definition of a false memory, as these shocks actually did occur, but a different context. I therefore found the results of the 2015 paper to be much more convincing. I appreciated how Ramirez distinguished between anxiety and depression paradigms; he also used multiple paradigms to induce a depressive state to strengthen their findings that positive memories can suppress depressive behavior. I also appreciated how Ramirez displayed that the positive memory alone does not suppress depressive behavior, but the activation of cells associated with the positive memory is required to ameliorate depressive symptoms.

The therapeutic value of the 2015 paper is fascinating; optigenetic controls could potentially be applied to humans in the future to alleviate depressive symptoms. While Ramirez mentioned that anxiety symptoms were not recovered through activation of positive memories, I would be interested to see more research if anxiety or other psychiatric illnesses could be ameliorated in animal models through other forms of optigenetic control.