This week articles focused on the same theme in two different directions: fear memories. In the Han article from 2009, the team identified a group of high-excitable neurons with over expression of the binding protein CREB, as a target in the lateral amygdala (LA). Their goals was to determine wether or not a fear conditioned memory could be erased, and undetectable through a mouse's behavioral expression of anxiety. Juxtaposing this paradigm, the Yiu article from 2013 took a different approach to examining the fear memory trace, investigating the inducibility of a fear response.
The conclusions of these articles were very similar: a select group of neurons in the LA with high excitability and high expression of CREB, are highly involved in the trace memory associated with fear conditioning. Given the reproducibility of the results and the build each article has had off previous research I am convinced of the legitimacy of their findings. I think this research is moving in line with the popular direction of identifying specific sets of neurons and their functions in order to form a more clear map of the brain.
In our previous class discussions two common topics have repeatedly emerged: we have questioned the methods of articles and their ability to distinguish between depression and anxiety, and we have pondered the possible clinical applications and relevance of the animal models we are studying. The two studies, while both looking at sea conditioning, took different approaches in measuring the anxiety of their subjects. In Han's they measures freezing (which we have discussed may not always be an accurate measurement given different expressions of fear in mice such as darting), and Yiu's article looks at classic measurements of anxiety including the open field test and elevated plus maze. I think it would have been interesting the compare more similar measures of fear or anxiety to see more similarities (or differences) among these studies. In addition, the concept of "weak" vs. "strong" memories stood out to me in particular. Similar to when we compared chromic mild stress to more severe and acute stress in mice I was curious where the threshold lies and how the experimenters determined where to draw the theoretical line between small, or more severe "traumas".
In terms of clinical applications, I assume this research would be transformed into anxiety or PTSD treatments in humans. Being able to identify the networks controlling these fear conditioned responses in humans would be a major mile stone in finding treatment for panic disorders. However, the ability to directly target such deep brain structures in human subjects is so limited. As we have discussed in previous classes I wonder how we would translate this knowledge into a clinical setting where similar protocols would not be possible. While I think this research could help us greatly in identifying the networks involved in fear trace memories, I think further research in how this would be able to translate towards treatment would be a challenging and interesting approach in a new direction.
The conclusions of these articles were very similar: a select group of neurons in the LA with high excitability and high expression of CREB, are highly involved in the trace memory associated with fear conditioning. Given the reproducibility of the results and the build each article has had off previous research I am convinced of the legitimacy of their findings. I think this research is moving in line with the popular direction of identifying specific sets of neurons and their functions in order to form a more clear map of the brain.
In our previous class discussions two common topics have repeatedly emerged: we have questioned the methods of articles and their ability to distinguish between depression and anxiety, and we have pondered the possible clinical applications and relevance of the animal models we are studying. The two studies, while both looking at sea conditioning, took different approaches in measuring the anxiety of their subjects. In Han's they measures freezing (which we have discussed may not always be an accurate measurement given different expressions of fear in mice such as darting), and Yiu's article looks at classic measurements of anxiety including the open field test and elevated plus maze. I think it would have been interesting the compare more similar measures of fear or anxiety to see more similarities (or differences) among these studies. In addition, the concept of "weak" vs. "strong" memories stood out to me in particular. Similar to when we compared chromic mild stress to more severe and acute stress in mice I was curious where the threshold lies and how the experimenters determined where to draw the theoretical line between small, or more severe "traumas".
In terms of clinical applications, I assume this research would be transformed into anxiety or PTSD treatments in humans. Being able to identify the networks controlling these fear conditioned responses in humans would be a major mile stone in finding treatment for panic disorders. However, the ability to directly target such deep brain structures in human subjects is so limited. As we have discussed in previous classes I wonder how we would translate this knowledge into a clinical setting where similar protocols would not be possible. While I think this research could help us greatly in identifying the networks involved in fear trace memories, I think further research in how this would be able to translate towards treatment would be a challenging and interesting approach in a new direction.
Comments
Post a Comment