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Fear memories and CREB

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In order for a fear memory to encoded, neurons must be recruited to a trace or engram in which become responsible not just for encoding that memory but in subsequent recall. It is speculated currently what determines a neurons affinity to be recruited as such. Both papers from Sheena Josselyn’s lab present convincing evidence of a mechanism behind the likelihood of a fear memory to be encoded. Through both inhibition of the CREB transcription factor, it is implicated that a higher expression of this transcription factor that is responsive to Ca2+/cAMP binding. 
In the first paper, Han et al. 2009, a tool is established to selectively kill lateral amygdala neurons in order to erase a fear memory. While this is substantially shown given the lower freezing recall after erasure. But, the data does not necessarily conclude how this model may affect encoding. As these neurons were only killed after the fear memory was encoded, it is possible that they are only responsible for the retrieval through the lateral amygdala. As much communication is bidirectional in the lateral amygdala, it might be interesting to see if they are responsible for the initial encoding as well. For example, If these neurons were selectively killed before the training, they might show the same decreased recall affect, implicating them in the true scope of the memory. It is also interesting that all the DTR mice had a much lower freezing percentage at baseline before the tone plays. This might be indicative of some secondary effects of the vector or just bad sampling of mice. 
With respect to the next paper, Yiu et al 2014, the study aims to narrow on this overexpression of CREB’s ability to more selectively recruit neurons into a memory trace. It is clearly seen that CREB increases a neurons excitability and memory retrieval of a fearful stimulus. Interestingly, this population of LA neurons that over-expressed CREB were only a very small percentage. It is possible that these neurons are selective towards even subtypes of fear. To test this, it would be enlightening to see if the effect of CREB excitability in this subpopulation creates a reproducible effect in other contexts of fear. If so, then this finding has huge implications in overall brain functionality when responding to stress and recruiting cells to create memories. 
            

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