Excitatory neurons expressing CREB contribute to fear memory traces- Sierra Smith
Both Yiu et al and Han et al examined small populations of cells in the lateral amygdala of mice and identified the importance of CREB activity inducing excitatory states in neurons. While Han et al showed that CREB activity is necessary for memory formation, as when cells expressing CREB that had been activated during fear conditioning were ablated via inducing apoptosis, the memory formation was nulled in both short and long-term. Yiu et al were able to focus more on the sufficiency of CREB activity, and more specifically excitatory "primed" neurons in the formation of fear memories, especially during the reconsolidation phase of memory retrieval.
I was curious after reading this paper what the difference may be between the memory engrams that we observed while studying the two Ramirez et al group papers and the memory traces referenced in Yiu et al and Han et al based in neuronal excitability. According to Yiu et al, increasing CREB expression in random subsets of 10% of excitatory LA neurons is sufficient to enhance fear memory encoding. Both Han et al and Yiu et al show that different excitatory neurons can be recruited into fear memory formation depending on the degree to which CREB signaling is occurring within the neuron, which I thought was interesting given the neuron-by-neuron specificity of memory formation witnessed in the memory engrams of the dentate gyrus of the hippocampus. I would like to be able to examine data looking at CREB activity in the previously examined DG cells underlying memory engram recruitment and formation, and whether or not simply increasing CREB activity could also promote stronger fear memory formation in those contexts.
I also thought it was incredible that in both Yiu et al and Han et al, fear memory effects regulated by CREB activity showed permanency, at least on the order of several days. I wonder if it would be possible to mute fear memory formation in overly fearful human patients, for example in patients who experience phobias to either social situations or objects that interfere with their daily lives, by decreasing CREB activity in certain subsets of neurons in the LA similarly to what was done in Han et al by inducing apoptosis in cells activated by the fearful memories.
I was curious after reading this paper what the difference may be between the memory engrams that we observed while studying the two Ramirez et al group papers and the memory traces referenced in Yiu et al and Han et al based in neuronal excitability. According to Yiu et al, increasing CREB expression in random subsets of 10% of excitatory LA neurons is sufficient to enhance fear memory encoding. Both Han et al and Yiu et al show that different excitatory neurons can be recruited into fear memory formation depending on the degree to which CREB signaling is occurring within the neuron, which I thought was interesting given the neuron-by-neuron specificity of memory formation witnessed in the memory engrams of the dentate gyrus of the hippocampus. I would like to be able to examine data looking at CREB activity in the previously examined DG cells underlying memory engram recruitment and formation, and whether or not simply increasing CREB activity could also promote stronger fear memory formation in those contexts.
I also thought it was incredible that in both Yiu et al and Han et al, fear memory effects regulated by CREB activity showed permanency, at least on the order of several days. I wonder if it would be possible to mute fear memory formation in overly fearful human patients, for example in patients who experience phobias to either social situations or objects that interfere with their daily lives, by decreasing CREB activity in certain subsets of neurons in the LA similarly to what was done in Han et al by inducing apoptosis in cells activated by the fearful memories.
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