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 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.

scholarly journals The reuniens and rhomboid nuclei are necessary for contextual fear memory persistence in rats

2020 ◽  
Vol 225 (3) ◽  
pp. 955-968 ◽  
Author(s):  
Etienne Quet ◽  
Monique Majchrzak ◽  
Brigitte Cosquer ◽  
Thomas Morvan ◽  
Mathieu Wolff ◽  
...  
Keyword(s):  
Fear Memory ◽  
Contextual Fear ◽  
Contextual Fear Memory ◽  
Memory Persistence

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.

scholarly journals Hippocampal neurogenesis enhancers promote forgetting of remote fear memory after hippocampal reactivation by retrieval

eLife ◽  
2016 ◽  
Vol 5 ◽  
Author(s):  
Rie Ishikawa ◽  
Hotaka Fukushima ◽  
Paul W Frankland ◽  
Satoshi Kida
Keyword(s):  
Fear Memory ◽  
Hippocampal Neurogenesis ◽  
Remote Memory ◽  
Traumatic Memory ◽  
Post Traumatic Stress ◽  
Contextual Fear ◽  
Contextual Fear Memory ◽  
Long Time ◽  
Post Traumatic ◽  
Dependent State

Forgetting of recent fear memory is promoted by treatment with memantine (MEM), which increases hippocampal neurogenesis. The approaches for treatment of post-traumatic stress disorder (PTSD) using rodent models have focused on the extinction and reconsolidation of recent, but not remote, memories. Here we show that, following prolonged re-exposure to the conditioning context, enhancers of hippocampal neurogenesis, including MEM, promote forgetting of remote contextual fear memory. However, these interventions are ineffective following shorter re-exposures. Importantly, we find that long, but not short re-exposures activate gene expression in the hippocampus and induce hippocampus-dependent reconsolidation of remote contextual fear memory. Furthermore, remote memory retrieval becomes hippocampus-dependent after the long-time recall, suggesting that remote fear memory returns to a hippocampus dependent state after the long-time recall, thereby allowing enhanced forgetting by increased hippocampal neurogenesis. Forgetting of traumatic memory may contribute to the development of PTSD treatment.

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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