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Source—Privy Council Science and Technology Editor—Wang Sizhen, Fang Yiyi, Editor—Xia Ye
In the rapidly changing natural environment, animals need to flexibly extract memories
according to their environment and state.
However, how everyday emotions quickly and directly affect the retrieval efficiency of memory engrams is currently elucidated
.
Memories are thought to be stored in a collection of neurons called engram cells, and there are multiple states such as silent (non-extractable), latent (can be extracted), and active (being extracted) [1-2].
。 Under pathological or artificial conditions, memories can form silent traces, which cannot be extracted by presenting conditioned stimuli, and in the silent state, only artificially activated trace cells can induce memory expression, allowing natural recall
.
Latent trace cells, on the other hand, can be activated by natural stimuli to make them active for memory retrieval [3-5].
However, the physiological significance of the different states of memory traces, especially the silent state, remains unclear
.
Recently, Professor Zhong Yi's research group at the School of Life Sciences of Tsinghua University published a paper entitled "Social experiences switch states of memory engrams through regulating hippocampal Rac1" in the journal Proceedings of the National Academy of Sciences (PNAS).
activity" research paper
.
The authors show that social rewards transform silent memory traces into latent states
.
Instead, social pressure transforms latent traces of memory into a state of silence, which in turn leads to brief forgetting
.
This two-way transition between the latent and silent states of emotion-driven memory traces is mediated
by the regulation of reversible amnesia that is activity-dependent on hippocampal Rac1.
Stress-activated Rac1 inhibits memory retrieval, while Reward restores silent memories
in amnesiac states by inhibiting Rac1.
These data suggest that hippocampal Rac1 activity underlies
emotion-mediated latent and silent memory trace transformations to achieve emotion-driven behavioral flexibility.
1.
Social rewards transform memory traces from a silent state to a latent state
Immediately after conditioning (associated conditioned fear, CFC) training, the protein synthesis inhibitor anisiromycin (ANI) is injected, which puts memory trace cells into a silent state and inhibits the formation
of fear memories.
However, if mice were given social rewards before memory testing, the fear memory level of mice could be enhanced (Figure 1).
Using viral means to label memory trace cells, ANI was found to significantly reduce the number of memory trace cells in the hippocampal brain area, while social reward processing could restore the number of
memory trace cells.
It is explained that social rewards can transform the memory traces of the silent state into a latent state (Figure 1).
Figure 1.
Social rewards shift memory traces from a silent state to a latent state
(Source: Lei B, et al.
, PNAS, 2022).
2.
Social pressure promotes the transition of memory traces from a latent state to a silent state
.
The memory trace cells in the hippocampal brain region of the mouse were labeled, and it was found that the number of memory trace cells increased significantly after conditioned fear training, but the number of activated memory trace cells was reduced after social stress treatment (Figure 2).
Figure 2 Social stress promotes the transition of memory traces from latent to silent
(Source: Lei B, et al.
, PNAS, 2022).
3.
The activity of Rac1 in the hippocampal brain area regulates the state of memory traces
。 To confirm the regulatory relationship between Rac1 and memory traces, the researchers injected AAV virus targeting to induce decreased activity of excitatory neurons in the hippocampus brain region and found Rac1 Reduced activity does restore conditioned fear memory for ANI injury (Figure 3).
Figure 3 The activity of Rac1 in the hippocampal brain region regulates the state of memory traces
(Source: Lei B, et al.
, PNAS, 2022).
4.
Social experiences affect the state of memory traces by regulating the activity of Rac1
in Rac1 activity caused by ANI.
Memory trace cells were tested and found to increase the number of
memory trace cells by either social reward or Ehop016, an inhibitor of intraperitoneal injection of Rac1.
Overexpression of Rac1 in excitatory neurons cancels the effect of social rewards (Figure 4).
Figure 4 Social rewards downregulate the activity of Rac1 to increase the number of memory trace cells
(Source: Lei B, et al.
, PNAS, 2022).
After social stress, the activity of Rac1 in the hippocampal brain area was tested, and it was found that social stress did increase the activity
of Rac1 in the hippocampal brain area.
The use of Ehop016, an inhibitor of Rac1, restores fearful memories
with reduced social pressure.
The memory trace cells were tested and found that social stress reduced the number of memory trace cells, while the number of memory trace cells could be restored using Ehop016 (Figure 5).
Figure 5.
Social stress increases the activity of Rac1 and reduces the number of memory trace cells
(Source: Lei B, et al.
, PNAS, 2022).
Figure 6.
Pattern diagram: Neural mechanisms by which emotional experiences regulate the cellular state of memory traces
(Source: Tsinghua Academy of Health Sciences official website)
In this paper, it is found that the emotional state in social communication can regulate the storage state of memory traces in both directions, and social rewards can transform the memory traces of the silent state into a latent state by inhibiting the activity of Rac1.
Social stress, on the other hand, changes the memory trace from a latent state to a silent state
by increasing the activity of Rac1.
This study provides a novel neurobiological mechanism to help us understand how daily mood changes flexibly regulate memory retrieval in response to environmental changes by switching the state of memory traces in the hippocampus (Figure 6).
Original link: https://doi.
org/10.
1186/s12974-022-02621-9
Lei Bo, a 2016 PhD student at the School of Life Sciences, Tsinghua University, Lv Li, a 2015 PTN PhD student (graduated), and PTN in 2018 PhD student Shiqiang Hu is the co-first author of this paper, and Professor Zhong Yi and PhD student Lei Bo are the co-corresponding authors
of this paper.
Tang Yikai, a postdoctoral fellow at the School of Life Sciences, Tsinghua University, made important contributions to
this research.
This research was supported by the National Natural Science Foundation of China and the Tsinghua-Beijing Center for Life Sciences.
Professor Zhong Yi
(Photo source: Privy Seal)
Corresponding author profile:
Zhong Yi is a professor at the School of Life Sciences, Tsinghua University, PI of Tsinghua-IDG/McGovern Institute for Brain Science, and PI of Tsinghua Peking University Joint Center for Life Sciences.He is currently the executive director of the Chinese Society of Neuroscience and the chairman of the Basic and Clinical Branch of
Learning and Memory.
He has long been engaged in the research of the biological mechanisms of learning, memory and forgetting, and is committed to advancing the research on the pathological mechanisms of human memory-related diseases and the development of
potential therapeutic drugs.
It has achieved a number of influential research results and published them in international high-level journals such as Nature, Science, and Cell
.
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Welcome to "Logical Neuroscience"[1]" "Logical Neuroscience" Recruitment for Editor/Operation Positions ( Online Office)[2] Talent Recruitment - " Logical Neuroscience " Recruitment Article Interpretation/Writing Position ( Online Part-time, Online Office) Reference (slide up and down to read)1.
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