scholarly journals Reversible Inactivation of the Higher Order Auditory Cortex during Fear Memory Consolidation Prevents Memory-Related Activity in the Basolateral Amygdala during Remote Memory Retrieval

2017 ◽  
Vol 11 ◽  
Author(s):  
Marco Cambiaghi ◽  
Annamaria Renna ◽  
Luisella Milano ◽  
Benedetto Sacchetti
Keyword(s):  
Auditory Cortex ◽  
Memory Consolidation ◽  
Memory Retrieval ◽  
Basolateral Amygdala ◽  
Fear Memory ◽  
Higher Order ◽  
Remote Memory ◽  
Related Activity ◽  
Reversible Inactivation

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

scholarly journals Convergent coding of recent and remote fear memory in the basolateral amygdala

2021 ◽  
Author(s):  
Jianfeng Liu ◽  
Michael S. Totty ◽  
Laila Melissari ◽  
Stephen Maren
Keyword(s):  
Basolateral Amygdala ◽  
Conditioned Fear ◽  
Fear Memory ◽  
Remote Memory ◽  
Storage Site ◽  
Long Term Storage ◽  
Behavioral Design ◽  
Within Subjects ◽  
Conditioned Freezing ◽  
Evoked Activity

Animals must learn to anticipate recently encountered threats as well as dangers experienced long ago. In both rodents and humans, the basolateral amygdala (BLA) is essential for the encoding and retrieval conditioned fear memories. Although the BLA is a putative storage site for aversive memory, recent evidence suggests that these memories undergo time-dependent reorganization and no longer require the BLA after the passage of time. To explore this question, we systematically examined the role for the BLA in recent and remote fear memory using optogenetic, electrophysiological, and calcium imaging methods in male and female Long-Evans rats. Critically, we used a behavioral design that permits within-subjects comparison of recent and remote memory at the same time point. We found that BLA c-Fos expression was similar after the retrieval of recent (1 day) or remote (2 weeks) fear memories. Extracellular recordings in awake, behaving animals revealed that the majority of BLA neurons encoded both recent and remote memories, suggesting substantial overlap in the allocation of temporally distinct events. Fiber photometric recordings of BLA principal neurons also revealed similar patterns of CS-evoked activity to recent and remote CSs. Consistent with these results, continuous or CS-specific optogenetic inhibition of BLA principal neurons impaired conditioned freezing to both recent and remote CSs. Collectively, these data reveal that single BLA neurons encode both recent and remote fear memories. This may underlie the broad generalization of fear memories across both space and time. Ultimately, these results provide robust evidence that the BLA is a long-term storage site for emotional memories.

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.

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.

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