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55 results for “fear memory”
The entorhinal cortex modulates trace fear memory formation and neuroplasticity in the lateral amygdala via cholecystokinin
<p>Although the neural circuitry underlying fear memory formation is important in fear-related mental disorders, it is incompletely understood. Here, we utilized trace fear conditioning to study the formation of trace fear memory. We identified the entorhinal cortex (EC) as a critical component of sensory signaling to the amygdala. Moreover, we used the loss of function and rescue experiments to demonstrate that release of the neuropeptide cholecystokinin (CCK) from the EC is required for trace fear memory formation. We discovered that CCK-positive neurons extend from the EC to the lateral nuclei of the amygdala (LA), and inhibition of CCK-dependent signaling in the EC prevented long-term potentiation of sensory signals to the LA and formation of trace fear memory. Altogether, we suggest a model where sensory stimuli trigger the release of CCK from EC neurons, which potentiates sensory signals to the LA, ultimately influencing neural plasticity and trace fear memory formation.</p>
raw data for Optogenetic Stimulation of Prelimbic Pyramidal Neurons Maintains Fear Memories and Modulates Amygdala Pyramidal Neuron Transcriptome
<p>Figure Legend </p> <p>Modulation of cellular excitability of Prelimbic (PrL) pyramidal neurons by optogenetic stimulation. (<strong>A</strong>) Representative traces in current-clamp configuration reporting evoked firing activity triggered by a series of depolarizing current steps (0 to 400 pA) applied to PrL pyramidal neurons of SHAM FEAR (black, <em>n</em> = 8 neurons from 5 mice), OPTO FEAR (red, <em>n</em>= 8 neurons from 5 mice), and No-EX (green, <em>n</em> = 5 neurons from 3 mice) groups. The cumulative plot shows the changes in firing activity. (<strong>B</strong>) Representative traces of PrL pyramidal neurons of SHAM FEAR (black, <em>n</em> = 8 neurons from 5 mice), OPTO FEAR (red, <em>n</em>= 8 neurons from 5 mice), and No-EX (green, <em>n</em> = 5 neurons from 3 mice) groups showing the firing activity triggered by linear depolarization from 0 to 800 pA. Graph (on the right) reports the effects of optogenetic stimulation on rheobase value. Namely, PrL pyramidal neurons of OPTO FEAR and No-EX groups recorded after optogenetic stimulation showed a clear reduction in the rheobase value in comparison to neurons of SHAM FEAR group (* at least <em>p</em>= 0.01). (<strong>C</strong>) Representative traces of Excitatory Post-Synaptic Currents (EPSC) of PrL pyramidal neurons of SHAM FEAR (black, <em>n</em> = 8 neurons from 5 mice), OPTO FEAR (red, <em>n</em>= 8 neurons from 5 mice), and No-EX (green, <em>n</em> = 5 neurons from 3 mice) groups. Graph plot (in the middle) and cumulative curve (on the right) depict the clear increase in firing frequency in PrL pyramidal neurons of OPTO FEAR and No-EX groups (* at least <em>p</em> = 0.01). (<strong>D</strong>) Graphs and cumulative curves report no significant differences in cellular excitability in PrL pyramidal neurons of SHAM NOT FEAR (black) and OPTO NOT FEAR (blue) groups. Data are reported as median with interquartile range.</p>
The entorhinal cortex modulates trace fear memory formation and neuroplasticity in the lateral amygdala via cholecystokinin
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Data from: Network-level changes in the brain underlie fear memory strength
<p>The strength of a fear memory significantly influences whether it drives adaptive or maladaptive behavior in the future. Yet, how mild and strong fear memories differ in underlying biology is not well understood. We hypothesized that this distinction may not be exclusively the result of changes within specific brain regions, but rather the outcome of collective changes in connectivity across multiple regions within the neural network. To test this, rats were fear conditioned in protocols of varying intensities to generate mild or strong memories. Neuronal activation driven by recall was measured using cfos immunohistochemistry in 12 brain regions implicated in fear learning and memory. The interregional coordinated brain activity was computed and graph-based functional networks were generated to compare how mild and strong fear memories differ at the systems level. Our results show that mild fear recall is supported by a well-connected brain network with small-world properties in which the amygdala is well-positioned to be modulated by other regions. In contrast, this connectivity is disrupted in strong fear memories and the amygdala is isolated from other regions. These findings indicate that the neural systems underlying mild and strong fear memories differ, with implications for understanding and treating disorders of fear dysregulation.</p>
Memory and Fear Study (Fear of Memory Loss Study)
ClinicalTrials.gov study NCT04821960. IPD Sharing: NO. Countries: 1. Publications: 2.
Extinction of Fear Memories With Glucocorticoids in Veterans With PTSD
ClinicalTrials.gov study NCT01090180. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Data from: Network-level changes in the brain underlie fear memory strength
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Activation of astrocytes in hippocampus decreases fear memory through adenosine A1 receptors
<p>Astrocytes respond to and regulate neuronal activity, yet their role in mammalian behavior remains incompletely understood. Especially unclear is whether, and if so how, astrocyte activity regulates contextual fear memory, the dysregulation of which leads to pathological fear-related disorders. We generated <i>GFAP-ChR2-EYFP</i> rats to allow the specific activation of astrocytes in vivo by optogenetics. We found that after memory acquisition within a temporal window, astrocyte activation disrupted memory consolidation and persistently decreased contextual but not cued fear memory accompanied by reduced fear-related anxiety behavior. In vivo microdialysis experiments showed astrocyte photoactivation increased extracellular ATP and adenosine concentrations. Intracerebral blockade of adenosine A<sub>1</sub> receptors (A<sub>1</sub>Rs) reversed the attenuation of fear memory. Furthermore, intracerebral or intraperitoneal injection of A<sub>1</sub>R agonist mimicked the effects of astrocyte activation. Therefore, our findings provide a deeper understanding of the astrocyte-mediated regulation of fear memory, and suggest a new and important therapeutic strategy against pathological fear-related disorders.</p>
Source Data for Infralimbic activity during REM sleep facilitates fear extinction memory
<p>Source data for the manuscript Infralimbic activity during REM sleep facilitates fear extinction memory</p>
Effects of Delta9-tetrahydrocannabinol (THC) on Retention of Memory for Fear Extinction Learning in PTSD: R33 Study
ClinicalTrials.gov study NCT04080427. IPD Sharing: NO. Countries: 1. Publications: 1.
Activation of astrocytes in hippocampus decreases fear memory through adenosine A1 receptors
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Data from: Noradrenergic projections from the locus coeruleus to the amygdala constrain fear memory reconsolidation
<p>Memory reconsolidation is a fundamental plasticity process in the brain that allows established memories to be changed or erased. However, certain boundary conditions limit the parameters under which memories can be made plastic. Strong memories do not destabilize, for instance, although why they are resilient is mostly unknown. Here, we extend the understanding of the mechanisms implicated in reconsolidation-resistant memories by<i> </i>investigating the hypothesis that specific modulatory signals shape memory formation into a state that lacks lability. We find that the activation of the noradrenaline-locus coeruleus system (NOR-LC) during strong fear memory encoding increases molecular mechanisms of stability at the expense of lability in the amygdala. Preventing the NOR-LC from modulating strong fear encoding results in the formation of memories that can undergo reconsolidation within the amygdala and thus are vulnerable to post-reactivation interference. Thus, the memory strength boundary condition on reconsolidation is set at the time of encoding by the action of the NOR-LC.</p>
Data from: Disruption of memory reconsolidation erases a fear memory trace in the human amygdala: An 18-month follow-up
Fear memories can be attenuated by reactivation followed by disrupted reconsolidation. Using functional magnetic resonance imaging we recently showed that reactivation and reconsolidation of a conditioned fear memory trace in the basolateral amygdala predicts subsequent fear expression over two days, while reactivation followed by disrupted reconsolidation abolishes the memory trace and suppresses fear. In this follow-up study we demonstrate that the behavioral effect persists over 18 months reflected in superior reacquisition after undisrupted, as compared to disrupted reconsolidation, and that neural activity in the basolateral amygdala representing the initial fear memory predicts return of fear. We conclude that disrupting reconsolidation have long lasting behavioral effects and may permanently erase an amygdala-dependent fear memory.
Data from: Chemogenetic interrogation of a brain-wide fear memory network in mice
Behavior depends on coordinated activity across multiple brain regions. Within such networks, highly connected hub regions are assumed to disproportionately influence behavioral output, although this hypothesis has not been systematically evaluated. Previously, by mapping brain-wide expression of the activity-regulated gene c-fos, we identified a network of brain regions co-activated by fear memory. To test the hypothesis that hub regions are more important for network function, here, we simulated node deletion in silico in this behaviorally defined functional network. Removal of high degree nodes produced the greatest network disruption (e.g., reduction in global efficiency). To test these predictions in vivo, we examined the impact of post-training chemogenetic silencing of different network nodes on fear memory consolidation. In a series of independent experiments encompassing 25% of network nodes (i.e., 21/84 brain regions), we found that node degree accurately predicted observed deficits in memory consolidation, with silencing of highly connected hubs producing the largest impairments.
The Effect of Intravenous Anesthetics on Fear Learning and Memory
ClinicalTrials.gov study NCT00767767. IPD Sharing: NO. Countries: 1. Publications: 0.
The Effect of Oxytocin on Fear Memory Consolidation Novel Intervention to Prevent Posttraumatic Stress Disorder (PTSD)
ClinicalTrials.gov study NCT01466127. IPD Sharing: Not stated. Countries: 1. Publications: 0.
Effects of Delta-9 Tetrahydrocannabinol (THC) on Retention of Memory for Fear Extinction Learning in PTSD: R61 Study
ClinicalTrials.gov study NCT03008005. IPD Sharing: NO. Countries: 1. Publications: 0.
Data from: Competition between engrams influences fear memory formation and recall
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Data from: Noradrenergic projections from the locus coeruleus to the amygdala constrain fear memory reconsolidation
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Data from: Chemogenetic interrogation of a brain-wide fear memory network in mice
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Allen Brain Atlas
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Annotated Behaviour and Observability Dataset (ABODe)
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