scholarly journals Myosin II motor activity in the lateral amygdala is required for fear memory consolidation

2011 ◽  
Vol 19 (1) ◽  
pp. 9-14 ◽  
Author(s):  
C. F. Gavin ◽  
M. D. Rubio ◽  
E. Young ◽  
C. Miller ◽  
G. Rumbaugh
Keyword(s):  
Motor Activity ◽  
Memory Consolidation ◽  
Myosin Ii ◽  
Fear Memory ◽  
Lateral Amygdala

scholarly journals Epigenetic Alterations Are Critical for Fear Memory Consolidation and Synaptic Plasticity in the Lateral Amygdala

PLoS ONE ◽  
2011 ◽  
Vol 6 (5) ◽  
pp. e19958 ◽  
Author(s):  
Melissa S. Monsey ◽  
Kristie T. Ota ◽  
Irene F. Akingbade ◽  
Ellie S. Hong ◽  
Glenn E. Schafe
Keyword(s):  
Synaptic Plasticity ◽  
Memory Consolidation ◽  
Fear Memory ◽  
Epigenetic Alterations ◽  
Lateral Amygdala

scholarly journals Increasing Synaptic GluN2B levels within the Basal and Lateral Amygdala Enables the Modification of Strong Reconsolidation Resistant Fear Memories

2019 ◽  
Author(s):  
Christopher A. de Solis ◽  
Cuauhtémoc U. Gonzalez ◽  
Mario A. Galdamez ◽  
John M. Perish ◽  
Samuel W. Woodard ◽  
...  
Keyword(s):  
Point Mutation ◽  
Memory Consolidation ◽  
Memory Retrieval ◽  
Therapeutic Strategy ◽  
Fear Memory ◽  
Lateral Amygdala ◽  
Neuronal Synapses ◽  
Stabilization Phase ◽  
Excitatory Neurons ◽  
Novel Therapeutic

AbstractReconsolidation disruption has been proposed as a method to attenuate pathological memories in disorders such as PTSD. However, studies from our group and others indicate that strong memories are resistant to becoming destabilized following reactivation, rendering them impervious to agents that disrupt the re-stabilization phase of reconsolidation. Thus, therapies designed to attenuate maladaptive memories by disrupting reconsolidation updating have not been adequately developed. We previously determined that animals possessing strong auditory fear memories, compared to animals with weaker fear memories, are associated with an enduring increase in the synaptic GluN2A/GluN2B ratio in neurons of the mouse basal and lateral amygdala (BLA). In this study, we determined whether increasing GluN2B levels within BLA excitatory neuronal synapses is sufficient to enable modification of strong fear memories via reconsolidation. To accomplish this, we utilized a combinatorial genetic strategy to express GluN2B or GluN2B(E1479Q) in excitatory neurons of the mouse BLA before or after fear memory consolidation. GluN2B(E1479Q) contains a point mutation that increases synaptic expression of the subunit by interfering with phosphorylation-driven endocytosis. At the time of memory retrieval, increasing synaptic GluN2B levels by expression of GluN2B(E1479Q), but not GluN2B(WT), enhanced the induction of reconsolidation rendering the strong fear memory modifiable. GluN2B(WT) or GluN2B(E1479Q) expression did not influence fear memory maintenance or extinction. Fear memory consolidation, however, was enhanced when GluN2B(E1479Q) was expressed in the BLA at the time of training. These findings indicate that enhancing GluN2B synaptic trafficking may provide a novel therapeutic strategy to enhance modification of pathological memories.

Neurons Activated During Fear Memory Consolidation and Reconsolidation are Mapped to a Common and New Topography in the Lateral Amygdala

2013 ◽  
Vol 26 (3) ◽  
pp. 468-478 ◽  
Author(s):  
Hadley C. Bergstrom ◽  
Craig G. McDonald ◽  
Smita Dey ◽  
Gina M. Fernandez ◽  
Luke R. Johnson
Keyword(s):  
Memory Consolidation ◽  
Fear Memory ◽  
Lateral Amygdala ◽  
Memory Consolidation And Reconsolidation

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.

Ketamine anesthesia enhances fear memory consolidation via noradrenergic activation in the basolateral amygdala

2021 ◽  
Vol 178 ◽  
pp. 107362
Author(s):  
Maria Morena ◽  
Paola Colucci ◽  
Giulia F. Mancini ◽  
Valentina De Castro ◽  
Andrea Peloso ◽  
...  
Keyword(s):  
Memory Consolidation ◽  
Basolateral Amygdala ◽  
Fear Memory ◽  
Ketamine Anesthesia
Sign in / Sign up

Export Citation Format

Share Document