The Han et al. (2009) paper does a very thorough job of showing that this subpopulation of lateral amygdala neurons is an essential component of the memory trace. However, for further research, I’d like to know what other parts of the brain are essential or involved in the fear memory formation. It’d be fascinating to be able to plot out a whole or most of a memory trace since it likely is not isolated in a single region of the brain, and be able to understand how all these different brain regions are interacting to produce a single behavioral response.
These papers show how CREB expression enhances memory and that, by killing a specific subpopulation of neurons, a fear memory can be deleted which are important and interesting findings. However, I don’t see a clear clinical application for the results of these experiments. The experiments from the Han et al. (2009) paper require killing neurons in order to remove the fear memory from the rodents. Killing an entire area of the brain in a patient suffering from let’s say PTSD is risky and probably not realistic (I don’t know enough about severe PTSD treatments or clinical research to know if this is considered). The next steps I’d like to see in this line of research is if it is possible to take these neurons that can be identified to be in the memory trace and remove them from the memory trace/remove the memory trace from the neurons without killing the neurons. Is there a limit to how many memory traces a neuron can be recruited into? Neurons can be part of multiple memory traces so if researchers were to rewire lateral amygdala neurons in order to erase the memory trace from specific neurons, a major challenge would be to remove one memory trace without significantly disrupting others. Something the Han et al. (2009) paper lacked is an investigation into the unintentional effects of killing the targeted neurons. They could’ve done two separate fear trainings and see if/how killing the neurons encoding one fear memory affects the other fear memory.
These papers show how CREB expression enhances memory and that, by killing a specific subpopulation of neurons, a fear memory can be deleted which are important and interesting findings. However, I don’t see a clear clinical application for the results of these experiments. The experiments from the Han et al. (2009) paper require killing neurons in order to remove the fear memory from the rodents. Killing an entire area of the brain in a patient suffering from let’s say PTSD is risky and probably not realistic (I don’t know enough about severe PTSD treatments or clinical research to know if this is considered). The next steps I’d like to see in this line of research is if it is possible to take these neurons that can be identified to be in the memory trace and remove them from the memory trace/remove the memory trace from the neurons without killing the neurons. Is there a limit to how many memory traces a neuron can be recruited into? Neurons can be part of multiple memory traces so if researchers were to rewire lateral amygdala neurons in order to erase the memory trace from specific neurons, a major challenge would be to remove one memory trace without significantly disrupting others. Something the Han et al. (2009) paper lacked is an investigation into the unintentional effects of killing the targeted neurons. They could’ve done two separate fear trainings and see if/how killing the neurons encoding one fear memory affects the other fear memory.
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