Isoproterenol injected into the basolateral amygdala rescues amyloid β1-42-induced conditioned fear memory deficit via reducing intracellular Zn2+ toxicity

2021 ◽  
pp. 136353
Author(s):  
Yudai Ishikawa ◽  
Ryusei Itoh ◽  
Rin Tsujimoto ◽  
Haruna Tamano ◽  
Atsushi Takeda
Keyword(s):  
Basolateral Amygdala ◽  
Conditioned Fear ◽  
Fear Memory ◽  
Memory Deficit

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 MPP2 Interacts With SK2 Rescue The Excitability of Glutamatergic Neurons in The BLA and Facilitate The Extinction of Conditioned Fear in Mice

2021 ◽  
Author(s):  
Xiao-Han Peng ◽  
Pan-Pan Chen ◽  
Yang Zhang ◽  
Ke Wu ◽  
Ningning Ji ◽  
...  
Keyword(s):  
Fear Conditioning ◽  
Basolateral Amygdala ◽  
Conditioned Fear ◽  
Fear Memory ◽  
Fear Extinction ◽  
Definitive Evidence ◽  
Glutamatergic Neurons ◽  
Integral Role ◽  
Calcium Activated Potassium Channel ◽  
Increased Activity

Abstract Posttraumatic stress disorder (PTSD) and other anxiety disorders stem from dysregulated fear memory in which the basolateral amygdala (BLA) plays an integral role. The excitability of glutamatergic neurons in the BLA correlates with fear memory, and the afterhyperpolarization current (IAHP) mediated by small-conductance calcium-activated potassium channel subtype 2 (SK2) dominates the excitability of glutamatergic neurons. However, definitive evidence for the involvement of the SK2 channel in the BLA in fear extinction is lacking. Here, we discovered that fear conditioning decreased the levers of synaptic SK2 channels in the BLA, which were restored following fear extinction. Notably, reduced expression of synaptic SK2 channels in the BLA during fear conditioning was caused by the increased activity of protein kinase A (PKA), while increased levers of synaptic SK2 channels in the BLA during fear extinction were mediated by interactions with membrane palmitoylated protein 2 (MPP2). Collectively, our results revealed that MPP2 interacts with the SK2 channels and rescues the excitability of glutamatergic neurons by increasing the expression of synaptic SK2 channels in the BLA to promote the normalization of fear memory. These findings expand our understanding of the neurobiological mechanism of PTSD and provide a new direction for PTSD treatment.

scholarly journals P2-044: THE EFFECT OF STANDARDIZED EXTRACT OF ASIAN HERB IM01 ON CONDITIONED FEAR MEMORY DEFICIT OF 3XTG-AD MICE

2019 ◽  
Vol 15 ◽  
pp. P588-P588
Author(s):  
Tanita Pairojana ◽  
Sarayut Phasuk ◽  
Shun-Ping Huang ◽  
Mayuree Tantisira ◽  
Supin Chompoopong ◽  
...  
Keyword(s):  
Conditioned Fear ◽  
Fear Memory ◽  
Memory Deficit

scholarly journals Evaluation of an angiotensin Type 1 receptor blocker on the reconsolidation of fear memory

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Adam P. Swiercz ◽  
Laxmi Iyer ◽  
Zhe Yu ◽  
Allison Edwards ◽  
N. M. Prashant ◽  
...  
Keyword(s):  
Rna Sequencing ◽  
Cardiovascular Reactivity ◽  
Basolateral Amygdala ◽  
Conditioned Fear ◽  
Fear Memory ◽  
Whole Genome ◽  
Extinction Learning ◽  
Single Intraperitoneal Injection ◽  
Angiotensin Type

Abstract Inhibition of the angiotensin type 1 receptor (AT1R) has been shown to decrease fear responses in both humans and rodents. These effects are attributed to modulation of extinction learning, however the contribution of AT1R to alternative memory processes remains unclear. Using classic Pavlovian conditioning combined with radiotelemetry and whole-genome RNA sequencing, we evaluated the effects of the AT1R antagonist losartan on fear memory reconsolidation. Following the retrieval of conditioned auditory fear memory, animals were given a single intraperitoneal injection of losartan or saline. In response to the conditioned stimulus (CS), losartan-treated animals exhibited significantly less freezing at 24 h and 1 week; an effect that was dependent upon memory reactivation and independent of conditioned cardiovascular reactivity. Using an unbiased whole-genome RNA sequencing approach, transcriptomic analysis of the basolateral amygdala (BLA) identified losartan-dependent differences in gene expression during the reconsolidation phase. These findings demonstrate that post-retrieval losartan modifies behavioral and transcriptomic markers of conditioned fear memory, supporting an important regulatory role for this receptor in reconsolidation and as a potential pharmacotherapeutic target for maladaptive fear disorders such as PTSD.

scholarly journals Amygdala Reward Neurons Form and Store Fear Extinction Memory

2019 ◽  
Author(s):  
Xiangyu Zhang ◽  
Joshua Kim ◽  
Susumu Tonegawa
Keyword(s):  
Emotional Disorders ◽  
Basolateral Amygdala ◽  
Conditioned Fear ◽  
Fear Memory ◽  
Fear Extinction ◽  
Neuronal Population ◽  
Post Traumatic Stress ◽  
Extinction Memory ◽  
Memory Engram ◽  
Reward Behaviors

SummaryThe ability to extinguish conditioned fear memory is critical for adaptive control of fear response, and its impairment is a hallmark of emotional disorders like post-traumatic stress disorder (PTSD). Fear extinction is thought to take place when animals form a new memory that suppresses the original fear memory. However, little is known about the nature and the site of formation and storage of the new extinction memory. Here, we demonstrate that a fear extinction memory engram is formed and stored in a genetically distinct basolateral amygdala (BLA) neuronal population that drive reward behaviors and antagonize the BLA’s original fear neurons. The activation of the fear extinction engram neurons and natural reward-responsive neurons overlap extensively in the BLA. Furthermore, these two neuron subsets are mutually interchangeable in driving reward behaviors and fear extinction behaviors. Thus, fear extinction memory is a newly formed reward memory.

A Retrieval-Extinction Paradigm to Treat Conditioned Fear Memory

2014 ◽  
Vol 22 (3) ◽  
pp. 431
Author(s):  
Xiangxing ZENG ◽  
Yanhui XIANG ◽  
Juan DU ◽  
Xifu ZHENG
Keyword(s):  
Conditioned Fear ◽  
Fear Memory

scholarly journals Environmental enrichment prevents the late effect of acute stress-induced fear extinction deficit: the role of hippocampal AMPA-GluA1 phosphorylation

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Leonardo Santana Novaes ◽  
Letícia Morais Bueno-de-Camargo ◽  
Carolina Demarchi Munhoz
Keyword(s):  
Environmental Enrichment ◽  
Basolateral Amygdala ◽  
Acute Stress ◽  
Fear Memory ◽  
Fear Extinction ◽  
Post Traumatic Stress ◽  
Related Disorder ◽  
Memory Extinction ◽  
Post Traumatic

AbstractThe persistence of anxiety and the deficit of fear memory extinction are both phenomena related to the symptoms of a trauma-related disorder, such as post-traumatic stress disorder (PTSD). Recently we have shown that single acute restraint stress (2 h) in rats induces a late anxiety-related behavior (observed ten days after stress), whereas, in the present work, we found that the same stress impaired fear extinction in animals conditioned ten days after stress. Fourteen days of environmental enrichment (EE) prevented the deleterious effect of stress on fear memory extinction. Additionally, we observed that EE prevented the stress-induced increase in AMPA receptor GluA1 subunit phosphorylation in the hippocampus, but not in the basolateral amygdala complex and the frontal cortex, indicating a potential mechanism by which it exerts its protective effect against the stress-induced behavioral outcome.

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

Lack of effect of propranolol on the reconsolidation of conditioned fear memory due to a failure to engage memory destabilisation

Neuroscience ◽  
2021 ◽  
Author(s):  
Federico Rotondo ◽  
Kathryn Biddle ◽  
John Chen ◽  
Josh Ferencik ◽  
Mathilde d'Esneval ◽  
...  
Keyword(s):  
Conditioned Fear ◽  
Fear Memory
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