When I first began reading Ramirez et al's paper titled "Creating a False Memory in the Hippocampus," I was quite skeptical of the way they would induce and represent a false memory. I was actually quite surprised and impressed with the way they were able to identify naturally activated cells in a certain context and then associate them with a foot shock, therefore creating a "false memory" (or perhaps more like a false association). The various scenarios and experimental groups/controls that they used provided a great deal of evidence to support their hypotheses (although I did have some trouble understanding the figures and am looking forward to further clarification in class). Ramirez et al. were able to successfully isolate a certain group of cells that are naturally activated in a novel context, associate those cells with a foot shock, and then reactivate those cells in either the original or a new context to show the newly formed false memory. Furthermore, they switched the order of events so that they were exposed to both of the contexts before forming the association, and their hypothesis still stood.
Next, they measured the amount of freezing when re-exposing the animals to Context B, where they were shocked. Due to two simultaneous CSs, the animals then froze less. I was a little confused about this section of the paper (specifically Figure 3), but it seems that having two conditioned stimuli (Contexts A and B) cause an overall lower amount of freezing in the mice as compared to just one conditioned stimulus. The researchers touched on this a bit more in the discussion, mentioning competition and interference of stimuli, and I'd be interested to learn more about this, as I'm sure in human representations of fear, there is often more than one stimulus.
Finally, Ramirez et al also conducted a conditioned place-avoidance paradigm in which they found that the experimental group preferred the unlabeled chamber whereas the control groups had no preference. In addition, each of these significant results were regarding cells in the DG. All of their experiments done with CA1 cells lacked significant results, which I found to be interesting. I wonder if they were correct in assuming that CA1 engrams are more temporally dependent, accounting for the lack of results. I did notice however that there were very small groups, which always leads me to take study results with a grain of salt. They also mentioned spatial and temporal importance when justifying why their results differed from previous studies, which I appreciated.
After I finished reading this paper, I was quite impressed with the way they were able to induce the false memory. However, it did cause me to think about possible applications. While I've heard of many human studies that investigate false memories (I believe they mentioned them in this paper), this seems to be more of a "false association" than a "false memory." These researchers used fear conditioning in order to induce it, but I would see the applications to be the opposite - rather than showing a possible reason for the formation of false memories in humans, I saw this to be a potential treatment for PTSD, phobias, or other fear-related issues. While Ramirez et al speculated that false memories in humans "may occur in natural settings through the internally driven retrieval of a previously formed memory..." (p390), I thought of this experimental method to have possible applications in inducing false associations with positive stimuli (rather than fearful ones) to help abolish irrational or extensive fears. Of course this entire field demands much more extensive research, but I could see possible exploration of the use of false associations/memories to treat fear disorders.
In contrast to Ramirez et al, Yiu et al's paper was much longer but also much clearer. It explained each step the researchers took as well as the reasoning behind it, which was very helpful. Results were clearly stated and I found their overall hypothesis about neuron excitability influencing memory trace to be quite fascinating. When there is so much yet to learn about memory formation and recall, Yiu et al did a good job of focusing on a specific aspect of memory formation. They were able to show that the "excitability" of a neuron (or its potential for firing) directly influences its chance of being part of the memory trace. In other words, the more excitable a neuron is (or, the more CREB a neuron has), the more likely it is to be part of the memory trace. We have learned that the nervous system is extremely complex and that there are very specific neuronal types/functions, and this is further confirmation of that. Specifically, Yiu et al showed how memory allocation is also (at least partially) based on excitability at time of training. I also found it interesting that increasing CREB not only influenced that neuron to be allocated to the memory trace, but it discouraged neighboring neurons, allowing it to keep the size of the LA memory trace relatively stable. It's always incredible to me the way the brain can monitor itself in these ways, not only with positive signals but with inhibitory ones as well.
While I don't quite see a direct application to PTSD or other fear-related disorders in humans from Yiu et al's study, I see great potential for future research and investigation of memory formation and consolidation. It seems as if they are on the right track for determining exactly how memories are formed and what factors are influential in the process. Perhaps once we are able to determine exactly which neurons are allocated in memory formation and how the entire process unfolds, we will be able to selectively target neurons in humans to attempt to relieve fear in PTSD and related disorders.
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