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Week 4 Memory Engrams

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            After reading both research papers, it is unclear to me what the clinical significance is. I understand that the 10% of LA neurons that had more excitability before fear training were significantly more likely to be allocated into the memory trace and enhance memory formation. However, in all cases, the excitability of the neurons was artificial, whether it be due to optogenetics or a CNO injection. In the discussion of the second paper, it was said that endogenous changes in intrinsic excitability are linked to learning. There was one sentence that alluded to what is possibly happening naturally. Do we endogenously express varying levels of CREB in our LA neurons, and whichever ones are randomly excited at the moment right before an experience get allocated into the memory trace? What are the endogenous changes in excitability and how does this paper relate to them? It was also determined that expressing Kir2.1, which decreases excitability, did not affect memory formation. So, animals without this increase in excitability performed similar to the control. Doesn’t this show that we don’t need excitable neurons to form normal fear memories?
            In the first paper, a fear memory was erased via apoptosis. In an ideal world, this would be extremely relevant if we could, for example, erase the fear memory of a trauma. I’d be curious about the overlap if researchers increased CREB with one technique, fear conditioned with one tone, and then increased CREB via another technique to fear condition with another tone. Since only about 10% of LA neurons are recruited for one fear memory trace, there must be some overlap with fear memories, given how many people have. If this is the case, there would be no way to erase one fear memory without disrupting several others. So again, I do not see the clinical significance. We seemingly cannot decrease fear and I can’t imagine a scenario where we would want an increased fear memory as opposed to a normal fear memory.

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