scholarly journals Optogenetic stimulation of a hippocampal engram activates fear memory recall

Nature ◽  
2012 ◽  
Vol 484 (7394) ◽  
pp. 381-385 ◽  
Author(s):  
Xu Liu ◽  
Steve Ramirez ◽  
Petti T. Pang ◽  
Corey B. Puryear ◽  
Arvind Govindarajan ◽  
...  
Keyword(s):  
Fear Memory ◽  
Memory Recall ◽  
Optogenetic Stimulation ◽  
Stimulation Of

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 Reactivating Hippocampal-Mediated Memories to Disrupt the Reconsolidation of Fear

2021 ◽  
Author(s):  
Stephanie L Grella ◽  
Amanda H Fortin ◽  
John H Bladon ◽  
Leanna F Reynolds ◽  
Evan Ruesch ◽  
...  
Keyword(s):  
Dentate Gyrus ◽  
Conditioned Fear ◽  
Large Population ◽  
Fear Memory ◽  
Memory Recall ◽  
Negative Experiences ◽  
Operant Responding ◽  
Small Set ◽  
The Brain ◽  
Stimulation Of

Memories are stored in the brain as cellular ensembles activated during learning and reactivated during retrieval. Using the Tet-tag system, we labeled dorsal dentate gyrus (dDG) neurons activated by positive, neutral or negative experiences with channelrhodopsin-2. Following fear-conditioning, these cells were artificially reactivated during fear memory recall. Optical stimulation of a competing positive memory was sufficient to disrupt reconsolidation, thereby reducing conditioned fear acutely and enduringly. Moreover, mice demonstrated operant responding for reactivation of a positive memory, confirming its reward-like properties. These results show that interference from a rewarding experience can counteract negative states. While interference induced by memory reactivation involved a relatively small set of neurons, we also found that activating a large population of randomly labeled dDG neurons was effective at disrupting fear reconsolidation. Importantly, reconsolidation-interference was specific to the fear memory. These findings implicate the dDG as a potential therapeutic node for modulating memories to suppress fear.

scholarly journals Incerto-thalamic modulation of fear via GABA and dopamine

2021 ◽  
Author(s):  
Archana Venkataraman ◽  
Sarah C. Hunter ◽  
Maria Dhinojwala ◽  
Diana Ghebrezadik ◽  
JiDong Guo ◽  
...  
Keyword(s):  
Brain Regions ◽  
Zona Incerta ◽  
Dependent Manner ◽  
Post Traumatic Stress ◽  
Functional Roles ◽  
Functional Connections ◽  
Optogenetic Stimulation ◽  
Fear Generalization ◽  
Stimulation Of

AbstractFear generalization and deficits in extinction learning are debilitating dimensions of Post-Traumatic Stress Disorder (PTSD). Most understanding of the neurobiology underlying these dimensions comes from studies of cortical and limbic brain regions. While thalamic and subthalamic regions have been implicated in modulating fear, the potential for incerto-thalamic pathways to suppress fear generalization and rescue deficits in extinction recall remains unexplored. We first used patch-clamp electrophysiology to examine functional connections between the subthalamic zona incerta and thalamic reuniens (RE). Optogenetic stimulation of GABAergic ZI → RE cell terminals in vitro induced inhibitory post-synaptic currents (IPSCs) in the RE. We then combined high-intensity discriminative auditory fear conditioning with cell-type-specific and projection-specific optogenetics in mice to assess functional roles of GABAergic ZI → RE cell projections in modulating fear generalization and extinction recall. In addition, we used a similar approach to test the possibility of fear generalization and extinction recall being modulated by a smaller subset of GABAergic ZI → RE cells, the A13 dopaminergic cell population. Optogenetic stimulation of GABAergic ZI → RE cell terminals attenuated fear generalization and enhanced extinction recall. In contrast, optogenetic stimulation of dopaminergic ZI → RE cell terminals had no effect on fear generalization but enhanced extinction recall in a dopamine receptor D1-dependent manner. Our findings shed new light on the neuroanatomy and neurochemistry of ZI-located cells that contribute to adaptive fear by increasing the precision and extinction of learned associations. In so doing, these data reveal novel neuroanatomical substrates that could be therapeutically targeted for treatment of PTSD.

scholarly journals Causal role for sleep-dependent reactivation of learning-activated sensory ensembles for fear memory consolidation

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Brittany C. Clawson ◽  
Emily J. Pickup ◽  
Amy Ensing ◽  
Laura Geneseo ◽  
James Shaver ◽  
...  
Keyword(s):  
Visual Cortex ◽  
Primary Visual Cortex ◽  
Memory Consolidation ◽  
Critical Role ◽  
Visual Presentation ◽  
Fear Memory ◽  
Memory Recall ◽  
Visual Cue ◽  
V1 Neurons ◽  
Targeted Recombination

AbstractLearning-activated engram neurons play a critical role in memory recall. An untested hypothesis is that these same neurons play an instructive role in offline memory consolidation. Here we show that a visually-cued fear memory is consolidated during post-conditioning sleep in mice. We then use TRAP (targeted recombination in active populations) to genetically label or optogenetically manipulate primary visual cortex (V1) neurons responsive to the visual cue. Following fear conditioning, mice respond to activation of this visual engram population in a manner similar to visual presentation of fear cues. Cue-responsive neurons are selectively reactivated in V1 during post-conditioning sleep. Mimicking visual engram reactivation optogenetically leads to increased representation of the visual cue in V1. Optogenetic inhibition of the engram population during post-conditioning sleep disrupts consolidation of fear memory. We conclude that selective sleep-associated reactivation of learning-activated sensory populations serves as a necessary instructive mechanism for memory consolidation.

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