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 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 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 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

Striatal dopamine mediates hallucination-like perception in mice

Science ◽  
2021 ◽  
Vol 372 (6537) ◽  
pp. eabf4740
Author(s):  
K. Schmack ◽  
M. Bosc ◽  
T. Ott ◽  
J. F. Sturgill ◽  
A. Kepecs
Keyword(s):  
Psychotic Disorders ◽  
Neural Circuit ◽  
Dopamine Neurons ◽  
Striatal Dopamine ◽  
Model Organisms ◽  
High Confidence ◽  
Optogenetic Stimulation ◽  
The Brain ◽  
Central Symptom ◽  
Stimulation Of

Hallucinations, a central symptom of psychotic disorders, are attributed to excessive dopamine in the brain. However, the neural circuit mechanisms by which dopamine produces hallucinations remain elusive, largely because hallucinations have been challenging to study in model organisms. We developed a task to quantify hallucination-like perception in mice. Hallucination-like percepts, defined as high-confidence false detections, increased after hallucination-related manipulations in mice and correlated with self-reported hallucinations in humans. Hallucination-like percepts were preceded by elevated striatal dopamine levels, could be induced by optogenetic stimulation of mesostriatal dopamine neurons, and could be reversed by the antipsychotic drug haloperidol. These findings reveal a causal role for dopamine-dependent striatal circuits in hallucination-like perception and open new avenues to develop circuit-based treatments for psychotic disorders.

scholarly journals Parylene photonics: a flexible, broadband optical waveguide platform with integrated micromirrors for biointerfaces

2020 ◽  
Vol 6 (1) ◽  
Author(s):  
Jay W. Reddy ◽  
Maya Lassiter ◽  
Maysamreza Chamanzar
Keyword(s):  
Optical Waveguides ◽  
Brain Activity ◽  
Low Loss ◽  
Parylene C ◽  
Optogenetic Stimulation ◽  
Patterned Illumination ◽  
The Brain ◽  
532 Nm ◽  
Stimulation Of

Abstract Targeted light delivery into biological tissue is needed in applications such as optogenetic stimulation of the brain and in vivo functional or structural imaging of tissue. These applications require very compact, soft, and flexible implants that minimize damage to the tissue. Here, we demonstrate a novel implantable photonic platform based on a high-density, flexible array of ultracompact (30 μm × 5 μm), low-loss (3.2 dB/cm at λ = 680 nm, 4.1 dB/cm at λ = 633 nm, 4.9 dB/cm at λ = 532 nm, 6.1 dB/cm at λ = 450 nm) optical waveguides composed of biocompatible polymers Parylene C and polydimethylsiloxane (PDMS). This photonic platform features unique embedded input/output micromirrors that redirect light from the waveguides perpendicularly to the surface of the array for localized, patterned illumination in tissue. This architecture enables the design of a fully flexible, compact integrated photonic system for applications such as in vivo chronic optogenetic stimulation of brain activity.

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