scholarly journals Chronic Vortioxetine Treatment Reduces Exaggerated Expression of Conditioned Fear Memory and Restores Active Coping Behavior in Chronically Stressed Rats

2016 ◽  
pp. pyw105 ◽  
Author(s):  
Lauren Hatherall ◽  
Connie Sánchez ◽  
David A. Morilak
Keyword(s):  
Conditioned Fear ◽  
Coping Behavior ◽  
Fear Memory ◽  
Active Coping

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

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

Acquisition of Fear and Extinction in Lateral Amygdala: A Modeling Study

2010 ◽  
Author(s):  
Sandeep Pendyam ◽  
Dongbeom Kim ◽  
Gregory J. Quirk ◽  
Satish S. Nair
Keyword(s):  
Pyramidal Neurons ◽  
Conditioned Fear ◽  
Fear Memory ◽  
Fear Learning ◽  
Cell Populations ◽  
Storage Site ◽  
Somatosensory Information ◽  
Cortical Inputs ◽  
Lateral Nucleus ◽  
And Storage

The lateral nucleus of amygdala (LA) is known to be a critical storage site for conditioned fear memory. Synaptic plasticity at auditory inputs to the dorsal LA (LAd) is critical for the formation and storage of auditory fear memories. Recent evidence suggests that two different cell populations (transient- and long-term plastic cells) are present in LAd and are responsible for fear learning. However, the mechanisms involved in the formation and storage of fear are not well understood. As an extension of previous work, a biologically realistic computational model of the LAd circuitry is developed to investigate these mechanisms. The network model consists of 52 LA pyramidal neurons and 13 interneurons. Auditory and somatosensory information reaches LA from both thalamic and cortical inputs. The model replicated the tone responses observed in the two LAd cell populations during conditioning and extinction. The model provides insights into the role of thalamic and cortical inputs in fear memory formation and storage.

Is There a Science of Psychotherapy?

2018 ◽  
Author(s):  
Jack M. Gorman
Keyword(s):  
Anxiety Disorders ◽  
Life Experience ◽  
Conditioned Fear ◽  
Fear Memory ◽  
Cognitive Behavioral ◽  
Psychoanalytic Psychotherapy ◽  
Laboratory Animals ◽  
Psychiatric Illnesses ◽  
Brain Pathways ◽  
Unconscious Memory

Traditionally, psychotherapists have been reluctant to embrace neuroscience, incorrectly believing that it is solely devoted to finding more drugs for psychiatric illnesses. By thinking of psychotherapy as a type of life experience, however, we see that many aspects of neurobiology are relevant to psychotherapy and strengthen our understanding of how psychotherapy works. One example is studies showing that the same brain pathways involved in the acquisition and extinction of conditioned fear in laboratory animals and in anxiety disorders in humans are also affected by cognitive behavioral psychotherapy. Another example is the similarity of the ability to permanently abolish fear memory by blocking its reconsolidation and the reframing of a previously unconscious memory during psychoanalytic psychotherapy. A neuroscience of psychotherapy is certainly conceivable.

Biological Systems that Control Conditioned Fear Memory

2014 ◽  
Vol 5 (2) ◽  
pp. 85-92
Author(s):  
Masayuki Sekiguchi
Keyword(s):  
Conditioned Fear ◽  
Biological Systems ◽  
Fear Memory

scholarly journals Layer- and subregion-specific differences in the neurophysiological properties of rat medial prefrontal cortex pyramidal neurons

2018 ◽  
Vol 119 (1) ◽  
pp. 177-191 ◽  
Author(s):  
Chenghui Song ◽  
James R. Moyer
Keyword(s):  
Prefrontal Cortex ◽  
Medial Prefrontal Cortex ◽  
Pyramidal Neurons ◽  
Conditioned Fear ◽  
Input Resistance ◽  
Underlying Mechanism ◽  
Fear Memory ◽  
Membrane Properties ◽  
Spike Threshold ◽  
Memory Acquisition

Medial prefrontal cortex (mPFC) is critical for the expression of long-term conditioned fear. However, the neural circuits involving fear memory acquisition and retrieval are still unclear. Two subregions within mPFC that have received a lot of attention are the prelimbic (PL) and infralimbic (IL) cortices (e.g., Santini E, Quirk GJ, Porter JT. J Neurosci 28: 4028–4036, 2008; Song C, Ehlers VL, Moyer JR Jr. J Neurosci 35: 13511–13524, 2015). Interestingly, PL and IL may play distinct roles during fear memory acquisition and retrieval but the underlying mechanism is poorly understood. One possibility is that the intrinsic membrane properties differ between these subregions. Thus, the current study was carried out to characterize the basic membrane properties of mPFC neurons in different layers and subregions. We found that pyramidal neurons in L2/3 were more hyperpolarized and less excitable than in L5. This was observed in both IL and PL and was associated with an enhanced h-current in L5 neurons. Within L2/3, IL neurons were more excitable than those in PL, which may be due to a lower spike threshold and higher input resistance in IL neurons. Within L5, the intrinsic excitability was comparable between neurons obtained in IL and PL. Thus, the heterogeneity in physiological properties of mPFC neurons may underlie the observed subregion-specific contribution of mPFC in cognitive function and emotional control, such as fear memory expression. NEW & NOTEWORTHY This is the first study to demonstrate that medial prefrontal cortical (mPFC) neurons are heterogeneous in both a layer- and a subregion-specific manner. Specifically, L5 neurons are more depolarized and more excitable than those neurons in L2/3, which is likely due to variations in h-current. Also, infralimbic neurons are more excitable than those of prelimbic neurons in layer 2/3, which may be due to differences in certain intrinsic properties, including input resistance and spike threshold.

scholarly journals SUN-235 Deficient Fear Extinction in PRKAR1A-Defective Mice

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Margaret Keil ◽  
Enrica Paradiso ◽  
Rita S Keil ◽  
Maddalena Ugolini ◽  
Evan Harris ◽  
...  
Keyword(s):  
Gene Expression ◽  
Fear Conditioning ◽  
Conditioned Fear ◽  
Critical Role ◽  
Fear Memory ◽  
Brain Regions ◽  
Fear Extinction ◽  
Carney Complex ◽  
Bdnf Gene ◽  
Extinction Learning

Abstract Background: The role of the cAMP/PKA signaling in molecular pathways involved in fear memory is well established: PKA is required for fear memory formation and is a constraint for fear extinction. Previously we reported that a Prkar1a heterozygote (HZ) mouse that was developed in our lab to investigate Carney complex (CNC), the disease caused by PRKAR1A mutations, showed brain region-specific increased PKA activity that was associated with anxiety-like behavioral phenotype and threat bias (Keil, 2010, 2013). We hypothesized that Prkar1a+/- (HZ) mice would have deficits in fear extinction behavior. Brain derived neurotrophic factor (BDNF) has a critical role in formation of fear memory and its transcription is regulated by PKA/CREB. A mouse model with down regulation of PKA provides an opportunity for the first time to investigate the effect of altered PKA signaling on fear conditioning and extinction. Method: Fear conditioning, fear extinction learning, and fear extinction recall were tested in adult male HZ and wild-type (WT) mice as follows: fear conditioning training followed 24hr later by extinction training (new context), then 24hr later by extinction recall training. Percentage of time freezing was used to assess conditioned fear response. We measured BDNF gene expression in brain regions after completion of extinction recall training. Results: As expected, fear conditioning (learning) behavior was similar in HZ and WT mice. However, HZ mice showed a significant deficit in the early phase of fear extinction learning compared to WT. There was no difference in extinction recall between genotypes. Alterations in BDNF gene expression in the prefrontal cortex and amygdala was associated with deficit in fear extinction. Conclusion: Mice with a downregulation of Prkar1a gene demonstrate intact fear conditioning but impaired fear extinction learning, consistent with prior studies that report that PKA inhibition is necessary to facilitate extinction learning. Prkar1a+/- mice provide a valuable model to investigate impaired fear extinction to identify mechanisms for therapeutic targets for anxiety and trauma-related disorders.

scholarly journals Gender difference in retrieval-extinction of conditioned fear memory

2021 ◽  
Vol 53 (10) ◽  
pp. 1082
Author(s):  
Wei CHEN ◽  
Xiaoyi LIN ◽  
Junjiao LI ◽  
Wenxi ZHANG ◽  
Nan SUN ◽  
...  
Keyword(s):  
Gender Difference ◽  
Conditioned Fear ◽  
Fear Memory

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 Dopamine and fear memory formation in the human amygdala

2021 ◽  
Author(s):  
Andreas Frick ◽  
Johannes Björkstrand ◽  
Mark Lubberink ◽  
Allison Eriksson ◽  
Mats Fredrikson ◽  
...  
Keyword(s):  
Fear Conditioning ◽  
Dopamine Release ◽  
Conditioned Fear ◽  
Fear Memory ◽  
Memory Formation ◽  
Fear Learning ◽  
Causative Role ◽  
Endogenous Dopamine ◽  
Positron Emission ◽  
Endogenous Dopamine Release

AbstractLearning which environmental cues that predict danger is crucial for survival and accomplished through Pavlovian fear conditioning. In humans and rodents alike, fear conditioning is amygdala-dependent and rests on similar neurocircuitry. Rodent studies have implicated a causative role for dopamine in the amygdala during fear memory formation, but the role of dopamine in aversive learning in humans is unclear. Here, we show dopamine release in the amygdala and striatum during fear learning in humans. Using simultaneous positron emission tomography and functional magnetic resonance imaging, we demonstrate that the amount of dopamine release is linked to strength of conditioned fear responses and linearly coupled to learning-induced activity in the amygdala. Thus, like in rodents, formation of amygdala-dependent fear memories in humans seems to be facilitated by endogenous dopamine release, supporting an evolutionary conserved neurochemical mechanism for aversive memory formation.

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