Relevant bibliographies by topics / Fear circuit

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  2. Dissertations / Theses
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  4. Book chapters
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Academic literature on the topic 'Fear circuit'

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Published: 2 November 2024

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Journal articles on the topic "Fear circuit"

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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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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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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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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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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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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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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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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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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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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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Dissertations / Theses on the topic "Fear circuit"

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Wright, Kristina M. "Revising the Role of the Ventrolateral Periaqueductal Gray in the Fear Circuit:." Thesis, Boston College, 2021. http://hdl.handle.net/2345/bc-ir:109159.

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Thesis advisor: Michael A. McDannald
Thesis advisor: John P. Christianson
The ability to accurately evaluate and respond to threats is vital to survival. Disruptions in neural circuits of fear give rise to maladaptive threat responding, and have clinical implications in fear and anxiety disorders. To better inform therapeutic interventions, it is imperative that roles for regions classically associated with fear continue to be refined, and that novel nodes are incorporated into what is most certainly a larger fear circuit. In the canonical view, threat estimates are generated at the level of the amygdala and sent to the ventrolateral periaqueductal gray (vlPAG), which organizes an appropriate behavioral response, most notably freezing. Despite a multitude of studies successfully linking the vlPAG and Pavlovian fear behavior, evidence of a direct neural correlate for fear expression in the vlPAG is lacking. By contrast, a role for the caudal substantia nigra (cSN) in fear, stands apart from its canonical associations with movement and reward processes. Although there is new interest in examining a role for the nigra in fear modulation, this is essentially an uncharted area of discovery. The goals of this dissertation are three-fold. First, to propose a role for vlPAG activity in threat estimation, a function previously restricted to the upstream amygdala. Second, to scrutinize vlPAG neural activity using a novel multi-cue Pavlovian procedure and identify the long-anticipated, direct neural correlate for fear expression. Third, to present causal evidence supporting the cSN as a potential node in a circuit that most certainly extends beyond regions canonically associated with fear
Thesis (PhD) — Boston College, 2021
Submitted to: Boston College. Graduate School of Arts and Sciences
Discipline: Psychology
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Yuzhe, Li. "Computational Investigations on Uncertainty-Dependent Extinction of Fear Memory." 京都大学 (Kyoto University), 2017. http://hdl.handle.net/2433/225756.

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Pagani, Jerome H. "The medial hypothalamic defensive circuit and predator odor-induced fear a comparison of electrolytic and neurotoxic lesions /." Access to citation, abstract and download form provided by ProQuest Information and Learning Company; downloadable PDF file, 127 p, 2007. http://proquest.umi.com/pqdweb?did=1397903941&sid=8&Fmt=2&clientId=8331&RQT=309&VName=PQD.

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Aime, Mattia. "Circuit mechanisms for encoding discriminative learning in the dorsal prefrontal cortex of behaving mice." Thesis, Bordeaux, 2017. http://www.theses.fr/2017BORD0805/document.

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Chez les mammifères, le néocortex constitue une structure remarquablement plastique assurant leurs multiples capacités d’adaptation et d’apprentissage. Par exemple, l’apprentissage associatif permet à chaque individu d’apprendre les relations entre un événement particulier (un danger par exemple) et les signaux environnementaux qui y sont associés, afin d’en anticiper les conséquences s’il se reproduit dans le futur. Dans le cas de la peur conditionnée, l'apprentissage associatif améliore les capacités de discrimination des signaux de menace et de sécurité, garantissant ainsi une représentation précise de l'environnement. Ce processus comportemental est en partie dépendant de l'interaction entre deux structures cérébrales: le cortex préfrontal (PFC) et le complexe basolatéral de l'amygdale (BLA). Bien que le PFC puisse encoder à la fois les mémoires de menace et de sécurité qui seraient recrutées préférentiellement après l'apprentissage, on ignore toujours si une telle représentation discriminative existe réellement, et si oui, les mécanismes neuronaux et synaptiques qui en sont à l'origine. Au cours de mon travail de thèse, j'ai démontré que l'activité des neurones excitateurs du PFC est nécessaire à la discrimination entre les signaux de menace et de sécurité grâce à la formation d'ensembles spécifiques de neurones. Au cours de l'apprentissage, les neurones pyramidaux sont potentialisés et recrutés au sein de ses ensembles grâce à l'association au niveau dendritique d'événements synaptiques non-linéaires issus des entrées sensorielles avec des entrées synaptiques provenant de la BLA. En conclusion, nos données fournissent la preuve d'un nouveau mécanisme synaptique qui associe, pendant l'apprentissage, l'expérience perçue avec l’état émotionnel transmis par la BLA permettant ainsi la formation d'ensembles neuronaux dans le cortex préfrontal
The ability of an organism to predict forthcoming events is crucial for survival, and depends on the repeated contingency and contiguity between sensory cues and the events (i.e. danger) they must predict. The resulting learned association provides an accurate representation of the environment by increasing discriminative skills between threat and safety signals, most likely as a result of the interaction between the prefrontal cortex (PFC) and the basolateral amygdala (BLA). Although it suggests that local neuronal networks in the PFC might encode opposing memories that are preferentially selected during recall by recruiting specific cortical or subcortical structures, whether such a discriminative representation is wired within discrete prefrontal circuits during learning and by which synaptic mechanisms remain unclear. Here, the work at issue demonstrates that discrimination learning of both safe and fear-conditioned stimuli depends on full activity of the frontal association cortex, and is associated with the formation of cue-specific neuronal assemblies therein. During learning, prefrontal pyramidal neurons were potentiated through sensory-driven dendritic non-linearities supported by the activation of long-range inputs from the basolateral amygdala (BLA). Taken together, these data provide evidence for a new synaptic level mechanism that coincidently link (or meta-associate) during learning features of perceived experience with BLA mediated emotional state into prefrontal memory assemblies
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Lima, Miguel Antonio Xavier de. "Investigação da circuitaria cortical envolvida no processamento do medo contextual à ameça predatória." Universidade de São Paulo, 2015. http://www.teses.usp.br/teses/disponiveis/42/42131/tde-17022016-135344/.

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Lesões na parte ventral do núcleo anteromedial do tálamo (AMv) interferem no processamento da memória aversiva predatória sem no entanto influenciar as respostas de defesa inatas do animal frente a um predador. O escopo deste trabalho foi entender melhor o papel do AMv e investigar se seus alvos de projeção corticais também interferem no processamento da memória aversiva. No primeiro experimento detectamos que o AMv participa da aquisição da memória aversiva. As áreas corticais pré-límbica, cingulada anterior, visual anteromedial e retroesplenial ventral, recebem e integram entre si projeções oriundas do AMv, além de enviar projeções para a amígdala e hipocampo. Estas áreas corticais estão seletivamente recrutadas durante a exposição ao predador, e observamos que lesões neuroquímicas afetaram severamente a formação da memória aversiva. Nossos dados sugerem que há um circuito de áreas corticais que está criticamente envolvido no processo mnemônico aqui abordado, e fornece as primeiras evidências para a hipótese de módulos corticais a partir do conectoma do rato.
Neurochemical lesions placed into ventral part of anteromedial thalamic nucleus (AMv) disrupt contextual, but not innate, fear responses to predatory threats. In the present investigation, we determined whether the AMv is involved in the acquisition and/or retrieval of the conditioned responses, and if its cortical targets are involved in the fear memory processing. In the first assay, we found that AMv has a critical role in the acquisition of conditioned responses. The cortical areas prelimbic (PL), anterior cingulate area (ACA), anteromedial visual area (VISam) and the ventral part of retrosplenial area (RSPv), receive projections from AMv and are recruited during predator exposure. The integrity of these cortical areas is required for the processing of the mnemonic processes here addressed. Our data corroborate current ideas on functional cortical modules, and help to elucidate how they are involved in the acquisition of fear memories related to life threatening situations.
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Bouarab, Chloe. "Modifications post-traductionnelles des histones au sein du circuit hippocampo-amygdalien déterminant le passage d'une mémoire de peur normale à une mémoire traumatique." Thesis, Bordeaux, 2016. http://www.theses.fr/2016BORD0261/document.

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Les altérations mnésiques associées au trouble de stress post-traumatique (TSPT) constituent un aspect fondamental de la symptomatologie de cette pathologie. Cette altération qualitative de la mémoire inclut à la fois une hypermnésie, c’est-à-dire une intensification de la mémoire vis-à-vis du coeur de l’événement traumatique, et une amnésie de type déclaratif pour les éléments contextuels péri-traumatiques. Les données chez l’Homme suggèrent que ces altérations mnésiques pourraient être sous-tendues par une hyper-activation amygdalienne et un dysfonctionnement hippocampique, respectivement. Cependant, les bases neurobiologiques, et en particulier moléculaires, du TSPT restent largement méconnues. Un modèle comportemental développé chez la souris au laboratoire et basé sur un conditionnement aversif permet précisément de comparer une mémoire de peur normale, c’est-à-dire « contextualisée » et adaptée, à une mémoire pathologique de type TSPT, c’est-à-dire « décontextualisée » et focalisée sur un élément saillant du trauma. Dans la mesure où il a été montré que le développement d’une mémoire de peur contextuelle implique certaines modifications épigénétiques spécifiques, nos travaux ont eu pour objectif de déterminer les altérations des modifications post-traductionnelles d’histones qui sous-tendent le développement d’une mémoire traumatique au lieu d’une mémoire de peur normale. Nos résultats révèlent (1) que des profils spécifiques différents des états d’acétylation/méthylation de l’histone H3 dans le réseau hippocampo-amygdalien sont associés à une mémoire de peur normale et à une mémoire traumatique de type TSPT. Spécifiquement, une mémoire de peur normale est associée à une forte acétylation de H3K9 hippocampique, tandis qu’une mémoire traumatique de type TSPT s’accompagne d’une hyperméthylation de H3K9 dans l’hippocampe, traduisant une répression transcriptionnelle, ainsi que d’une diminution de la tri-méthylation de H3K27 dans l’amygdale latérale, caractéristique d’une activation transcriptionnelle. De plus, nos travaux montrent (2) qu’une modulation pharmacologique de la balance des états d’acétylation/méthylation de H3K9 dans l’hippocampe permet de promouvoir ou de prévenir le développement d’une mémoire traumatique. Enfin, (3) une dernière série d’expériences révèle (i) qu’un stress prénatal est un facteur de risque au développement d’une mémoire traumatique, (ii) que cette dernière est associée à des profils épigénétiques spécifiques, et (iii) qu’une telle vulnérabilité peut se transmettre de manière intergénérationnelle
Memory alterations associated with post-traumatic stress disorder (PTSD) are a fundamental feature of this pathology. PTSD is characterized both by hypermnesia for simple salient trauma-related stimuli and amnesia for peri-traumatic contextual cues. In humans, this disorder is associated with hippocampal hypofunction and amygdalar hyperfunction, which may underlie such paradoxical memory pattern. However, neurobiological bases of PTSD, particularly at the molecular level, remain largely unknown. A behavioral model based on aversive conditioning was developed in mice by our team. This model allows the comparison between a normal, i.e. “contextualized” and adaptive, fear memory, and a PTSD-like pathological fear memory, i.e. “decontextualized” and focused on a salient cue of the trauma. Since specific epigenetic alterations have been involved in the development of contextual fear memory, our aim was the identification of the alterations in post-translational histone modifications underlying the development of traumatic memory instead of normal fear memory. Our results first reveal that normal and PTSD-like fear memory are associated with distinct acetylation/methylation profiles of histone H3 in the hippocampal-amygdalar network. Specifically, we show that, compared to normal fear memory, PTSD-like memory is associated with a switch from H3K9 hyperacetylation (marker of transcriptional activation) to H3K9 hypermethylation (marker of transcriptional repression) in hippocampal CA1, as well as a significant reduction of H3K27 trimethylation, which results in an increased transcription, in the lateral amygdala. Second, we show that the pharmacological manipulation of the acetylation/methylation balance of H3K9 in the hippocampus can prevent or promote the development of PTSD-like memory. Finally, a last series of experiments shows that (i) prenatal stress is a risk factor for the development of PTSD-like memory, (ii) which is associated with specific epigenetic alterations and (iii) that such vulnerability to stress can be transmitted to subsequent generations
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SILVA, BIANCA AMBROGINA. "INDEPENDENT HYPOTHALAMIC CIRCUITS FOR SOCIAL AND PREDATOR FEAR." Doctoral thesis, Università degli Studi di Milano, 2014. http://hdl.handle.net/2434/229915.

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Fear is a distressing negative sensation induced by a perceived threat. This emotion is necessary for the survival of the individual, since it guarantees appropriate responses to life challenging threats. In the last decades research on the neural mechanisms underling such emotion both in humans and in animal models have been mostly focused on the amygdala. In particular fear models in rodents typically rely on foot shock based paradigms. However, innate and learned fear elicited by other stimuli such as predators or aggressive members of the same species has been shown to be regulated by other circuits where the triggering, coordination and the expression of fear seem to be centered in the hypothalamus and periaqueductal grey. Nevertheless very little is known about the function and physiology of these structures in fear processing. To study the function of the medial hypothalamic fear circuit, we developed a novel behavioral paradigm to measure innate and conditioned fear responses to social and predator threats in mice. We subsequently created tools to selectively inhibit specific hypothalamic nuclei during the fear and we observed the inhibition of the ventromedial hypothalamus, a nucleus previously studied for its function in feeding, sex and aggression, specifically impaired social and predator fear but not foot shock fear. Moreover we demonstrated that different portions of this nucleus account for fear to different threats with the dorsomedial portion, previously implicated in feeding function, processing predator fear, and the ventrolateral portion, previously implicated in sex and aggression, processing social fear. Our results demonstrate that the hypothalamus plays a crucial role in fear processing even if it is not recruited during foot shock exposure, suggesting that it might be a good target for the treatment of fear related disorders like panic or phobias and we are now trying to identify possible drugs specifically acting in this area. On the other hand, we showed that specific hypothalamic subnuclei are recruited selectively during social or predator fear, corroborating the hypothesis that different types of fear are processed by separate brain circuits. Such evidence opens the possibility of targeted therapy of pathological fear in humans. Interestingly these same hypothalamic structures are fundamental regulators of non-fear motivated behaviors that are essential for survival such as feeding behavior, aggression and sex and we are now investigating how the same nuclei can orchestrate multiple functions.
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Carey, Guillaume. "Imaging anxiety in Parkinson's disease." Electronic Thesis or Diss., Université de Lille (2022-....), 2024. https://pepite-depot.univ-lille.fr/ToutIDP/EDBSL/2024/2024ULILS023.pdf.

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L'anxiété dans la maladie de Parkinson (MP) est un symptôme non-moteur fréquent et invalidant dont la prise en charge est difficile. La faible connaissance des mécanismes impliqués est une limite à sa prise en charge. L'objectif de ce travail était d'identifier les mécanismes sous-jacents de l'anxiété liée à la MP, via une approche IRM cérébrale multimodale.Une revue systématique de la littérature portant sur les données d'imagerie dans l'anxiété liée à la MP a d'abord été réalisée, permettant de générer de premières hypothèses. Ensuite, plusieurs études incluant des analyses en IRM cérébrale structurale et fonctionnelle ont été menées chez des patients atteints de MP et présentant ou non une anxiété cliniquement significative. Nos analyses se sont focalisées sur le circuit de la peur, connu pour être impliqué dans les troubles anxieux, et le circuit cortico-striato-thalamo-cortical limbique, connu pour son implication dans les symptômes psycho-comportementaux de la MP.Nos résultats suggèrent que l'anxiété liée à la MP serait la conséquence d'un déséquilibre fonctionnel et structural entre ces deux circuits. Certaines structures communes, comme le thalamus, le striatum ou les noyaux du tronc cérébral, pourraient être des zones clés dont l'altération pourrait expliquer la forte prévalence de ces troubles dans la MP. D'autres travaux s'appuyant notamment sur les avancées technologiques en imagerie et sur de nouveaux concepts concernant la physiopathologie de la MP, seront nécessaires pour répondre à ces questions
Anxiety in Parkinson's disease (PD) is a frequent and disabilitating non-motor symptom. It is difficult to manage, partly due to a poor knowledge of the underlying mechanisms. The objective of this thesis was to identify the underlying mechanisms of PD-related anxiety, using multimodal brain MRI.A systematic review of the literature on imaging data in PD-related anxiety was first carried out, allowing the generation of initial hypotheses. Then, several studies including structural and functional brain MRI analyses were carried out in PD patients with or without clinically significant anxiety. Our analyses focused on the fear circuit, known to be involved in anxiety disorders and fear processing, and the limbic cortico-striato-thalamo-cortical circuit, known for its involvement in the neuropsychiatric symptoms of PD.Our results suggest that PD-related anxiety is the consequence of a functional and structural imbalance between these two circuits. Certain overlapping structures, such as the thalamus, the striatum or the brainstem nuclei, could be key areas whose alteration could explain the high prevalence of these disorders in PD. Further works based in particular on technological advances in imaging and new concepts concerning the pathophysiology of PD will be necessary to answer the remaining questions
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Joly, Fanny. "Impacts d’une perturbation de la voie TSC2/mTOR dans l’amygdale dès l’adolescence sur le comportement de peur et la fonctionnalité du cortex préfrontal chez le rat adulte Disruption of Amygdala Tsc2 in Adolescence Leads to Changed Prelimbic Cellular Activity and Generalized Fear Responses at Adulthood in Rats." Thesis, université Paris-Saclay, 2021. http://www.theses.fr/2021UPASL016.

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L’adolescence est une période développementale vulnérable marquée par d’intenses modifications structurelles et fonctionnelles des réseaux qui assurent la régulation des comportements émotionnels et cognitifs. Les processus de maturation de ces réseaux sont influencés par les facteurs environnementaux et génétiques. Le syndrome de stress post-traumatique (PTSD) est un trouble psychiatrique caractérisé par des peurs exagérées, des généralisations de la peur et des déficits d’extinction de peur. Les facteurs de prédisposition au PTSD sont peu connus, mais nous savons qu’un stress intense subi au cours de l’adolescence favorise son apparition à l’âge adulte lorsqu’un individu est confronté à un nouvel événement traumatique.Au cours de cette thèse, nous avons étudié la fonctionnalité de deux structures du circuit de la peur, l’amygdale et le cortex préfrontal, qui suivent une maturation asynchrone. L’amygdale étant fonctionnellement mature à l’âge juvénile, elle est en position de modifier la maturation tardive du cortex préfrontal (mPFC). Nous avons donc voulu tester l’impact d’une dérégulation de la voie Tsc2/mTOR dans les cellules excitatrices du noyau basolatéral de l’amygdale (BLA) du rat au début (25 jours post-natal, PN25), ou à la fin (PN50) de l’adolescence. Le comportement émotionnel à l’âge adulte a été évalué à l’aide d’un conditionnement Pavlovien et l’activité basale du mPFC par la mesure de l’expression du gène immédiat précoce c-FOS. Nous montrons que seuls les rats altérés à l’adolescence (PN25) présentent à l’âge adulte des symptômes typiques du PTSD (déficit d’extinction et généralisation de la peur), associés à une augmentation de l’activité basale du mPFC, en particulier dans les couches corticales impliquées dans le maintien de la mémoire de peur. Ainsi, une modification de la fonctionnalité de l’amygdale au début de l’adolescence pourrait être un facteur de prédisposition à l’apparition d’un PTSD à l’âge adulte
Adolescence is a highly sensitive developmental period characterized by massive structural and functional changes in networks regulating emotional and cognitive behaviors, with maturational processes influenced by environmental and genetical factors. Post-traumatic stress disorder (PTSD) is a psychiatric disorder characterized by an exaggerated fear, overgeneralization, and deficits in fear extinction. Nowadays, genetical and/or environmental predisposal factors for PTSD are not fully understood, but we know that an intense stress or a trauma endured during adolescence promotes the appearance of PTSD at adulthood following a novel trauma exposure.In this thesis, we particularly studied two structures that belong to the fear-network, the amygdala and prefrontal cortex, which follow an asynchronous maturation. While the amygdala is functionally mature at a juvenile age, its activity could impact the late maturation of the medial prefrontal cortex (mPFC). We aimed to study the impact of a disruption of Tsc2/mTOR pathway in the excitatory cells of the basolateral nucleus of the amygdala (BLA) in rats at young adolescence (post-natal day 25, PN25) or at the end of adolescence (PN50). When animals had reached adulthood, we assessed emotional behavior through a Pavlovian fear conditioning protocol, and the basal mPFC activity through the measure of expression of immediate early gene c-FOS. We show that only animals altered during young adolescence presented at the adult age typical symptoms of PTSD (fear extinction deficits, overgeneralization of fear), associated with an increase of mPFC basal activity, especially in cortical layers known to be involved in the maintenance of fear memory and expression. Thus, we suggest that a developmental dysfunction of the amygdala early in adolescence could be a predisposal factor to PTSD appearance at adulthood
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Hancock, Kate. "Women's perceptions of safety : CCTV in an inner city setting." Thesis, Edith Cowan University, Research Online, Perth, Western Australia, 2004. https://ro.ecu.edu.au/theses/801.

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To date, most research on closed circuit television (CCTV) has come out of the United Kingdom (UK) where the growth of CCTV has reached immense proportions with wide support and funding from the Home Office. There are 33 systems operating in Australia, with the focus of this research on the first system installed in Perth, Western Australia in 1991. There is a dearth of information on CCTV in Australia, and little research looking at the link between CCTV, women’s safety and fear of crime. The literature on fear of crime shows that women are more fearful than men even though they are less likely to be offended against. Many reasons are proposed in the literature including vulnerability, victimisation and past experience of crime, environmental factors, and psychological factors to explain women’s fear. Many methodological problems are presented in the fear of crime literature. The core aim of this research was to collect information attitudes, knowledge and opinions about closed circuit television (CCTV) and women’s safety. Six qualitative interviews were conducted with women who work in the fields related to CCTV and women’s safety or who have a keen interest in the field. A further 295 women in the community were surveyed about issues relating to the purpose and effectiveness of CCTV, attitudes about CCTV and general feelings towards crime and safety. The findings show that women are overwhelmingly supportive of CCTV in public spaces and believe CCTV reduces crime and increases feelings of safety. However, women consider the current level of surveillance to be sufficient, and would like to see more police officers, women police and improved street lighting. Women are fearful for their safety at night and are afraid of personal crimes more than property crimes. Women are fearful at the railway station, when they are alone, in car parks and walkways and when waiting for taxis. Older women are more supportive of CCTV than younger women and all women would like to be made more aware the CCTV system.
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Books on the topic "Fear circuit"

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Stujenske, Joseph Matthew. Prefrontal-Amygdala Circuits Regulating Fear and Safety. [New York, N.Y.?]: [publisher not identified], 2016.

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ill, Wiley Nancy 1964, ed. The blammo--surprise! book: A story to help children overcome fears. New York: Magination Press, 1988.

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Bourguignon, Laurence. A friend for Tiger. Mahwah, NJ: BridgeWater Books, 1994.

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Gavin, Andrews, ed. Stress-induced and fear circuitry disorders: Advancing the research agenda for DSM-V. Washington, DC: American Psychiatric Pub., 2009.

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Pedrozo, Sebastián. Abejas y flores marchitas. Montevideo, Uruguay: Alfaguara, 2007.

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McCully, Emily Arnold. Juliette et Bellini. [France]: Kaléidoscope, 1994.

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Michael, Zulli, and Cooper Alice, eds. The compleat Alice Cooper: Incorporating the three acts of Alice Cooper - the last temptation. New York: Marvel Comics, 1994.

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When Panic Happens: Short-Circuit Anxiety and Fear in the Moment Using Neuroscience and Polyvagal Theory. New Harbinger Publications, 2024.

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Sargin, Derya, Chen Yan, and Sheena Josselyn. Genetic Tools in the Erasure of Emotional Memory. Edited by Turhan Canli. Oxford University Press, 2013. http://dx.doi.org/10.1093/oxfordhb/9780199753888.013.004.

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Fear is an important emotion; remembering fearful events/places/stimuli is key for survival. However, dysregulation of fear may underlie the etiology of several psychiatric diseases. Inappropriate storage and/or recall of fearful events can lead to maladaptive fear behaviors and physiological responses that contribute to emotional disorders. Much research has provided insights into the neural processes mediating the formation of fear memories. In addition, some new research has begun to provide insights into how fear memories may be weakened. A more thorough understanding of the molecular, cellular, and circuit basis of the formation and storage of fear memories may one day provide insights into how we can rid ourselves of aberrant fear memories associated with psychopathological responses.
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Cuthbert, Bruce N. The Nimh Research Domain Criteria Project. Edited by Dennis S. Charney, Eric J. Nestler, Pamela Sklar, and Joseph D. Buxbaum. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190681425.003.0071.

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The Research Domain Criteria (RDoC) project grew from recognized deficiencies in currently used diagnostic schemes for mental illness, such as the Diagnostic and Statistical Manual of Mental Disorders (DSM). While the latter is based on a series of signs and symptoms of illnesses that can co-occur in groups of individuals, without consideration of underlying biological factors, RDoC is based on the increasing ability to relate normal as well as abnormal behavior to particular molecules and circuits in the brain across animal species and humans. Behavioral domains include negative valence systems (e.g., fear and anxiety), positive valence systems (e.g., reward and motivation), cognitive systems, social processes, and arousal and regulatory systems, several of which might be affected in a given DSM disease classification. RDoC is seen as a step toward a “precision psychiatry,” where increasing knowledge of the genetic, molecular, cellular, and circuit basis of mental illness will yield biologically based diagnoses that offer important pathophysiological, treatment, and prognostic implications.
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Book chapters on the topic "Fear circuit"

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Ren, Chaoran, and Qian Tao. "Neural Circuits Underlying Innate Fear." In Advances in Experimental Medicine and Biology, 1–7. Singapore: Springer Singapore, 2020. http://dx.doi.org/10.1007/978-981-15-7086-5_1.

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Kawai, Nobuyuki. "The Underlying Neuronal Circuits of Fear Learning and the Snake Detection Theory (SDT)." In The Fear of Snakes, 33–58. Singapore: Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-13-7530-9_3.

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Marek, Roger, and Pankaj Sah. "Neural Circuits Mediating Fear Learning and Extinction." In Advances in Neurobiology, 35–48. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-94593-4_2.

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Tait, Peta. "Technologies of Risk, Fear and Fun: Human and Nonhuman Circus Performance." In Circus, Science and Technology, 101–20. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-43298-0_6.

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Lal, Pradeep, Hideyuki Tanabe, and Koichi Kawakami. "Genetic Identification of Neural Circuits Essential for Active Avoidance Fear Conditioning in Adult Zebrafish." In Methods in Molecular Biology, 169–81. New York, NY: Springer US, 2023. http://dx.doi.org/10.1007/978-1-0716-3401-1_11.

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Moulédous, L., P. Roullet, and Bruno P. Guiard. "Brain Circuits Regulated by the 5-HT2A Receptor: Behavioural Consequences on Anxiety and Fear Memory." In 5-HT2A Receptors in the Central Nervous System, 231–58. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-70474-6_10.

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Frank, Guido K. W. "Interactions Between Fear-Driven Food Avoidance and the Ventral Striatal-Hypothalamic Circuitry Reinforce Eating Disorder Behaviors." In Handbook of the Biology and Pathology of Mental Disorders, 1–20. Cham: Springer International Publishing, 2024. http://dx.doi.org/10.1007/978-3-031-32035-4_49-1.

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Rosenbaum, Blake L., Kara K. Cover, Huijin Song, and Mohammed R. Milad. "Neural Circuit Mechanisms of Fear Extinction." In Anxiety Disorders, 343–54. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199395125.003.0024.

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Panksepp, Jaak. "The Sources of Fear and Anxiety in the Brain." In Affective Neuroscience, 206–22. Oxford University PressNew York, NY, 1998. http://dx.doi.org/10.1093/oso/9780195096736.003.0011.

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Abstract Contrary to traditional thinking on the topic, which taught that fears simply reflect learned anticipation of harmful events, it now appears that the potential for fear is a genetically ingrained function of the nervous system. This should come as no surprise. An organism’s ability to perceive and anticipate dangers was of such obvious importance during evolution that it was not simply left to the vagaries of individual learning. Even though learning is essential for animals to utilize their fear systems effectively in the real world, learning does not create fear by pasting together a variety of external experiences. Evolution created several coherently operating neural systems that help orchestrate and coordinate perceptual, behavioral, and physiological changes that promote survival in the face of danger. The emotional experience of fear appears to arise from a conjunction of neural processes that prompt animals to hide (freeze) if danger is distant or inescapable, or to flee when danger is close but can be avoided. To understand the deep experiential nature of fear in humans, we must probe the genetically ingrained neural components that mediate homologous fearful states in other mammals. Our understanding of the neuro-biology of human fears has emerged largely from basic research on the brains of “lower” animals. These investigations indicate that the capacity to experience fear, along with fear-typical patterns of autonomic and behavioral arousal, emerges primarily from a FEAR circuit that courses between the central amygdala and the periaqueductal gray of the midbrain. Fear behaviors can be evoked by artificially activating this circuit, and conditioned fears can be developed by pairing neutral stimuli with unconditional stimuli, such as electric shock, that can arouse this emotional system. In other words, conditioned fears emerge by neutral stimuli gaining access to this system via learning. Higher cortical processes are not necessary for the activation of learned fears, although those processes refine the types of perceptions that can instigate fear. The neurochemistries that control this emotional system include excitatory amino acids such as glutamate and a variety of neuropeptides (e.g., CRF, a-MSH, ACTH, CCK, and DBI), each of which may eventually be found to instigate slightly different anxieties-for instance, fear of pain, fear of heights, fear of predators. Minor tranquilizers of the benzodiazepine (BZ) class act by partially dampening activity in this emotional system, through GABA-mediated neural inhibition. Other antianxiety drugs such as buspirone are able to attenuate anxiety in totally different ways, such as by modifying serotonin sensitivity in the brain. New agents-for instance, those that inhibit cholecystokinin (CCK) and other neuropeptide receptor systems (especially CRF) as well as those that stimulate neuropeptide Y and oxytocin systems-show considerable promise of yielding a new generation of antianxiety agents. Others are bound to follow as our knowledge of the FEAR system becomes complete.
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Iqbal, Asifa. "Inclusive, Safe and Resilient Public Spaces: Gateway to Sustainable Cities?" In Urban Transition - Perspectives on Urban Systems and Environments [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.97353.

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The rapid urbanization process of cities is majorly coupled with extreme climate change, housing shortage and urban safety issues. These issues are raising new challenges to address the capability of urban resilience. Enhancing Urban Safety and Security is one of the major principles addressed by UN-Habitat in Sustainable Development Goal number 11. Making cities safe and sustainable means ensuring access to safe and affordable public spaces for all. This book chapter aims to highlight how do the city’s public spaces are linked and affected by crime and fear of crime? How do crime and fear of crime interconnect to the built environment in cities while promoting positive urban transitions in terms of safe and sustainable cities? This book chapter explores answers to these questions through the parks and public spaces of the city as a case study. In other words, the book chapter deals with the issue of safety and security by (1) showing links between parks and public spaces, and crime and fear of crime, (2) highlighting how different attributes in the built environment can affect people’s perception of safety, (3) understanding socio-technical perspectives i.e., how technological systems and equipment’s (such as lighting sensors, security alarms, security electronic devices, closed-circuit television (CCTV), smartphones or other technological instruments) are influencing safety/security and sustainability, (4) demonstrating the issues and challenges found in Stockholm, Sweden, and, (5) providing recommendations on how these places can be planned and designed to become more sustainable.
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Conference papers on the topic "Fear circuit"

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Carbonieri, Matteo, Daniel Bachinski Pinhal, Jonathan Godbehere, and Mircea Popescu. "FEA Augmented Equivalent Circuit for Accurate Performance Prediction of Induction Machines." In 2024 International Conference on Electrical Machines (ICEM), 1–7. IEEE, 2024. http://dx.doi.org/10.1109/icem60801.2024.10700286.

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Li, Guoshi, Gregory J. Quirk, and Satish S. Nair. "Regulation of Fear by Amygdala Intercalated Cells in a Network Model of Fear Acquisition and Extinction." In ASME 2008 Dynamic Systems and Control Conference. ASMEDC, 2008. http://dx.doi.org/10.1115/dscc2008-2403.

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A computational model of the fear circuit was developed to study regulation of fear by amygdala intercalated (ITC) neurons within the amygdala. A new biophysical model of an ITC neuron was developed first to capture its bistable behavior caused by an unusual slowly deinactivating current. An existing lateral amygdala network model was then extended into an overall fear circuit by adding ITC neurons, together with additional amygdaloid structures. Using a biophysical Hebbian learning rule for plastic synapses, the model successfully simulated the amygdala responses during acquisition, extinction, and recall of extinction in auditory fear conditioning. Results showed that fear could be regulated by the bistability of ITC neurons. The model also suggested additional sites for the storage fear and extinction memories.
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Ram, Rashmirekha, Hemanta Kumar Palo, and Mihir Narayan Mohanty. "Recognition of fear from speech using adaptive algorithm with MLP classifier." In 2016 International Conference on Circuit, Power and Computing Technologies (ICCPCT). IEEE, 2016. http://dx.doi.org/10.1109/iccpct.2016.7530149.

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Li, Guoshi, Stacy Cheng, Frank Ko, Scott L. Raunch, Gregory Quirk, and Satish S. Nair. "Computational Modeling of Lateral Amygdala Neurons During Acquisition and Extinction of Conditioned Fear, Using Hebbian Learning." In ASME 2006 International Mechanical Engineering Congress and Exposition. ASMEDC, 2006. http://dx.doi.org/10.1115/imece2006-15078.

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The amygdaloid complex located within the medial temporal lobe plays an important role in the acquisition and expression of learned fear associations (Quirk et al. 2003) and contains three main components: the lateral nucleus (LA), the basal nucleus (BLA), and the central nucleus (CE) (Faber and Sah, 2002). The lateral nucleus of the amygdala (LA) is widely accepted to be a key site of plastic synaptic events that contributes to fear learning (Pare, Quirk, LeDoux, 2004). There are two main types of neurons within the LA and the BLA: principal pyramidal-like cells which form projection neurons and are glutamatergic and local circuit GABAergic interneurons (Faber and Sah, 2002). In auditory fear conditioning, convergence of tone [conditioned stimulus (CS)] and foot-shock [unconditioned stimulus (US)] inputs potentiates the synaptic transmission containing CS information from the thalamus and cortex to LA, which leads to larger responses in LA in the presentation of subsequent tones only. The increasing LA responses disinhibit the CE neurons via the intercalated (ITC) cells, eliciting fear responses via excessive projections to brain stem and hypothalamic sites (Pare, Quirk, LeDoux, 2004). As a result, rats learn to freeze to a tone that predicts a foot-shock. Once acquired, conditioned fear associations are not always expressed and repeated presentation of the tone CS in the absence of US causes conditioned fear responses to rapidly diminish, a phenomenon termed fear extinction (Quirk et al. 2003). Extinction does not erase the CS-US association, instead it forms a new memory that inhibits conditioned response (Quirk et al. 2003)
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Miranda, Jose A., Manuel F. Canabal, Jose M. Lanza-Gutierrez, Marta Portela Garcia, and Celia Lopez-Ongil. "Toward Fear Detection using Affect Recognition." In 2019 XXXIV Conference on Design of Circuits and Integrated Systems (DCIS). IEEE, 2019. http://dx.doi.org/10.1109/dcis201949030.2019.8959852.

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Yang, Ruoting, K. Sriram, and Francis J. Doyle. "Control circuitry for fear conditioning associated with Post-Traumatic Stress Disorder (PTSD)." In 2010 49th IEEE Conference on Decision and Control (CDC). IEEE, 2010. http://dx.doi.org/10.1109/cdc.2010.5717136.

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Pendyam, Sandeep, Dongbeom Kim, Gregory J. Quirk, and Satish S. Nair. "Acquisition of Fear and Extinction in Lateral Amygdala: A Modeling Study." In ASME 2010 Dynamic Systems and Control Conference. ASMEDC, 2010. http://dx.doi.org/10.1115/dscc2010-4218.

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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.
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Sharmili, S. Shahana, and R. Kanagaraj. "Live Beyond Fear: A Virtual Reality Serious Game Platform to Overcome Phobias." In 2020 5th International Conference on Devices, Circuits and Systems (ICDCS). IEEE, 2020. http://dx.doi.org/10.1109/icdcs48716.2020.243592.

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"Accurate Modeling and Simulation for the Circuit Behavior of Si-Tip FEA." In 10th International Conference on Vacuum Microelectronics. IEEE, 1997. http://dx.doi.org/10.1109/ivmc.1997.627653.

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Su, Zou, Li Chuanri, Xu Fei, and Qiao Liang. "Correlation Factor Analysis of FEA Model Simplification Methods of Printed Circuit Board." In 2011 Seventh International Conference on Computational Intelligence and Security (CIS). IEEE, 2011. http://dx.doi.org/10.1109/cis.2011.326.

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