Inhibitory Fear Memory Engram in the Mouse Central Lateral Amygdala

2022 ◽  
Author(s):  
Wen-Hsien Hou ◽  
Meet Jariwala ◽  
Kai-Yi Wang ◽  
Anna Seewald ◽  
Yu-Ling Lin ◽  
...  
Keyword(s):  
Fear Memory ◽  
Lateral Amygdala ◽  
Memory Engram

scholarly journals TMEM16B regulates anxiety-related behavior and GABAergic neuronal signaling in the central lateral amygdala

eLife ◽  
2019 ◽  
Vol 8 ◽  
Author(s):  
Ke-Xin Li ◽  
Mu He ◽  
Wenlei Ye ◽  
Jeffrey Simms ◽  
Michael Gill ◽  
...  
Keyword(s):  
Action Potential ◽  
Knockout Mice ◽  
Chloride Channel ◽  
Action Potential Duration ◽  
Fear Memory ◽  
Brain Regions ◽  
Gabaergic Neurons ◽  
Nerve Terminals ◽  
Lateral Amygdala ◽  
Presynaptic Nerve Terminals

TMEM16B (ANO2) is the Ca2+-activated chloride channel expressed in multiple brain regions, including the amygdala. Here we report that Ano2 knockout mice exhibit impaired anxiety-related behaviors and context-independent fear memory, thus implicating TMEM16B in anxiety modulation. We found that TMEM16B is expressed in somatostatin-positive (SOM+) GABAergic neurons of the central lateral amygdala (CeL), and its activity modulates action potential duration and inhibitory postsynaptic current (IPSC). We further provide evidence for TMEM16B actions not only in the soma but also in the presynaptic nerve terminals of GABAergic neurons. Our study reveals an intriguing role for TMEM16B in context-independent but not context-dependent fear memory, and supports the notion that dysfunction of the amygdala contributes to anxiety-related behaviors.

scholarly journals Reactivation maintains LTP at CS inputs to the lateral amygdala enabling selective fear memory persistence

IBRO Reports ◽  
2019 ◽  
Vol 6 ◽  
pp. S311-S312
Author(s):  
Jung-Pyo Oh ◽  
Jeong-Tae Kwon ◽  
Sangrak Jin ◽  
Miran Yoo ◽  
Hyung-Su Kim ◽  
...  
Keyword(s):  
Fear Memory ◽  
Lateral Amygdala ◽  
Memory Persistence

Population coding of fear memory retrieval in the lateral amygdala

2009 ◽  
Vol 65 ◽  
pp. S233
Author(s):  
Hiroshi Nomura ◽  
Koichi Hashikawa ◽  
Norio Matsuki
Keyword(s):  
Memory Retrieval ◽  
Fear Memory ◽  
Population Coding ◽  
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 Persistence of Fear Memory Depends on a Delayed Elevation of BAF53b and FGF1 Expression in the Lateral Amygdala

2020 ◽  
Vol 40 (37) ◽  
pp. 7133-7141
Author(s):  
Miran Yoo ◽  
Seongwan Park ◽  
Inkyung Jung ◽  
Jin-Hee Han
Keyword(s):  
Fear Memory ◽  
Lateral Amygdala

scholarly journals Role of cGMP-dependent protein kinases for fear memory formation in the lateral amygdala

2009 ◽  
Vol 9 (Suppl 1) ◽  
pp. S21
Author(s):  
Cindy Paul ◽  
Florian Schöberl ◽  
Pascal Weinmeister ◽  
Vincenzo Micale ◽  
Carsten Wotjak ◽  
...  
Keyword(s):  
Protein Kinases ◽  
Fear Memory ◽  
Memory Formation ◽  
Lateral Amygdala ◽  
Dependent Protein

scholarly journals Arp2/3 and VASP Are Essential for Fear Memory Formation in Lateral Amygdala

eNeuro ◽  
2016 ◽  
Vol 3 (6) ◽  
pp. ENEURO.0302-16.2016 ◽  
Author(s):  
Sreetama Basu ◽  
Irina Kustanovich ◽  
Raphael Lamprecht
Keyword(s):  
Fear Memory ◽  
Memory Formation ◽  
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.

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