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Journal articles on the topic 'Fear circuit'

Author: Grafiati
Published: 2 November 2024

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1

Sah, Pankaj, and R. Frederick Westbrook. "The circuit of fear." Nature 454, no. 7204 (July 2008): 589–90. http://dx.doi.org/10.1038/454589a.

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2

Sekiguchi, Masayuki. "Fear Circuit and Anxiety Disorders." Anxiety Disorder Research 10, no. 1 (October 31, 2018): 2–9. http://dx.doi.org/10.14389/jsad.10.1_2.

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3

Shultz, Brianna, Abigail Farkash, Bailey Collins, Negin Mohammadmirzaei, and Dayan Knox. "Fear learning-induced changes in AMPAR and NMDAR expression in the fear circuit." Learning & Memory 29, no. 3 (February 15, 2022): 83–92. http://dx.doi.org/10.1101/lm.053525.121.

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NMDA receptors (NMDARs) and AMPA receptors (AMPARs) in amygdala nuclei and the dorsal hippocampus (dHipp) are critical for fear conditioning. Enhancements in synaptic AMPAR expression in amygdala nuclei and the dHipp are critical for fear conditioning, with some studies observing changes in AMPAR expression across many neurons in these brain regions. Whether similar changes occur in other nodes of the fear circuit (e.g., ventral hippocampus [vHipp]) or changes in NMDAR expression in the fear circuit occur with fear conditioning have not been sufficiently examined. To address this we used near-infrared immunohistochemistry (IHC) to measure AMPAR and NMDAR subunit expression in several nodes of the fear circuit. Long-term changes in GluR1 and GluR2 expression in the ventral hippocampus (vHipp) and anterior cingulate cortex (ACC), enhanced NR2A expression in amygdala nuclei, and changes in the ratio of GluR1/NR2A and GluR2/NR2A in the dHipp was observed with fear conditioning. Most of these changes were dependent on protein synthesis during fear conditioning and were not observed immediately after fear conditioning. The results of the study suggest that global changes in AMPARs and NMDARs occur in multiple nodes within the fear circuit and raise the possibility that these changes contribute to fear memory. Further research examining how global changes in AMPAR, NMDAR, and AMPAR/NMDAR ratios within nodes of the fear circuit contribute to fear memory is needed.
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4

McNally, Gavan P., Joshua P. Johansen, and Hugh T. Blair. "Placing prediction into the fear circuit." Trends in Neurosciences 34, no. 6 (June 2011): 283–92. http://dx.doi.org/10.1016/j.tins.2011.03.005.

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5

Selemon, Lynn D., Keith A. Young, Dianne A. Cruz, and Douglas E. Williamson. "Frontal Lobe Circuitry in Posttraumatic Stress Disorder." Chronic Stress 3 (January 2019): 247054701985016. http://dx.doi.org/10.1177/2470547019850166.

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Symptoms of posttraumatic stress disorder include hyperarousal, avoidance of trauma-related stimuli, re-experiencing of trauma, and mood changes. This review focuses on the frontal cortical areas that form crucial links in circuitry pertinent to posttraumatic stress disorder symptomatology: (1) the conditioned fear extinction circuit, (2) the salience circuit, and (3) the mood circuit. These frontal areas include the ventromedial prefrontal cortex (conditioned fear extinction), the dorsal anterior cingulate and insular cortices (salience), and the lateral orbitofrontal and subgenual cingulate cortices (mood). Frontal lobe structural abnormalities in posttraumatic stress disorder, including volumetric reductions in the cingulate cortices, impact all three circuits. Functional analyses of frontal cortices in posttraumatic stress disorder show abnormal activation in all three according to task demand and emotional valence. Network analyses reveal altered amygdalo-frontal connectivity and failure to suppress the default mode network during cognitive engagement. Spine shape alterations also have been detected in the medial orbitofrontal cortex in posttraumatic stress disorder postmortem brains, suggesting reduced synaptic plasticity. Importantly, frontal lobe abnormalities in posttraumatic stress disorder extend beyond emotion-related circuits to include the lateral prefrontal cortices that mediate executive functions. In conclusion, widespread frontal lobe dysfunction in posttraumatic stress disorder provides a neurobiologic basis for the core symptomatology of the disorder, as well as for executive function impairment.
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6

Wang, Qin, Qi Wang, Xing-Lei Song, Qin Jiang, Yan-Jiao Wu, Ying Li, Ti-Fei Yuan, et al. "Fear extinction requires ASIC1a-dependent regulation of hippocampal-prefrontal correlates." Science Advances 4, no. 10 (October 2018): eaau3075. http://dx.doi.org/10.1126/sciadv.aau3075.

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Extinction of conditioned fear necessitates the dynamic involvement of hippocampus, medial prefrontal cortex (mPFC), and basolateral amygdala (BLA), but key molecular players that regulate these circuits to achieve fear extinction remain largely unknown. Here, we report that acid-sensing ion channel 1a (ASIC1a) is a crucial molecular regulator of fear extinction, and that this function requires ASIC1a in ventral hippocampus (vHPC), but not dorsal hippocampus, mPFC, or BLA. While genetic disruption or pharmacological inhibition of ASIC1a in vHPC attenuated the extinction of conditioned fear, overexpression of the channel in this area promoted fear extinction. Channelrhodopsin-2–assisted circuit mapping revealed that fear extinction involved an ASIC1a-dependent modification of the long-range hippocampal-prefrontal correlates in a projection-specific manner. Gene expression profiling analysis and validating experiments identified several neuronal activity–regulated and memory-related genes, including Fos, Npas4, and Bdnf, as the potential mediators of ASIC1a regulation of fear extinction. Mechanistically, genetic overexpression of brain-derived neurotrophic factor (BDNF) in vHPC or supplement of BDNF protein in mPFC both rescued the deficiency in fear extinction and the deficits on extinction-driven adaptations of hippocampal-prefrontal correlates caused by the Asic1a gene inactivation in vHPC. Together, these results establish ASIC1a as a critical constituent in fear extinction circuits and thus a promising target for managing adaptive behaviors.
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7

Birnie, Matthew T., and Tallie Z. Baram. "Principles of emotional brain circuit maturation." Science 376, no. 6597 (June 3, 2022): 1055–56. http://dx.doi.org/10.1126/science.abn4016.

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8

Amano, T., S. Duvarci, D. Popa, and D. Pare. "The Fear Circuit Revisited: Contributions of the Basal Amygdala Nuclei to Conditioned Fear." Journal of Neuroscience 31, no. 43 (October 26, 2011): 15481–89. http://dx.doi.org/10.1523/jneurosci.3410-11.2011.

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9

Coryell, Matthew W., Adam E. Ziemann, Patricia J. Westmoreland, Jill M. Haenfler, Zlatan Kurjakovic, Xiang-ming Zha, Margaret Price, Mikael K. Schnizler, and John A. Wemmie. "Targeting ASIC1a Reduces Innate Fear and Alters Neuronal Activity in the Fear Circuit." Biological Psychiatry 62, no. 10 (November 2007): 1140–48. http://dx.doi.org/10.1016/j.biopsych.2007.05.008.

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10

Bukalo, Olena, Courtney R. Pinard, Shana Silverstein, Christina Brehm, Nolan D. Hartley, Nigel Whittle, Giovanni Colacicco, et al. "Prefrontal inputs to the amygdala instruct fear extinction memory formation." Science Advances 1, no. 6 (July 2015): e1500251. http://dx.doi.org/10.1126/sciadv.1500251.

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Persistent anxiety after a psychological trauma is a hallmark of many anxiety disorders. However, the neural circuits mediating the extinction of traumatic fear memories remain incompletely understood. We show that selective, in vivo stimulation of the ventromedial prefrontal cortex (vmPFC)–amygdala pathway facilitated extinction memory formation, but not retrieval. Conversely, silencing the vmPFC-amygdala pathway impaired extinction formation and reduced extinction-induced amygdala activity. Our data demonstrate a critical instructional role for the vmPFC-amygdala circuit in the formation of extinction memories. These findings advance our understanding of the neural basis of persistent fear, with implications for posttraumatic stress disorder and other anxiety disorders.
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11

Hanchate, Naresh K., Eun Jeong Lee, Andria Ellis, Kunio Kondoh, Donghui Kuang, Ryan Basom, Cole Trapnell, and Linda B. Buck. "Connect-seq to superimpose molecular on anatomical neural circuit maps." Proceedings of the National Academy of Sciences 117, no. 8 (February 7, 2020): 4375–84. http://dx.doi.org/10.1073/pnas.1912176117.

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The mouse brain contains about 75 million neurons interconnected in a vast array of neural circuits. The identities and functions of individual neuronal components of most circuits are undefined. Here we describe a method, termed “Connect-seq,” which combines retrograde viral tracing and single-cell transcriptomics to uncover the molecular identities of upstream neurons in a specific circuit and the signaling molecules they use to communicate. Connect-seq can generate a molecular map that can be superimposed on a neuroanatomical map to permit molecular and genetic interrogation of how the neuronal components of a circuit control its function. Application of this method to hypothalamic neurons controlling physiological responses to fear and stress reveals subsets of upstream neurons that express diverse constellations of signaling molecules and can be distinguished by their anatomical locations.
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12

Li, Haohong, Mario A. Penzo, Hiroki Taniguchi, Charles D. Kopec, Z. Josh Huang, and Bo Li. "Experience-dependent modification of a central amygdala fear circuit." Nature Neuroscience 16, no. 3 (January 27, 2013): 332–39. http://dx.doi.org/10.1038/nn.3322.

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13

Twining, Robert C., Jaime E. Vantrease, Skyelar Love, Mallika Padival, and J. Amiel Rosenkranz. "An intra-amygdala circuit specifically regulates social fear learning." Nature Neuroscience 20, no. 3 (January 23, 2017): 459–69. http://dx.doi.org/10.1038/nn.4481.

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14

Penzo, Mario A., Vincent Robert, Jason Tucciarone, Dimitri De Bundel, Minghui Wang, Linda Van Aelst, Martin Darvas, et al. "The paraventricular thalamus controls a central amygdala fear circuit." Nature 519, no. 7544 (January 19, 2015): 455–59. http://dx.doi.org/10.1038/nature13978.

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15

Ozawa, Takaaki, and Joshua P. Johansen. "Neural circuit mechanism underlying learning asymptote in fear conditioning." Proceedings of the Annual Convention of the Japanese Psychological Association 79 (September 22, 2015): 3AM—084–3AM—084. http://dx.doi.org/10.4992/pacjpa.79.0_3am-084.

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16

Pendyam, Sandeep, Christian Bravo-Rivera, Anthony Burgos-Robles, Francisco Sotres-Bayon, Gregory J. Quirk, and Satish S. Nair. "Fear signaling in the prelimbic-amygdala circuit: a computational modeling and recording study." Journal of Neurophysiology 110, no. 4 (August 15, 2013): 844–61. http://dx.doi.org/10.1152/jn.00961.2012.

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The acquisition and expression of conditioned fear depends on prefrontal-amygdala circuits. Auditory fear conditioning increases the tone responses of lateral amygdala neurons, but the increase is transient, lasting only a few hundred milliseconds after tone onset. It was recently reported that that the prelimbic (PL) prefrontal cortex transforms transient lateral amygdala input into a sustained PL output, which could drive fear responses via projections to the lateral division of basal amygdala (BL). To explore the possible mechanisms involved in this transformation, we developed a large-scale biophysical model of the BL-PL network, consisting of 850 conductance-based Hodgkin-Huxley-type cells, calcium-based learning, and neuromodulator effects. The model predicts that sustained firing in PL can be derived from BL-induced release of dopamine and norepinephrine that is maintained by PL-BL interconnections. These predictions were confirmed with physiological recordings from PL neurons during fear conditioning with the selective β-blocker propranolol and by inactivation of BL with muscimol. Our model suggests that PL has a higher bandwidth than BL, due to PL's decreased internal inhibition and lower spiking thresholds. It also suggests that variations in specific microcircuits in the PL-BL interconnection can have a significant impact on the expression of fear, possibly explaining individual variability in fear responses. The human homolog of PL could thus be an effective target for anxiety disorders.
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17

Milad, Mohammed R., Sharon C. Furtak, Jennifer L. Greenberg, Aparna Keshaviah, Jooyeon J. Im, Martha J. Falkenstein, Michael Jenike, Scott L. Rauch, and Sabine Wilhelm. "Deficits in Conditioned Fear Extinction in Obsessive-Compulsive Disorder and Neurobiological Changes in the Fear Circuit." JAMA Psychiatry 70, no. 6 (June 1, 2013): 608. http://dx.doi.org/10.1001/jamapsychiatry.2013.914.

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18

Marvar, Paul, Zhe Yu, Laxmi Iyer, and Amy Bhatt. "Evaluation of a Brain Angiotensinergic Circuit in Fear-Related Behavior." Biological Psychiatry 89, no. 9 (May 2021): S50. http://dx.doi.org/10.1016/j.biopsych.2021.02.141.

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19

Marvar, Paul, Zhe Yu, Laxmi Iyer, and Amy Bhatt. "Evaluation of a Brain Angiotensinergic Circuit in Fear-Related Behavior." Biological Psychiatry 89, no. 9 (May 2021): S32. http://dx.doi.org/10.1016/j.biopsych.2021.02.098.

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20

Yu, Zhe, Amy Bhatt, and Paul J. Marvar. "Evaluation of a brain angiotensinergic circuit in fear‐related behavior." FASEB Journal 34, S1 (April 2020): 1. http://dx.doi.org/10.1096/fasebj.2020.34.s1.04887.

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21

Yu, Zhe, Amy Bhatt, and Paul Marvar. "Evaluation of a Brain Angiotensinergic Circuit in Fear-Related Behavior." Biological Psychiatry 87, no. 9 (May 2020): S171. http://dx.doi.org/10.1016/j.biopsych.2020.02.452.

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22

Kritman, Milly, and Mouna Maroun. "Inhibition of the PI3 kinase cascade in corticolimbic circuit: temporal and differential effects on contextual fear and extinction." International Journal of Neuropsychopharmacology 16, no. 4 (May 1, 2013): 825–33. http://dx.doi.org/10.1017/s1461145712000636.

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Abstract We studied the role of PI3K cascade in the basolateral amygdala (BLA) and the infralimbic region of the medial prefrontal cortex (IL-mPFC), in contextual fear learning and extinction in the rat. To that end, we micro-infused the phosphoinositide-3-kinase (PIK3) inhibitor LY294002 into either the mPFC or the BLA. Infusion of LY294002 into the BLA following fear conditioning was associated with enhanced freezing levels and impaired extinction in the subsequent sessions. Similarly, inhibition of PI3K in the BLA before the retrieval of fear memory was associated with impaired retrieval of the fear memory, which was expressed as reduced freezing levels that persisted over 2 d. In the IL-mPFC, only consolidation of fear extinction was impaired: micro-infusion of PI3K inhibitor following the retrieval of fear was associated with impaired extinction on the following days. These results indicate differences in the temporal parameters of the effects of PI3K inhibition in the IL-mPFC and in the BLA, which suggest differential involvement of these structures in long-term fear and in extinction of fear memory. Our findings provide additional evidence for the critical roles played by PI3K in intact formation of fear memory and in its extinction and add new evidence for a role of PI3K in consolidation of memory of extinction. Better understanding of the differential involvement of the PI3K cascade during acquisition and extinction of fear conditioning in the mPFC-amygdala circuit could potentially contribute to the understanding and treatment of anxiety disorders.
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23

Akirav, Irit, and Mouna Maroun. "The Role of the Medial Prefrontal Cortex-Amygdala Circuit in Stress Effects on the Extinction of Fear." Neural Plasticity 2007 (2007): 1–11. http://dx.doi.org/10.1155/2007/30873.

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Stress exposure, depending on its intensity and duration, affects cognition and learning in an adaptive or maladaptive manner. Studies addressing the effects of stress on cognitive processes have mainly focused on conditioned fear, since it is suggested that fear-motivated learning lies at the root of affective and anxiety disorders. Inhibition of fear-motivated response can be accomplished by experimental extinction of the fearful response to the fear-inducing stimulus. Converging evidence indicates that extinction of fear memory requires plasticity in both the medial prefrontal cortex and the amygdala. These brain areas are also deeply involved in mediating the effects of exposure to stress on memory. Moreover, extensive evidence indicates that gamma-aminobutyric acid (GABA) transmission plays a primary role in the modulation of behavioral sequelae resulting from a stressful experience, and may also partially mediate inhibitory learning during extinction. In this review, we present evidence that exposure to a stressful experience may impair fear extinction and the possible involvement of the GABA system. Impairment of fear extinction learning is particularly important as it may predispose some individuals to the development of posttraumatic stress disorder. We further discuss a possible dysfunction in the medial prefrontal cortex-amygdala circuit following a stressful experience that may explain the impaired extinction caused by exposure to a stressor.
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24

Liu, Keming. "Study on the progress of three pathways in anxiety disorders." Transactions on Materials, Biotechnology and Life Sciences 3 (March 24, 2024): 539–47. http://dx.doi.org/10.62051/b13xpe52.

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An overview is presented in this review, which delves into the neural pathways associated with anxiety disorders. The emphasis is placed on the amygdala and prefrontal cortex circuit, the GABAergic pathway, and the serotonin pathway. The amygdala-prefrontal cortex circuit is essential to processing fear and making decisions; anxiety disorders have been linked to disruption in this circuit. The GABAergic pathway, characterized by the release of GABA and inhibition of neuronal activity, is implicated in anxiety through its role in regulating neuronal excitability. Altered GABAergic function is associated with various anxiety disorders. The serotonin pathway, involving the release of serotonin and modulation of mood and stress responses, is also involved in anxiety disorders. Medications targeting these pathways can help modulate the circuits and alleviate anxiety symptoms. Awareness of these pathways is still limited, though, because anxiety is a complicated illness influenced by a number of factors. The main goals of future research should be the development of individualized treatment plans for anxiety disorders and better clarifying the processes of dysregulation.
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25

Chou, Tina, Marina Long, Ashley Hayden, Karianne Sretavan Wong, Benjamin Borron, Anish Kanabar, Thilo Deckersbach, and Darin Dougherty. "38. Transcranial Focused Ultrasound of the Amygdala Down-Modulates Fear Neural Circuit Activation and Facilitates Fear Extinction." Biological Psychiatry 93, no. 9 (May 2023): S84—S85. http://dx.doi.org/10.1016/j.biopsych.2023.02.221.

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26

Corcoran, Kevin A., and Gregory J. Quirk. "Recalling Safety: Cooperative Functions of the Ventromedial Prefrontal Cortex and the Hippocampus in Extinction." CNS Spectrums 12, no. 3 (March 2007): 200–206. http://dx.doi.org/10.1017/s1092852900020915.

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ABSTRACTAnxiety disorders are commonly treated with exposure-based therapies that rely on extinction of conditioned fear. Persistent fear and anxiety following exposure therapy could reflect a deficit in the recall of extinction learning. Animal models of fear learning have elucidated a neural circuit for extinction learning and recall that includes the amygdala, ventromedial prefrontal cortex (vmPFC), and hippocampus. Whereas the amygdala is important for extinction learning, the vmPFC is a site of neural plasticity that allows for the inhibition of fear during extinction recall. We suggest that the vmPFC receives convergent information from other brain regions, such as contextual information from the hippocampus, to determine the circumstances under which extinction or fear will be recalled. Imaging studies of human fear conditioning and extinction lend credence to this extinction network. Understanding the neural circuitry underlying extinction recall will lead to more effective therapies for disorders of fear and anxiety.
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27

Silva, Bianca A., Simone Astori, Allison M. Burns, Hendrik Heiser, Lukas van den Heuvel, Giulia Santoni, Maria Fernanda Martinez-Reza, Carmen Sandi, and Johannes Gräff. "A thalamo-amygdalar circuit underlying the extinction of remote fear memories." Nature Neuroscience 24, no. 7 (May 20, 2021): 964–74. http://dx.doi.org/10.1038/s41593-021-00856-y.

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28

Agetsuma, Masakazu, Issei Sato, Yasuhiro Tanaka, Atsushi Kasai, Yoshiyuki Arai, Miki Yoshitomo, Hitoshi Hashimoto, Junichi Nabekura, and Takeharu Nagai. "Optical and computational dissection of prefrontal neural circuit for fear memory." Proceedings for Annual Meeting of The Japanese Pharmacological Society 94 (2021): 2—S20–4. http://dx.doi.org/10.1254/jpssuppl.94.0_2-s20-4.

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29

Marek, Roger, Cornelia Strobel, Timothy W. Bredy, and Pankaj Sah. "The amygdala and medial prefrontal cortex: partners in the fear circuit." Journal of Physiology 591, no. 10 (April 9, 2013): 2381–91. http://dx.doi.org/10.1113/jphysiol.2012.248575.

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30

Bian, Xin-Lan, Cheng Qin, Cheng-Yun Cai, Ying Zhou, Yan Tao, Yu-Hui Lin, Hai-Yin Wu, Lei Chang, Chun-Xia Luo, and Dong-Ya Zhu. "Anterior Cingulate Cortex to Ventral Hippocampus Circuit Mediates Contextual Fear Generalization." Journal of Neuroscience 39, no. 29 (May 16, 2019): 5728–39. http://dx.doi.org/10.1523/jneurosci.2739-18.2019.

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31

Rigoli, Francesco, Michael Ewbank, Tim Dalgleish, and Andrew Calder. "Threat visibility modulates the defensive brain circuit underlying fear and anxiety." Neuroscience Letters 612 (January 2016): 7–13. http://dx.doi.org/10.1016/j.neulet.2015.11.026.

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32

Todd, Travis P., Matthew Y. Jiang, Nicole E. DeAngeli, and David J. Bucci. "A functional circuit for the retrieval of remote cued fear memory." Behavioral Neuroscience 132, no. 5 (October 2018): 403–8. http://dx.doi.org/10.1037/bne0000237.

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33

Kwapis, Janine L., Timothy J. Jarome, Nicole C. Ferrara, and Fred J. Helmstetter. "Updating Procedures Can Reorganize the Neural Circuit Supporting a Fear Memory." Neuropsychopharmacology 42, no. 8 (January 31, 2017): 1688–97. http://dx.doi.org/10.1038/npp.2017.23.

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34

Lahoud, Nisrine, and Mouna Maroun. "Oxytocinergic manipulations in corticolimbic circuit differentially affect fear acquisition and extinction." Psychoneuroendocrinology 38, no. 10 (October 2013): 2184–95. http://dx.doi.org/10.1016/j.psyneuen.2013.04.006.

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35

Keinath, Alexandra T. "Contextualizing a Prefrontal-to-Lateral Entorhinal Cortex Circuit Mediating Fear Expression." Biological Psychiatry 94, no. 3 (August 2023): e11-e13. http://dx.doi.org/10.1016/j.biopsych.2023.05.011.

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36

Bühler, Anja, and Matthias Carl. "Zebrafish Tools for Deciphering Habenular Network-Linked Mental Disorders." Biomolecules 11, no. 2 (February 20, 2021): 324. http://dx.doi.org/10.3390/biom11020324.

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The prevalence of patients suffering from mental disorders is substantially increasing in recent years and represents a major burden to society. The underlying causes and neuronal circuits affected are complex and difficult to unravel. Frequent disorders such as depression, schizophrenia, autism, and bipolar disorder share links to the habenular neural circuit. This conserved neurotransmitter system relays cognitive information between different brain areas steering behaviors ranging from fear and anxiety to reward, sleep, and social behaviors. Advances in the field using the zebrafish model organism have uncovered major genetic mechanisms underlying the formation of the habenular neural circuit. Some of the identified genes involved in regulating Wnt/beta-catenin signaling have previously been suggested as risk genes of human mental disorders. Hence, these studies on habenular genetics contribute to a better understanding of brain diseases. We are here summarizing how the gained knowledge on the mechanisms underlying habenular neural circuit development can be used to introduce defined manipulations into the system to study the functional behavioral consequences. We further give an overview of existing behavior assays to address phenotypes related to mental disorders and critically discuss the power but also the limits of the zebrafish model for identifying suitable targets to develop therapies.
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37

Vergara, Pablo, Deependra Kumar, Sakthivel Srinivasan, Iyo Koyanagi, Toshie Naoi, Sima Singh, and Masanori Sakaguchi. "Remapping of Adult-Born Neuron Activity during Fear Memory Consolidation in Mice." International Journal of Molecular Sciences 22, no. 6 (March 12, 2021): 2874. http://dx.doi.org/10.3390/ijms22062874.

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The mammalian hippocampal dentate gyrus is a unique memory circuit in which a subset of neurons is continuously generated throughout the lifespan. Previous studies have shown that the dentate gyrus neuronal population can hold fear memory traces (i.e., engrams) and that adult-born neurons (ABNs) support this process. However, it is unclear whether ABNs themselves hold fear memory traces. Therefore, we analyzed ABN activity at a population level across a fear conditioning paradigm. We found that fear learning did not recruit a distinct ABN population. In sharp contrast, a completely different ABN population was recruited during fear memory retrieval. We further provide evidence that ABN population activity remaps over time during the consolidation period. These results suggest that ABNs support the establishment of a fear memory trace in a different manner to directly holding the memory. Moreover, this activity remapping process in ABNs may support the segregation of memories formed at different times. These results provide new insight into the role of adult neurogenesis in the mammalian memory system.
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38

Tieu, Kinh H., Andrew L. Keidel, John P. McGann, Billie Faulkner, and Thomas H. Brown. "Perirhinal-amygdala circuit-level computational model of temporal encoding in fear conditioning." Psychobiology 27, no. 1 (March 1999): 1–25. http://dx.doi.org/10.3758/bf03332095.

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39

Yang, Ben, Javier Sanches-Padilla, Jyothisri Kondapalli, Sage L. Morison, Eric Delpire, Rajeshwar Awatramani, and D. James Surmeier. "Locus coeruleus anchors a trisynaptic circuit controlling fear-induced suppression of feeding." Neuron 109, no. 5 (March 2021): 823–38. http://dx.doi.org/10.1016/j.neuron.2020.12.023.

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40

Marcinkiewcz, Catherine A., Christopher M. Mazzone, Giuseppe D’Agostino, Lindsay R. Halladay, J. Andrew Hardaway, Jeffrey F. DiBerto, Montserrat Navarro, et al. "Serotonin engages an anxiety and fear-promoting circuit in the extended amygdala." Nature 537, no. 7618 (August 24, 2016): 97–101. http://dx.doi.org/10.1038/nature19318.

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41

Fadok, Jonathan P., Sabine Krabbe, Milica Markovic, Julien Courtin, Chun Xu, Lema Massi, Paolo Botta, et al. "A competitive inhibitory circuit for selection of active and passive fear responses." Nature 542, no. 7639 (January 25, 2017): 96–100. http://dx.doi.org/10.1038/nature21047.

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42

McClure, Erin B., Christopher S. Monk, Eric E. Nelson, Jessica M. Parrish, Abby Adler, R. James R. Blair, Stephen Fromm, et al. "Abnormal Attention Modulation of Fear Circuit Function in Pediatric Generalized Anxiety Disorder." Archives of General Psychiatry 64, no. 1 (January 1, 2007): 97. http://dx.doi.org/10.1001/archpsyc.64.1.97.

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43

Yan, Xiaoling, Liming Wang, Xing Xu, and Xiangjun Wang. "Discussion on Political Construction of Circuit Course." SHS Web of Conferences 157 (2023): 03018. http://dx.doi.org/10.1051/shsconf/202315703018.

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Under the background of engineering, in order to achieve the teaching goal of “Cultivate people with virtue”, the ideological and political construction of engineering courses pays more attention to strengthening students’ engineering ethics education, cultivating students’ spirit of striving for excellence as a great country craftsman, stimulating students’ feelings and mission of serving the country with science and technology, so that to help students get better knowledge and skills. The paper takes the course of circuit as an example, organically integrates the ideological and political elements of the curriculum into the learning process of the circuit curriculum so that to eliminate students’ fear of difficulties in curriculum learning, and increase their self-confidence by excavating the ideological and political elements in the circuit curriculum, carrying out reasonable curriculum design.
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44

Dicle, Mehmet F., and Kendra Reed. "Asymmetric return response to expected risk: policy implications." Journal of Financial Regulation and Compliance 27, no. 3 (July 8, 2019): 345–56. http://dx.doi.org/10.1108/jfrc-01-2018-0004.

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Purpose As investors’ fear has an impact on their risk-return tradeoff, this fear leaves markets susceptible to sudden and large fluctuations. The purpose of this study is to suggest regulators to amend their precautionary methods to recognize the difference in investor behavior for high-risk periods versus low-risk periods. Design/methodology/approach The authors empirically show the difference in investor response to changes in expected risk as a function of level of risk. They then show different return patterns for high-risk and low-risk days. Their approach is implemented to evaluate whether investors’ reaction is the same to changes in risk during high-risk versus low-risk periods. Findings The results indicate that the negative return response to incremental increases in risk is significantly higher for periods of high versus low expected risk, with high defined as risk levels above long-run normal. Research limitations/implications Investors’ increased response to changes in risk exposes financial markets to higher likelihood of sudden and larger fluctuations during high-risk periods. Regulator-imposed circuit breakers are designed to protect markets against such market crashes. However, circuit breakers are not designed to account for investor behavior changes. The results show that circuit breakers should be different for high- versus low-risk periods. Practical implications A circuit breaker that is designed to protect investors against large drops should be amended to have a lower threshold during high-risk periods. Originality/value The contribution is, to the authors’ knowledge, the first research effort to evaluate the effects of differences in investor behavior on investor reactions and regulator imposed fail-safes. During the times of extreme market risk, the proposed changes may enable circuit breakers function their intended purposes.
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45

Zahm, Daniel S., and Michael Trimble. "The Dopaminergic Projection System, Basal Forebrain Macrosystems, and Conditioned Stimuli." CNS Spectrums 13, no. 1 (January 2008): 32–40. http://dx.doi.org/10.1017/s1092852900016138.

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ABSTRACTThis review begins with a description of some problems that recently have beset an influential circuit model of fear conditioning and goes on to look at neuroanatomy that may subserve conditioning viewed in a broader perspective, including not only fear but also appetitive conditioning. The column will then focus on basal forebrain functional-anatomical systems, or macrosystems, as they have come to be called. Yet, more specific attention is then given to the relationships of the dorsal and ventral striatopallidal systems and extended amygdala with the dopaminergic mesotelencephalic projection systems, culminating with the hypothesis that all macrosystems contribute to behavioral conditioning.
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46

Ke, Shuo, Feiyu Wang, Chuanyu Fu, Huiwu Mao, Yixin Zhu, Xiangjing Wang, Changjin Wan, and Qing Wan. "Artificial fear neural circuit based on noise triboelectric nanogenerator and photoelectronic neuromorphic transistor." Applied Physics Letters 123, no. 12 (September 18, 2023). http://dx.doi.org/10.1063/5.0167011.

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Fear neural circuits can recognize precisely threatening stimuli and enable the early-warning for the individual in the real world. In this regard, implementation of fear neural circuits functions by neuromorphic devices could potentially improve the intelligent adaptability and cognition of humanoid robots. Here, an artificial fear neural circuit is proposed, which consists of a noise triboelectric nanogenerator (N-TENG) and an amorphous indium gallium zinc oxide based photoelectronic neuromorphic transistor (IGZO-PNT). Such an artificial fear neural circuit collects sound wave and light signals from the N-TENG and a-IGZO channel, respectively, converts these signals to electrical signals and integrates them into excitatory postsynaptic currents by the IGZO-PNT. The innate-fear and learned-fear behaviors are emulated by our artificial fear neural circuit. Furthermore, as a proof of concept, the escape behavior after fear triggered is realized by using a vibrator. Our biomimetic design can promote the developments of next-generation photoelectronic neuromorphic systems and humanoid robots.
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47

Correia, Susana S., Anna G. McGrath, Allison Lee, Ann M. Graybiel, and Ki A. Goosens. "Amygdala-ventral striatum circuit activation decreases long-term fear." eLife 5 (September 27, 2016). http://dx.doi.org/10.7554/elife.12669.

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In humans, activation of the ventral striatum, a region associated with reward processing, is associated with the extinction of fear, a goal in the treatment of fear-related disorders. This evidence suggests that extinction of aversive memories engages reward-related circuits, but a causal relationship between activity in a reward circuit and fear extinction has not been demonstrated. Here, we identify a basolateral amygdala (BLA)-ventral striatum (NAc) pathway that is activated by extinction training. Enhanced recruitment of this circuit during extinction learning, either by pairing reward with fear extinction training or by optogenetic stimulation of this circuit during fear extinction, reduces the return of fear that normally follows extinction training. Our findings thus identify a specific BLA-NAc reward circuit that can regulate the persistence of fear extinction and point toward a potential therapeutic target for disorders in which the return of fear following extinction therapy is an obstacle to treatment.
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48

Cheung, Hoiyin, Tong-Zhou Yu, Xin Yi, Yan-Jiao Wu, Qi Wang, Xue Gu, Miao Xu, et al. "An ultra-short-acting benzodiazepine in thalamic nucleus reuniens undermines fear extinction via intermediation of hippocamposeptal circuits." Communications Biology 7, no. 1 (June 14, 2024). http://dx.doi.org/10.1038/s42003-024-06417-w.

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AbstractBenzodiazepines, commonly used for anxiolytics, hinder conditioned fear extinction, and the underlying circuit mechanisms are unclear. Utilizing remimazolam, an ultra-short-acting benzodiazepine, here we reveal its impact on the thalamic nucleus reuniens (RE) and interconnected hippocamposeptal circuits during fear extinction. Systemic or RE-specific administration of remimazolam impedes fear extinction by reducing RE activation through A type GABA receptors. Remimazolam enhances long-range GABAergic inhibition from lateral septum (LS) to RE, underlying the compromised fear extinction. RE projects to ventral hippocampus (vHPC), which in turn sends projections characterized by feed-forward inhibition to the GABAergic neurons of the LS. This is coupled with long-range GABAergic projections from the LS to RE, collectively constituting an overall positive feedback circuit construct that promotes fear extinction. RE-specific remimazolam negates the facilitation of fear extinction by disrupting this circuit. Thus, remimazolam in RE disrupts fear extinction caused by hippocamposeptal intermediation, offering mechanistic insights for the dilemma of combining anxiolytics with extinction-based exposure therapy.
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Riccardo, Barchiesi, Chanthongdee Kanat, Petrella Michele, Xu Li, Söderholm Simon, Domi Esi, Augier Gaelle, et al. "An epigenetic mechanism for over-consolidation of fear memories." Molecular Psychiatry, September 21, 2022. http://dx.doi.org/10.1038/s41380-022-01758-6.

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AbstractExcessive fear is a hallmark of anxiety disorders, a major cause of disease burden worldwide. Substantial evidence supports a role of prefrontal cortex-amygdala circuits in the regulation of fear and anxiety, but the molecular mechanisms that regulate their activity remain poorly understood. Here, we show that downregulation of the histone methyltransferase PRDM2 in the dorsomedial prefrontal cortex enhances fear expression by modulating fear memory consolidation. We further show that Prdm2 knock-down (KD) in neurons that project from the dorsomedial prefrontal cortex to the basolateral amygdala (dmPFC-BLA) promotes increased fear expression. Prdm2 KD in the dmPFC-BLA circuit also resulted in increased expression of genes involved in synaptogenesis, suggesting that Prdm2 KD modulates consolidation of conditioned fear by modifying synaptic strength at dmPFC-BLA projection targets. Consistent with an enhanced synaptic efficacy, we found that dmPFC Prdm2 KD increased glutamatergic release probability in the BLA and increased the activity of BLA neurons in response to fear-associated cues. Together, our findings provide a new molecular mechanism for excessive fear responses, wherein PRDM2 modulates the dmPFC -BLA circuit through specific transcriptomic changes.
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50

Yau, Joanna Oi-Yue, Amy Li, Lauren Abdallah, Leszek Lisowksi, and Gavan P. McNally. "State- and circuit-dependent opponent-processing of fear." Journal of Neuroscience, July 26, 2024, e0857242024. http://dx.doi.org/10.1523/jneurosci.0857-24.2024.

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The presence of valence coding neurons in the basolateral amygdala (BLA) that form distinct projections to other brain regions implies functional opposition between aversion and reward during learning. However, evidence for opponent interactions in fear learning is sparse and may only be apparent under certain conditions. Here we test this possibility by studying the roles of the BLA→central amygdala (CeA) and BLA→nucleus accumbens (Acb) pathways in fear learning in male rats. First, we assessed the organisation of these pathways in the rat brain. BLA→CeA and BLA→Acb pathways were largely segregated in the BLA but shared overlapping molecular profiles. Then we assessed activity of the BLA→CeA and BLA→Acb pathways during two different forms of fear learning - fear learning in a neutral context and fear learning in a reward context. BLA → CeA neurons were robustly recruited by footshock regardless of where fear learning occurred whereas recruitment of BLA→Acb neurons was state-dependent because footshock only recruited this pathway in a reward context. Finally, we assessed the causal roles of activity in these pathways in fear learning. Photoinhibition of the BLA→CeA pathway during the footshock US impaired fear learning, regardless of where fear learning occurred. In contrast, photoinhibition of the BLA→Acb pathway augmented fear learning, but only in the reward context. Taken together, our findings show circuit- and state-dependent opponent processing of fear. Footshock activity in the BLA → Acb pathway limits how much fear is learned.Significance StatementHere we identify a fear opponent process in the brain. We show that an aversive event can recruit distinct populations of neurons in the rat basolateral amygdala. One population projects to the central amygdala to promote fear learning. A second population projects to the nucleus accumbens to oppose fear learning. These nucleus accumbens projecting neurons limit how much fear is learned and are candidates for therapeutic targeting to minimize the amount of fear learned after a traumatic experience.
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