Week 4 Papers

This Han et al. paper brings evidence to the table that auditory fear memories are specific to neurons in the LA, and that these neurons having been activated during the formation of this memory, now hold the memory within their function. Thus, through the abolition of these specific memory holding cells, memories such as fear response memories can be deleted. Although the paper was short, it had many control groups that tended to rule out many of the externalities that could have influenced the memory deletion. The length of time was manipulated, the activation or presence of CREB was manipulated, and relearning tasks were manipulated all to show that the abolition of a subset of cells in the LA could have drastic effects on memory of the rodents. The authors admit that the cells they are targeting most likely only play a role in a much broader network, that CREB could be mediating many affects, and that there could be multiple memory traces that utilize similar neurons but these consequences are set ups for future experiments or more broad research. This group showed that their experiment was successful and that when cells in the LA are expressing CREB that they hold the memory traces from fear conditioning.

            The second paper by Yiu et al. built upon the first just as was predicted. That the memory traces had to be looked at more broadly and that CREB’s role in neuronal excitability needed to be tested. The finding that relative neuronal excitability in the LA is the cause of which neurons are recruited for a memory trace is an important one. Although through the experiment even with the numerous controls put into place, it is still unknown if the memory trace lies within these specific neurons. Their freezing behavior is mediated by these neurons and this may suggest that memory of the fear conditioning causes this but the actual level of recall or feeling that comes from this activation cannot be known. It is difficult to say that these findings are imperfect as the data is quite compelling but the disconnect between mice memory and human memory is so great that the answer may not be as simple as differing levels of neuronal excitability. Overall with the multiple controls put into place by both groups of researchers and their findings, it’s clear that the neuronal excitability in the LA neurons plays a role in which cells are encoded with the memory trace and that activation or abolition of these cells can bring about previous fear behavior affects or amnesic behavioral affects from these animals.