Week IV

    I found this week's set of papers worked very well in tandem and complimented each other nicely. Han et al. studied the effect(s) of deleting neurons with the CREB-cre vector to determine if the loss of these cells resulted in the loss of the fear memory. They found that the loss of CREB-cre neurons blocked the fear memory and that these effects were long-lasting. I thought Han et al. were thorough in investigating the effects of ablating CREB-cre neurons. Their result that ablating CREB-overexpressing neurons did not block expression of a memory acquired before surgery helped to convince me that specific populations of neurons encode specific memories. This could be a very useful clinical finding in terms of treating certain psychiatric illnesses such as PTSD or anxiety. Could clinicians locate neuronal populations that encoded certain fear memories and then selectively ablate them to rid the patient of the traumatic memories?

Yui et al. found that increased neuronal excitability was the explanation for why CREB-overexpressing cells were recruited to encode memories. Going off of this line of thought I thought about what Charles wrote, about using the finding in this study to help prevent soldiers from developing PTSD. He mentioned possibly decreasing neuronal excitability in order to prevent the formation of a strong fear memory. My question would be how would this work on a human time-scale. For example in the study mice the HSV was used to express Kir2.1 to decrease action potential firing. Would soldiers pre-emptively be injected with the virus every few weeks to help ensure the prevention of traumatic memories and how long would it take for the phenotype to apepar? I think Charles brings up a very interesting concept that I would be interested in exploring.

Although both of these studies only dealt with fear memory, I wonder if these results apply to positive or neutral memories as well. Could positive memories be enhanced and if so could this be used as a treatment for depression? Last week Ramirez et al. (2015) found that activation of a positive memory helps to suppress depressive behaviors. Could the results from both of these studies be combined to create a novel form of depression treatment? Could clinicians increase neuronal excitability prior to the formation of a positive memory to enhance memory formation and then optogenetically activate the neurons coding for the enhanced positive memory to suppress depressive behaviors?

I believe the results of the papers we read this week have immense clinical implications in treating a variety of psychiatric conditions and would be very interested in the application of these finding.