scholarly journals Brain-wide mapping of contextual fear memory engram ensembles supports the dispersed engram complex hypothesis

2019 ◽  
Author(s):  
Dheeraj S Roy ◽  
Young-Gyun Park ◽  
Sachie K Ogawa ◽  
Jae H Cho ◽  
Heejin Choi ◽  
...  
Keyword(s):  
High Probability ◽  
Fear Memory ◽  
Brain Regions ◽  
Memory Recall ◽  
Contextual Fear ◽  
Contextual Fear Memory ◽  
Neuronal Ensembles ◽  
Specific Memory ◽  
Complex Hypothesis ◽  
Memory Engram

Neuronal ensembles that hold specific memory (memory engrams) have been identified in the hippocampus, amygdala, and cortex. It has been hypothesized that engrams for a specific memory are distributed among multiple brain regions that are functionally connected. Here, we report the hitherto most extensive engram map for contextual fear memory by characterizing activity-tagged neurons in 409 regions using SHIELD-based tissue phenotyping. The mapping was aided by a novel engram index, which identified cFos+ brain regions holding engrams with a high probability. Optogenetic manipulations confirmed previously known engrams and revealed new engrams. Many of these engram holding-regions were functionally connected to the CA1 or amygdala engrams. Simultaneous chemogenetic reactivation of multiple engrams, which mimics natural memory recall, conferred a greater level of memory recall than reactivation of a single engram ensemble. Overall, our study supports the hypothesis that a memory is stored in functionally connected engrams distributed across multiple brain regions.

Contextual Fear Memory Retrieval Is Vulnerable to Hippocampal Noise

2020 ◽  
Author(s):  
Satoshi Iwasaki ◽  
Yuji Ikegaya
Keyword(s):  
Memory Retrieval ◽  
Basolateral Amygdala ◽  
Fear Memory ◽  
Memory Recall ◽  
Contextual Fear ◽  
Contextual Fear Memory ◽  
Hippocampal Ca1 ◽  
Recall Memory ◽  
Neuron Ensemble ◽  
Memory Engram

Abstract Memory retrieval depends on reactivation of memory engram cells. Inadvertent activation of these cells is expected to cause memory-retrieval failure, but little is known about how noisy activity of memory-irrelevant neurons impacts mnemonic processes. Here, we report that optogenetic nonselective activation of only tens of hippocampal CA1 cells (∼0.01% of the total cells in the CA1 pyramidal cell layer) impairs contextual fear memory recall. Memory recall failure was associated with altered neuronal reactivation in the basolateral amygdala. These results indicate that hippocampal memory retrieval requires strictly regulated activation of a specific neuron ensemble and is easily disrupted by the introduction of noisy CA1 activity, suggesting that reactivating memory engram cells as well as silencing memory-irrelevant neurons are both crucial for memory retrieval.

Roles of CREB Signaling Pathway in Regulation of Fear Memory

2009 ◽  
Vol 24 (S1) ◽  
pp. 1-1
Author(s):  
S. Kida
Keyword(s):  
Gene Expression ◽  
Gene Expression Regulation ◽  
Fear Memory ◽  
Brain Regions ◽  
Contextual Fear ◽  
Contextual Fear Memory ◽  
New Gene ◽  
Activity Dependent

Activity-dependent gene expression through activation of Ca2+-CREB signal transduction pathways has been thought to play a central role in fear memory formation. On the other hand, retrieval of fear memory triggers two time-dependent phases of reactivated memory; reconsolidation and extinction. To understand the mechanisms for determining the fate of the reactivated fear memory, we investigated roles of CREB in reconsolidation and extinction of contextual fear memory and then analyzed the brain-regions regulating reconsolidation and extinction by identifying regions where CREB-mediated gene expression is activated and then examining the role of protein synthesis in those regions on reconsolidation and extinction. We first showed that activation of CREB-mediated transcription is required for reconsolidation and long-term extinction of contextual fear memory. Using immunocytochemical analyses, we demonstrated that CREB is activated in the hippocampus/amygdala and amygdala/medial prefrontal cortex (mPFC) in the reconsolidation and extinction phases, respectively. Similar results were observed by analyzing the expression of a CREB-dependent gene, Arc. We finally showed that reconsolidation and long-term extinction of the contextual fear memory depended on new gene expression in the hippocampus/amygdala and amygdala/mPFC, respectively. Thus reactivated contextual fear memory is reconsolidated or extinguished through distinct CREB-mediated gene expression regulation in the hippocampus, amygdala and mPFC.

Synapse-specific representation of the identity of overlapping memory engrams

Science ◽  
2018 ◽  
Vol 360 (6394) ◽  
pp. 1227-1231 ◽  
Author(s):  
Kareem Abdou ◽  
Mohammad Shehata ◽  
Kiriko Choko ◽  
Hirofumi Nishizono ◽  
Mina Matsuo ◽  
...  
Keyword(s):  
Retrograde Amnesia ◽  
Fear Memory ◽  
Memory Recall ◽  
Optogenetic Stimulation ◽  
Specific Memory ◽  
Memory Engram ◽  
And Storage ◽  
The Brain ◽  
Cell Ensemble ◽  
Stimulation Of

Memories are integrated into interconnected networks; nevertheless, each memory has its own identity. How the brain defines specific memory identity out of intermingled memories stored in a shared cell ensemble has remained elusive. We found that after complete retrograde amnesia of auditory fear conditioning in mice, optogenetic stimulation of the auditory inputs to the lateral amygdala failed to induce memory recall, implying that the memory engram no longer existed in that circuit. Complete amnesia of a given fear memory did not affect another linked fear memory encoded in the shared ensemble. Optogenetic potentiation or depotentiation of the plasticity at synapses specific to one memory affected the recall of only that memory. Thus, the sharing of engram cells underlies the linkage between memories, whereas synapse-specific plasticity guarantees the identity and storage of individual memories.

scholarly journals Developmental emergence of persistent memory for contextual and auditory fear in mice

2021 ◽  
Vol 28 (11) ◽  
pp. 414-421
Author(s):  
Rojina Samifanni ◽  
Mudi Zhao ◽  
Arely Cruz-Sanchez ◽  
Agarsh Satheesh ◽  
Unza Mumtaz ◽  
...  
Keyword(s):  
Early Life ◽  
Fear Memory ◽  
Remote Memory ◽  
Memory Recall ◽  
Time Line ◽  
Contextual Fear ◽  
Contextual Fear Memory ◽  
Persistent Memory ◽  
Memory Persistence ◽  
Precise Time

The ability to generate memories that persist throughout a lifetime (that is, memory persistence) emerges in early development across species. Although it has been shown that persistent fear memories emerge between late infancy and adolescence in mice, it is unclear exactly when this transition takes place, and whether two major fear conditioning tasks, contextual and auditory fear, share the same time line of developmental onset. Here, we compared the ontogeny of remote contextual and auditory fear in C57BL/6J mice across early life. Mice at postnatal day (P)15, 21, 25, 28, and 30 underwent either contextual or auditory fear training and were tested for fear retrieval 1 or 30 d later. We found that mice displayed 30-d memory for context– and tone–fear starting at P25. We did not find sex differences in the ontogeny of either type of fear memory. Furthermore, 30-d contextual fear retrieval led to an increase in the number of c-Fos positive cells in the prelimbic region of the prefrontal cortex only at an age in which the contextual fear memory was successfully retrieved. These data delineate a precise time line for the emergence of persistent contextual and auditory fear memories in mice and suggest that the prelimbic cortex is only recruited for remote memory recall upon the onset of memory persistence.

scholarly journals Photobiomodulation prevents PTSD-like memory impairments in rats

2021 ◽  
Author(s):  
Yong Li ◽  
Yan Dong ◽  
Luodan Yang ◽  
Lorelei Tucker ◽  
Xuemei Zong ◽  
...  
Keyword(s):  
Single Dose ◽  
Traumatic Event ◽  
Fear Memory ◽  
Etiologic Factor ◽  
Memory Recall ◽  
Memory Testing ◽  
Contextual Fear ◽  
Contextual Fear Memory ◽  
The Individual ◽  
High Level

AbstractA precise fear memory encoding a traumatic event enables an individual to avoid danger and identify safety. An impaired fear memory (contextual amnesia), however, puts the individual at risk of developing posttraumatic stress disorder (PTSD) due to the inability to identify a safe context when encountering trauma-associated cues later in life. Although it is gaining attention that contextual amnesia is a critical etiologic factor for PTSD, there is no treatment currently available that can reverse contextual amnesia, and whether such treatment can prevent the development of PTSD is unknown. Here, we report that (I) a single dose of transcranial photobiomodulation (PBM) applied immediately after tone fear conditioning can reverse contextual amnesia. PBM treatment preserved an appropriately high level of contextual fear memory in rats revisiting the “dangerous” context, while control rats displayed memory impairment. (II) A single dose of PBM applied after memory recall can reduce contextual fear during both contextual and cued memory testing. (III) In a model of complex PTSD with repeated trauma, rats given early PBM interventions efficiently discriminated safety from danger during cued memory testing and, importantly, these rats did not develop PTSD-like symptoms and comorbidities. (IV) Finally, we report that fear extinction was facilitated when PBM was applied in the early intervention window of memory consolidation. Our results demonstrate that PBM treatment applied immediately after a traumatic event or its memory recall can protect contextual fear memory and prevent the development of PTSD-like psychopathological fear in rats.

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