scholarly journals The NO-cGMP-PKG signaling pathway regulates synaptic plasticity and fear memory consolidation in the lateral amygdala via activation of ERK/MAP kinase

2008 ◽  
Vol 15 (10) ◽  
pp. 792-805 ◽  
Author(s):  
K. T. Ota ◽  
V. J. Pierre ◽  
J. E. Ploski ◽  
K. Queen ◽  
G. E. Schafe
Keyword(s):  
Synaptic Plasticity ◽  
Map Kinase ◽  
Signaling Pathway ◽  
Memory Consolidation ◽  
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 Memory Consolidation for Contextual and Auditory Fear Conditioning Is Dependent on Protein Synthesis, PKA, and MAP Kinase

1999 ◽  
Vol 6 (2) ◽  
pp. 97-110 ◽  
Author(s):  
Glenn E. Schafe ◽  
Nicole V. Nadel ◽  
Gregory M. Sullivan ◽  
Alexander Harris ◽  
Joseph E. LeDoux
Keyword(s):  
Protein Synthesis ◽  
Map Kinase ◽  
Fear Conditioning ◽  
Memory Consolidation ◽  
Molecular Mechanisms ◽  
Short Term Memory ◽  
Long Term Potentiation ◽  
Fear Memory ◽  
Term Memory

Fear conditioning has received extensive experimental attention. However, little is known about the molecular mechanisms that underlie fear memory consolidation. Previous studies have shown that long-term potentiation (LTP) exists in pathways known to be relevant to fear conditioning and that fear conditioning modifies neural processing in these pathways in a manner similar to LTP induction. The present experiments examined whether inhibition of protein synthesis, PKA, and MAP kinase activity, treatments that block LTP, also interfere with the consolidation of fear conditioning. Rats were injected intraventricularly with Anisomycin (100 or 300 μg), Rp-cAMPS (90 or 180 μg), or PD098059 (1 or 3 μg) prior to conditioning and assessed for retention of contextual and auditory fear memory both within an hour and 24 hr later. Results indicated that injection of these compounds selectively interfered with long-term memory for contextual and auditory fear, while leaving short-term memory intact. Additional control groups indicated that this effect was likely due to impaired memory consolidation rather than to nonspecific effects of the drugs on fear expression. Results suggest that fear conditioning and LTP may share common molecular mechanisms.

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 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 Axon TRAP reveals learning-associated alterations in cortical axonal mRNAs in the lateral amygdala

eLife ◽  
2019 ◽  
Vol 8 ◽  
Author(s):  
Linnaea E Ostroff ◽  
Emanuela Santini ◽  
Robert Sears ◽  
Zachary Deane ◽  
Rahul N Kanadia ◽  
...  
Keyword(s):  
Protein Synthesis ◽  
Synaptic Plasticity ◽  
Associative Memory ◽  
Memory Consolidation ◽  
Affinity Purification ◽  
Local Translation ◽  
Lateral Amygdala ◽  
Translation Machinery ◽  
Adult Rat ◽  
Neuronal Processes

Local translation can support memory consolidation by supplying new proteins to synapses undergoing plasticity. Translation in adult forebrain dendrites is an established mechanism of synaptic plasticity and is regulated by learning, yet there is no evidence for learning-regulated protein synthesis in adult forebrain axons, which have traditionally been believed to be incapable of translation. Here, we show that axons in the adult rat amygdala contain translation machinery, and use translating ribosome affinity purification (TRAP) with RNASeq to identify mRNAs in cortical axons projecting to the amygdala, over 1200 of which were regulated during consolidation of associative memory. Mitochondrial and translation-related genes were upregulated, whereas synaptic, cytoskeletal, and myelin-related genes were downregulated; the opposite effects were observed in the cortex. Our results demonstrate that axonal translation occurs in the adult forebrain and is altered after learning, supporting the likelihood that local translation is more a rule than an exception in neuronal processes.

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