Relevant bibliographies by topics / Fear conditioning

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Fear conditioning'

Author: Grafiati
Published: 4 June 2021
Last updated: 20 February 2023

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Journal articles on the topic "Fear conditioning"

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Dygdon, Judith A., Anthony J. Conger, and Esther Y. Strahan. "Multimodal Classical Conditioning of Fear: Contributions of Direct, Observational, and Verbal Experiences to Current Fears." Psychological Reports 95, no. 1 (August 2004): 133–53. http://dx.doi.org/10.2466/pr0.95.1.133-153.

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The authors propose that a multimodal classical conditioning model be considered when clinicians or clinical researchers study the etiology of fears and anxieties learned by human beings. They argue that fears can be built through the combined effects of direct, observed, and verbally presented classical conditioning trials. Multimodal classical conditioning is offered as an alternative to the three pathways to fear argument prominent in the human fear literature. In contrast to the three pathways position, the authors present theoretical arguments for why “learning by observation” and “learning through the receipt of verbal information” should be considered classical conditioning through observational and verbal modes. The paper includes a demonstration of how data, commonly collected in research on the three pathways to fear, would be studied differently using a multimodal classical conditioning perspective. Finally, the authors discuss implications for assessment, treatment, and prevention of learned fears in humans.
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Iwasaki, Satoshi, Tetsuya Sakaguchi, and Yuji Ikegaya. "Brief fear preexposure facilitates subsequent fear conditioning." Neuroscience Research 95 (June 2015): 66–73. http://dx.doi.org/10.1016/j.neures.2015.02.001.

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Serim-Yıldız, Begüm, Özgür Erdur-Baker, and Aslı Bugay. "The Common Fears and Their Origins Among Turkish Children and Adolescents." Behaviour Change 30, no. 3 (August 12, 2013): 199–209. http://dx.doi.org/10.1017/bec.2013.18.

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The present study aimed to investigate the common fears and their origins among children and adolescents from different age, gender, and socioeconomic levels (SES). The sample was comprised of 642 females (48.8%) and 673 males (51.2%) with a total of 1,315 participants aged between 8 and 18 (M = 13.15; SD = 3.18). The Fear interview was utilised to examine the common fears and the role of conditioning, modelling and negative information in the development of children's fears. The result showed that the most common fear in Turkey was ‘God’, followed by ‘losing my friends’ and ‘going to Hell’. In addition, the findings revealed that Turkish students are more likely to learn fears by modelling rather than negative information transmission and conditioning. The results also indicated that negative information transmission had a more intensifying effect on the children and adolescents’ existing fear rather than modelling and conditioning. Furthermore, multinomial logistic regression was conducted to examine the effects of age, gender and SES on the origins of fear. Results showed that age and gender were significant predictors of origins of fear.
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Izquierdo, Ivan, Cristiane R. G. Furini, and Jociane C. Myskiw. "Fear Memory." Physiological Reviews 96, no. 2 (April 2016): 695–750. http://dx.doi.org/10.1152/physrev.00018.2015.

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Fear memory is the best-studied form of memory. It was thoroughly investigated in the past 60 years mostly using two classical conditioning procedures (contextual fear conditioning and fear conditioning to a tone) and one instrumental procedure (one-trial inhibitory avoidance). Fear memory is formed in the hippocampus (contextual conditioning and inhibitory avoidance), in the basolateral amygdala (inhibitory avoidance), and in the lateral amygdala (conditioning to a tone). The circuitry involves, in addition, the pre- and infralimbic ventromedial prefrontal cortex, the central amygdala subnuclei, and the dentate gyrus. Fear learning models, notably inhibitory avoidance, have also been very useful for the analysis of the biochemical mechanisms of memory consolidation as a whole. These studies have capitalized on in vitro observations on long-term potentiation and other kinds of plasticity. The effect of a very large number of drugs on fear learning has been intensively studied, often as a prelude to the investigation of effects on anxiety. The extinction of fear learning involves to an extent a reversal of the flow of information in the mentioned structures and is used in the therapy of posttraumatic stress disorder and fear memories in general.
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Åsli, Ole, and Magne Arve Flaten. "How Fast is Fear?" Journal of Psychophysiology 26, no. 1 (January 2012): 20–28. http://dx.doi.org/10.1027/0269-8803/a000063.

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The minimum latency of potentiated startle after delay and trace fear conditioning was investigated. Delay conditioning is hypothesized to be mediated by automatic processes, whereas trace conditioning is hypothesized to involve controlled cognitive processes. In a group receiving delay conditioning, a tone conditioned stimulus (CS) signaled an electric shock unconditioned stimulus (US) presented 1,000 ms after CS onset. In a group receiving trace conditioning, a 200 ms tone CS was followed by an 800 ms gap prior to US presentation. Two control groups received unpaired CS/US presentations. It was hypothesized that fear-potentiated startle should be observed at shorter time intervals after CS onset in the group receiving delay conditioning compared to the group receiving trace conditioning. The results showed increased startle at 100 and 150 ms after CS onset in the group receiving delay conditioning compared to the unpaired group. In the group receiving trace conditioning, increased startle was observed at 1,500 ms after CS onset compared to the unpaired group. This supports the idea that conditioned fear after delay conditioning may be due to automatic processes, whereas trace conditioning is dependent on controlled processes.
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Carmel, D., C. Raio, E. A. Phelps, and M. Carrasco. "Fast unconscious fear conditioning." Journal of Vision 11, no. 11 (September 23, 2011): 314. http://dx.doi.org/10.1167/11.11.314.

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Critchley, Hugo D., Christopher J. Mathias, and Raymond J. Dolan. "Fear Conditioning in Humans." Neuron 33, no. 4 (February 2002): 653–63. http://dx.doi.org/10.1016/s0896-6273(02)00588-3.

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Lai, Cora Sau Wan, Avital Adler, and Wen-Biao Gan. "Fear extinction reverses dendritic spine formation induced by fear conditioning in the mouse auditory cortex." Proceedings of the National Academy of Sciences 115, no. 37 (August 27, 2018): 9306–11. http://dx.doi.org/10.1073/pnas.1801504115.

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Fear conditioning-induced behavioral responses can be extinguished after fear extinction. While fear extinction is generally thought to be a form of new learning, several lines of evidence suggest that neuronal changes associated with fear conditioning could be reversed after fear extinction. To better understand how fear conditioning and extinction modify synaptic circuits, we examined changes of postsynaptic dendritic spines of layer V pyramidal neurons in the mouse auditory cortex over time using transcranial two-photon microscopy. We found that auditory-cued fear conditioning induced the formation of new dendritic spines within 2 days. The survived new spines induced by fear conditioning with one auditory cue were clustered within dendritic branch segments and spatially segregated from new spines induced by fear conditioning with a different auditory cue. Importantly, fear extinction preferentially caused the elimination of newly formed spines induced by fear conditioning in an auditory cue-specific manner. Furthermore, after fear extinction, fear reconditioning induced reformation of new dendritic spines in close proximity to the sites of new spine formation induced by previous fear conditioning. These results show that fear conditioning, extinction, and reconditioning induce cue- and location-specific dendritic spine remodeling in the auditory cortex. They also suggest that changes of synaptic connections induced by fear conditioning are reversed after fear extinction.
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Nesse, Randolph M., and James L. Abelson. "Natural selection and fear regulation mechanisms." Behavioral and Brain Sciences 18, no. 2 (June 1995): 309–10. http://dx.doi.org/10.1017/s0140525x00038620.

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AbstractExpectations can facilitate rapid fear conditioning and this may explain some phenomena that have been attributed to preparedness. However, preparedness remains the best explanation for some aspects of clinical phobias and the difficulty of creating fears of modern dangers. Rapid fear conditioning based on expectancy is not an alternative to an evolutionary explanation, but has, like preparedness, been shaped by natural selection.
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Sarowar, Tasnuva, and Andreas M. Grabrucker. "Rho GTPases in the Amygdala—A Switch for Fears?" Cells 9, no. 9 (August 26, 2020): 1972. http://dx.doi.org/10.3390/cells9091972.

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Fear is a fundamental evolutionary process for survival. However, excess or irrational fear hampers normal activity and leads to phobia. The amygdala is the primary brain region associated with fear learning and conditioning. There, Rho GTPases are molecular switches that act as signaling molecules for further downstream processes that modulate, among others, dendritic spine morphogenesis and thereby play a role in fear conditioning. The three main Rho GTPases—RhoA, Rac1, and Cdc42, together with their modulators, are known to be involved in many psychiatric disorders that affect the amygdala′s fear conditioning mechanism. Rich2, a RhoGAP mainly for Rac1 and Cdc42, has been studied extensively in such regard. Here, we will discuss these effectors, along with Rich2, as a molecular switch for fears, especially in the amygdala. Understanding the role of Rho GTPases in fear controlling could be beneficial for the development of therapeutic strategies targeting conditions with abnormal fear/anxiety-like behaviors.
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Dissertations / Theses on the topic "Fear conditioning"

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Urcelay, Gonzalo Pablo. "Potentiation and overshadowing in Pavlovian fear conditioning." Diss., Online access via UMI:, 2008.

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Hakim, Marziah. "Neurogenesis and neuroplasticity following olfactory fear conditioning." Thesis, Queensland University of Technology, 2019. https://eprints.qut.edu.au/157474/1/Marziah_Hakim_Thesis.pdf.

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This dissertation focused on determining the neurocircuitry of olfactory fear conditioning in order to further understand the microanatomy of post-traumatic stress disorder and contribute towards the refinement of therapeutic innovations. The study determined that different subnuclei of the amygdala were involved in olfactory fear memory and that recollection of such memories enhanced neuroplasticity and increased the number of new born neurons and astrocytes in the brain regions associated with olfaction and memory processing. This study concluded that following olfactory fear conditioning, newborn neurons may undergo long term potentiation, which may support their survival up to 14 days after birth.
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Holahan, Matthew R. "Amygdala involvement in aversive conditioning." Thesis, McGill University, 2003. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=19529.

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Research over the past several decades has revealed that the amygdala is involved in aversive, or fear, conditioning. However, the precise nature of this involvement remains a matter of debate. One hypothesis suggests that disrupting amygdala function eliminates the storage of memories formed during aversive conditioning, eliminating the production of internal responses that alter the expression of observable behaviors. Alternatively, lesions or inactivation of the amygdala may impair the modulation of memories in other brain regions and disrupt the ability to perform certain observable behaviors. The experiments reported in the present thesis examined these arguments by making multiple behavioral measures during exposure to unconditioned (US) or conditioned (CS) aversive cues. Amygdala activity was inferred from changes in c-Fos protein expression or activity was temporarily suppressed with muscimol injections. The relationship between the behavioral measures and the role of the amygdala in producing them was examined. Amygdala neurons expressing the c-Fos protein tracked exposure to the US and CS but did not coincide with expression of freezing. Temporary inactivation of the amygdala with muscimol injections before presentation of the US or exposure to the CS attenuated the expression of freezing and active place avoidance; two incompatible behaviors. Finally, temporary inactivation of amygdala activity blocked freezing, place avoidance, and memory modulation produced by the same posttraining exposure to an aversive CS. Since amygdala activation alone was not sufficient to produce freezing and inactivation of the amygdala eliminated freezing, place avoidance, and memory modulation, the results cannot be interpreted as reflecting a direct role for the amygdala in production of observable behaviors. The results also preclude the idea that memory modulation is the only function of the amygdala. Rather, the results of all three studies suggest that the amygdala stores an aversive representation of the US which promotes the expression of various behaviors, possibly through the production of internal responses reflecting an aversive affective state.
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Antoniadis, Elena Anna. "Discriminative fear conditioning to context expressed by multiple measures of fear in the rat." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp01/MQ29181.pdf.

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Tinoco, González Daniella. "Fear conditioning to socially relevant stimuli in social anxiety." Doctoral thesis, Universitat Autònoma de Barcelona, 2013. http://hdl.handle.net/10803/120553.

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Los trastornos de ansiedad constituyen un reto para la psiquiatría y la psicología clínica. Cerca de un 30% de la población sufre, o ha sufrido, uno o más trastornos de ansiedad a lo largo de su vida, siendo dicho grupo de trastornos el más frecuente dentro del DSM-IV. Las aproximaciones teóricas basadas en los modelos de aprendizaje aversivo han ocupado un lugar muy importante entre los modelos etiológicos de dichos trastornos. A pesar de que el condicionamiento del miedo es un proceso adaptativo y de gran importancia para la supervivencia, puede acabar convirtiéndose en clínicamente relevante cuando la reactividad al Estímulo Condicionado (EC) persiste en ausencia de contingencia entre el EC y el Estímulo Incondicionado (EI). Mediante procesos de condicionamiento clásico aversivo pueda aparecer un trastorno de ansiedad durante o después de un acontecimiento traumático o en un período de estrés significativo. Sin embargo, no todas las personas expuestas a este tipo de sucesos acaban desarrollando un trastorno. Algunos estudios han demostrado un mayor condicionamiento y una mayor resistencia a la extinción en pacientes ansiosos comparados con controles sanos sugiriendo que pacientes con trastornos de ansiedad se caracterizan por una elevada condicionabilidad y que ésta es una de las razones por las que, en situaciones de exposición a incidentes aversivos, sólo algunos individuos desarrollan miedos patológicos, mientras que otros muestran una respuesta adaptativa de miedo. La mayoría de estudios han utilizado el reflejo de sobresalto como índice de procesamiento afectivo. Consiste en una respuesta defensiva súbita que presentan muchas especies animales ante un estímulo intenso e inesperado. En humanos, puede ser medido de forma bastante sencilla registrando la respuesta electromiográfica en el músculo orbicularis oculi. El incremento del reflejo de sobresalto cuando un individuo está experimentando un estado de miedo o ansiedad se denomina reflejo de sobresalto potenciado por miedo. Durante los últimos años, éste se ha convertido en una herramienta de gran utilidad para la investigación traslacional de los trastornos de ansiedad. La mayor parte de los trabajos han utilizado estímulos evolutivamente poco “preparados” y algunos no han demostrado mayor condicionabilidad en pacientes con trastornos de ansiedad. Esto nos alerta de la necesidad de emplear paradigmas que contemplen estímulos incondicionados más relevantes para el trastorno objeto de estudio. Por tanto, el objetivo general del presente proyecto fue investigar el papel del condicionamiento aversivo de estímulos socialmente relevantes como factor específico de vulnerabilidad a la fobia social, utilizando el reflejo de sobresalto en pacientes con fobia social respecto a pacientes con trastorno de pánico con agorafobia y controles sanos. Para llevarlo a cabo, se empleó un paradigma de condicionamiento diferencial desarrollado por Lissek et al. (2008) en el que imágenes de personas con una expresión facial neutra (EC) se aparearon con tres tipos de estímulos visuales/auditivos: insultos y expresiones faciales de crítica (EIneg); comentarios y expresiones faciales neutras (EIneu); y cumplidos y expresiones faciales positivas (EIpos). Los resultados del presente trabajo no demostraron una mayor condicionabilidad en pacientes con fobia social respecto a pacientes con trastorno de pánico con agorafobia y controles sanos. Es posible que otros procesos tanto asociativos (por ejemplo, extinción del miedo) como no asociativos (por ejemplo, procesos cognitivos y atencionales) tengan un papel más importante en la fobia social que un mayor condicionamiento.
Anxiety disorders represent a challenge for psychiatry and clinical psychology. Near 30 % of the population suffers, or has suffered, one or more anxiety disorder along his life, being this disorder the most frequent group of them inside the DSM-IV. The theoretical approximations based on aversive learning models have occupied traditionally a very important place among the etiological models of these disorders. Despite the fact that fear conditioning is an adaptative process of great importance for survival, it can turn into clinical relevant when the reactivity to the Conditioned Stimulus (CS) persists in absence of contingency between the CS and the Unconditioned Stimulus (US). By means of classical fear conditioning processes, an anxiety disorder could appear during or after a traumatic event or in a period of significant stress. Nevertheless, not all the persons exposed to this type of events end up developing a disorder. Some studies have demonstrated that patients with anxiety disorders are characterized by a high conditionability and resistance to extinction in anxiety patients compared to healthy controls suggesting that patients are characterized by en enhanced conditioning and that this is one of the reasons for which, in situations of exhibition to aversive incidents, only some individuals go on to develop pathological fears, whereas others show an adaptative response of fear. Many of these studies have use the startle reflex as an index of emotional activation. It consists of a defensive sudden response that many animal species present in presence of an intense and unexpected stimulus. In humans, it can be measured very simply by registering the electromyographic response in the orbicularis oculi muscle. The increase of the startle reflex when an individual is experiencing fear or anxiety is named fear potentiated startle. During the last years, it has been converted into a very useful tool for traslational investigation of anxiety disorders. Up to recent dates, most of the published studies with humans using classical conditioning paradigms have used evolutionarily “unprepared” stimuli to be conditioned, and many have not demonstrated an enhanced conditioning in anxiety patients. This alerts us of the importance to use paradigms that take into account unconditioned stimuli relevant to the disorder object of study. The overall goal of the present dissertation was to investigate fear conditioning processes in social anxiety using the fear potentiated startle in patients with social anxiety compared to patients with panic disorder with agoraphobia and healthy controls. To address this goal, we used a novel paradigm developed by Lissek et al. (2008) in which neutral facial expressions from three female actors served as the CS and were paired with one of three types audiovisual stimuli: insults and critical facial expressions (USneg); comments and neutral facial expressions (USneu); and compliments and positive facial expressions (USpos). Our results did not demonstrate an enhanced conditioning among patients with social anxiety compared to patients with panic disorder with agoraphobia and healthy controls. It is plausible that other associative (e.g. fear extinction) and non-associative processes (e.g cognitive and attentional processes) play a greater role in explaining social anxiety rather than enhanced fear conditioning.
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Hardwick, Sascha. "Startle modification during human fear conditioning : attention or emotion? /." [St. Lucia, Qld.], 2005. http://www.library.uq.edu.au/pdfserve.php?image=thesisabs/absthe19287.pdf.

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Angelhuber, Martin. "The neural circuitry of fear conditioning : a theoretical account." Thesis, Strasbourg, 2016. http://www.theses.fr/2016STRAJ082/document.

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Conditionnement à la peur est un paradigme réussi pour comprendre les substrats neuronaux de l’apprentissage et de l’émotion. Dans cette thèse, je présente deux modèles informatiques des structures du cerveau qui sous-tendent l'acquisition de la peur conditionnée. Le première modèle est utilisé pour enquêter sur l’effet des changements de l’inhibition tonique sur le traitement des informations reçues. On confirme que la diminution de l’inhibition tonique d’une population augmente la réactivité du réseau. Ensuite, le modèle est analysé d’une perspective fonctionnelle et des prédictions qui découlent de cette proposition sont discutées. En outre, je présenterai un modèle systématique, basé sur un type de modèle de conditionnement récemment introduit utilisant des variables latentes. Je propose que l’interaction entre les neurones dans l’amygdale basale code pour l’interface entre ces variables latentes. Le modèle couvre une large gamme d’effets et l’analyse produit un certain nombre de prédictions vérifiables
Fear conditioning is a successful paradigm for studying neural substrates of emotional learning. In this thesis, two computational models of the underlying neural circuitry are presented. First, the effects of changes in neuronal membrane conductance on input processing are analyzed in a biologically realistic model. We show that changes in tonic inhibitory conductance increase the responsiveness of the network to inputs. Then, the model is analyzed from a functional perspective and predictions that follow from this proposition are discussed. Next, a systems level model is presented based on a recent high-level approach to conditioning. It is proposed that the interaction between fear and extinction neurons in the basal amygdala is a neural substrate of the switching between latent states, allowing the animal to infer causal structure. Important behavioral and physiological results are reproduced and predictions and questions that follow from the main hypothesis are considered
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Garfield, Joshua Benjamin Bernard Psychology Faculty of Science UNSW. "FG7142 attenuates expression of overexpectation in Pavlovian fear conditioning." Publisher:University of New South Wales. Psychology, 2008. http://handle.unsw.edu.au/1959.4/43241.

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The experiments reported in this thesis studied the mechanisms of expression of overexpectation of conditioned fear, as measured by freezing. In Stage I, rats were conditioned to fear a tone and a flashing light conditioned stimulus (CS) through pairings with a 0.5 mA, 1 s shock. In Stage II, overexpectation was trained by the reinforcement of a compound of these CSs with a shock of the same magnitude. Two compound ?? shock pairings produced an overexpectation effect, as measured by freezing to presentations of the tone alone, while further Stage II training caused over-training of overexpectation. Expression of the overexpectation effect produced by two compound ?? shock pairings could be prevented by pre-test injection of the benzodiazepine partial inverse agonist FG7142. This effect was dose-dependent and not due to state-dependent memory. Control experiments suggested that it was also not due to any general effect of FG7142 on the Pavlovian freezing response. Freezing to a tone that had been conditioned, but not subjected to any decremental training procedures, was unaffected by administration of FG7142 before either the conditioning or test session. FG7142 also did not affect freezing to a tone that had been subjected to an associative blocking procedure. The hypothesis that overexpectation of conditioned fear may be context-dependent was also tested. However, renewal was not observed. Rats that received Stage II training in a context distinct from the Stage I training context showed equivalent expression of overexpectation regardless of whether testing was conducted in the Stage I or Stage II training context. These results are consistent with the hypothesis that overexpectation, like extinction, leads to the imposition of a GABAA receptor-mediated mask on the fear CR. Moreover, they suggest that this masking of fear is the specific consequence of negative predictive error.
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Merckelbach, Harald Lodewijk Gerardus Joseph. "Preparedness and classical conditioning of fear a critical inquiry /." [Maastricht : Maastricht : Rijksuniversiteit Limburg] ; University Library, Maastricht University [Host], 1989. http://arno.unimaas.nl/show.cgi?fid=5450.

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Mcguire, Joseph F. "Fear Conditioning and Extinction in Childhood Obsessive-Compulsive Disorder." Scholar Commons, 2015. http://scholarcommons.usf.edu/etd/5741.

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Fear conditioning and extinction are central in the cognitive behavioral model of obsessive-compulsive disorder (OCD), which underlies exposure-based cognitive behavioral therapy (CBT). Youth with OCD may have impairments in conditioning and extinction that carries treatment implications. The present study examined these processes using a differential conditioning paradigm. Forty-one youth (19 OCD, 22 community controls) and their parents completed a battery of clinical interviews, rating scales, and a differential conditioning task. Skin conductance response (SCR) served as the primary dependent measure across all three phases of the conditioning procedure (habituation, acquisition, and extinction). During habituation, no meaningful differences were observed between groups. During acquisition, differential fear conditioning was identified across groups evidenced by larger SCRs to the CS+ compared to CS-, with no significant group differences. During extinction, a three-way interaction and follow-up tests revealed youth with OCD failed to exhibit differential fear conditioning during early fear extinction; whereas community controls consistently exhibited differential fear conditioning throughout extinction. Across participants, the number and frequency of OCD symptoms was positively associated with fear acquisition and negatively associated with fear extinction to the conditioned stimulus. OCD symptom severity was negatively associated with differential SCR in early extinction. Youth with OCD exhibit a different pattern of fear extinction relative to community controls that may be accounted for by impaired inhibitory learning in early fear extinction. Findings suggest the potential benefit of augmentative retraining interventions prior to CBT. Therapeutic approaches to utilize inhibitory-learning principles and/or engage developmentally appropriate brain regions during exposures may serve to maximize CBT outcomes.
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Books on the topic "Fear conditioning"

1

Antoniadis, Elena Anna. Discriminative fear conditioning to context expressed by multiple measures of fear in the rat. Ottawa: National Library of Canada = Bibliothèque nationale du Canada, 1999.

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Landsberg, Judd Warren. Effect of manipulating intraamygdala levels of cGMP on fear conditioning. [New Haven, Conn: s.n.], 1996.

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Dunsmoor, Joseph E., and Rony Paz. Generalization of Learned Fear. Edited by Israel Liberzon and Kerry J. Ressler. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190215422.003.0004.

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Autonomic hyperarousal and avoidance in post-traumatic stress disorder (PTSD) can be triggered by a host of stimuli or situations that bear some similarity or association to the trauma event. As these triggers are often encountered in safe environments removed from the original trauma, this overgeneralization of fear and anxiety is a burden that can interfere with daily life. Recent efforts to understand the neurobiology of PTSD have relied on laboratory models of Pavlovian fear conditioning and extinction. This chapter reviews studies of fear generalization in animals and humans, which provide a valuable model to conceptualize the excessive fear generalization characteristic of PTSD.
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Bauer, Elizabeth P., and Denis Paré. Behavioral Neuroscience of Circuits Involved in Fear Processing. Edited by Israel Liberzon and Kerry J. Ressler. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190215422.003.0002.

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Normal fear regulation includes the ability to learn by experience that some circumstances predict danger. This process, which can be modeled in the laboratory using Pavlovian fear conditioning, appears to be disrupted in individuals with post-traumatic stress disorder (PTSD). Understanding of the mechanisms underlying fear learning has progressed tremendously in the last 25 years, and constitutes a promising paradigm to study the neural bases of PTSD. This chapter first reviews current knowledge of the brain structures involved in fear learning, expression and extinction, including the contributions of the amygdala and prefrontal cortex. It then addresses how these circuits are affected by PTSD and how fear processing is altered in PTSD. Understanding PTSD within a fear-conditioning and extinction framework provides insight into why certain individuals are susceptible to developing PTSD and suggests potential therapies.
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Antoniadis, Elena Anna. Discriminative fear conditioning to context and emotional memory systems in the brain of the rat. 2003.

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Fear and Anxiety in Virtual Reality: Investigations of cue and context conditioning in virtual environment. Springer, 2014.

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Genheimer, Hannah. Fear and Anxiety in Virtual Reality: Investigations of Cue and Context Conditioning in Virtual Environment. Springer Vieweg. in Springer Fachmedien Wiesbaden GmbH, 2015.

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Mehmet, Ali. Ideational conditioning: A new perspective on phobia acquisition : fear as a survival imperative : its experimental induction in human subjects through conditioning involving thoughts as stimuli. Bradford, 1986.

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Milad, Mohammed R., and Kylie N. Moore. Neurobiology and Neuroimaging of PTSD. Edited by Frederick J. Stoddard, David M. Benedek, Mohammed R. Milad, and Robert J. Ursano. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190457136.003.0015.

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This chapter provides a broad overview of the fear circuitry implicated in the development and maintenance of posttraumatic stress disorder. It begins by reviewing evidence from animal models of fear conditioning and extinction that unveiled the neural structures incorporated in the fear circuitry. Then it explores the translation of these findings to healthy human models of fear conditioning and finally examines the neural dysfunctions highlighted by neuroimaging studies of posttraumatic stress disorder (PTSD) in order to conceptualize mechanisms of fear extinction and the role of impaired fear extinction in contributing to the pathology of PTSD. The chapter ends with the potential therapeutic interventions for the treatment of PTSD in the scope of this model but with a note of caution regarding some of its limitations.
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Epstein, Joshua M. Mathematical Model. Princeton University Press, 2017. http://dx.doi.org/10.23943/princeton/9780691158884.003.0002.

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This part of the book describes explicit mathematical models for the affective, cognitive, and social components of Agent_Zero. It first considers some underlying neuroscience of fear and the role of the amygdala before turning to Rescorla–Wagner equations of conditioning. In particular, it explains how the fear circuit can be activated and how fear conditioning can occur unconsciously. It then reviews some standard nomenclature adopted by Ivan Pavlov in his study, Conditioned Reflexes: An Investigation of the Physiological Activity of the Cerebral Cortex, with emphasis on David Hume's “association of ideas,” the theory of conditioning, and the Rescorla–Wagner model. After examining “the passions,” the discussion focuses on reason, Agent_Zero's cognitive component, and the model's social component. The central case is that the agent initiates the group's behavior despite starting with the lowest disposition, with no initial emotional inclination, no evidence, the same threshold as all others, and no orders from above.
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Book chapters on the topic "Fear conditioning"

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Verster, Joris C., Thomas M. Tzschentke, Kieran O’Malley, Francis C. Colpaert, Bart Ellenbroek, Bart Ellenbroek, R. Hamish McAllister-Williams, et al. "Fear Conditioning." In Encyclopedia of Psychopharmacology, 532. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-540-68706-1_707.

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Hoyer, Daniel, Eric P. Zorrilla, Pietro Cottone, Sarah Parylak, Micaela Morelli, Nicola Simola, Nicola Simola, et al. "Classical Fear Conditioning." In Encyclopedia of Psychopharmacology, 290. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-540-68706-1_3139.

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Anagnostaras, Stephan G., Jennifer R. Sage, and Stephanie A. Carmack. "Pavlovian Fear Conditioning." In Encyclopedia of Psychopharmacology, 1237–40. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-36172-2_161.

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McAllister-Williams, R. Hamish, Daniel Bertrand, Hans Rollema, Raymond S. Hurst, Linda P. Spear, Tim C. Kirkham, Thomas Steckler, et al. "Pavlovian Fear Conditioning." In Encyclopedia of Psychopharmacology, 974–76. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-540-68706-1_161.

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Fanselow, Michael S., and Sarah R. Sterlace. "Pavlovian Fear Conditioning." In The Wiley Blackwell Handbook of Operant and Classical Conditioning, 117–41. Oxford, UK: John Wiley & Sons, Ltd, 2014. http://dx.doi.org/10.1002/9781118468135.ch6.

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Anagnostaras, Stephan G., Jennifer R. Sage, and Stephanie A. Carmack. "Pavlovian Fear Conditioning." In Encyclopedia of Psychopharmacology, 1–4. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-27772-6_161-2.

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Graham, Bronwyn M., and Mohammed R. Milad. "Fear Conditioning and Extinction." In Innovations in Cognitive Neuroscience, 139–55. Boston, MA: Springer US, 2016. http://dx.doi.org/10.1007/978-1-4614-3846-5_8.

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Schafe, G. E., and J. E. LeDoux. "Neurochemistry/Neuropharmacology of Fear and Fear Conditioning." In Handbook of Neurochemistry and Molecular Neurobiology, 689–707. Boston, MA: Springer US, 2007. http://dx.doi.org/10.1007/978-0-387-30405-2_18.

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Müller, Iris, and Markus Fendt. "Fear Conditioning in Laboratory Rodents." In Neuromethods, 119–60. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2748-8_8.

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Vervliet, Bram, Aaron Baker, and Michelle G. Craske. "Fear Conditioning in Animals and Humans." In Encyclopedia of the Sciences of Learning, 1273–76. Boston, MA: Springer US, 2012. http://dx.doi.org/10.1007/978-1-4419-1428-6_949.

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Conference papers on the topic "Fear conditioning"

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Pavlou, Athanasios, and Matthew Casey. "A computational platform for visual fear conditioning." In 2009 International Joint Conference on Neural Networks (IJCNN 2009 - Atlanta). IEEE, 2009. http://dx.doi.org/10.1109/ijcnn.2009.5178718.

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Plusnin, Viktor, Olga Ivashkina, Ksenia Toropova, Olga Rogozhnikova, and Konstantin Anokhin. "Behavior analysis tool for fear conditioning paradigm." In 2022 Fourth International Conference Neurotechnologies and Neurointerfaces (CNN). IEEE, 2022. http://dx.doi.org/10.1109/cnn56452.2022.9912477.

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Faghih, Rose T., Patrick A. Stokes, Marie-France Marin, Rachel G. Zsido, Sam Zorowitz, Blake L. Rosenbaum, Huijin Song, et al. "Characterization of fear conditioning and fear extinction by analysis of electrodermal activity." In 2015 37th Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC). IEEE, 2015. http://dx.doi.org/10.1109/embc.2015.7320204.

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Li, Xiaoyuan, Yun Liu, Zhenlong Wang, Yamin Chen, Qiang Liu, and Hongyu Si. "Establishment of Fear Conditioning on Visual Information in Long-Evans Rats." In ICBET 2020: 2020 10th International Conference on Biomedical Engineering and Technology. New York, NY, USA: ACM, 2020. http://dx.doi.org/10.1145/3397391.3397431.

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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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Navarro-Guerrero, Nicolas, Robert Lowe, and Stefan Wermter. "A neurocomputational amygdala model of auditory fear conditioning: A hybrid system approach." In 2012 International Joint Conference on Neural Networks (IJCNN 2012 - Brisbane). IEEE, 2012. http://dx.doi.org/10.1109/ijcnn.2012.6252392.

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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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XianLi An and XiGeng Zheng. "Post-training corticosterone opposingly modulates fear conditioning of high and low anxiety rats." In 2012 IEEE-EMBS International Conference on Biomedical and Health Informatics (BHI). IEEE, 2012. http://dx.doi.org/10.1109/bhi.2012.6211655.

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Fanhua, Meng, Ma Meifang, and Tian Xin. "Neuronal Ensemble Score Coding in the Anterior Cingulate Cortex of Rats under Fear Conditioning." In 2008 Second International Symposium on Intelligent Information Technology Application (IITA). IEEE, 2008. http://dx.doi.org/10.1109/iita.2008.478.

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Wenwen, Bai, Ma Meifang, and Tian Xin. "Neuronal Ensemble Entropy Coding in the Anterior Cingulate Cortex of Rats under Fear Conditioning." In 2008 International Workshop on Geoscience and Remote Sensing (ETT and GRS). IEEE, 2008. http://dx.doi.org/10.1109/ettandgrs.2008.348.

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Reports on the topic "Fear conditioning"

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Kaplan, Gary B. Fear Conditioning Effects on Sensitivity to Drug Reward. Fort Belvoir, VA: Defense Technical Information Center, June 2009. http://dx.doi.org/10.21236/ada538749.

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Kaplan, Gary. Fear Conditioning Effects on Sensitivity to Drug Reward. Fort Belvoir, VA: Defense Technical Information Center, June 2010. http://dx.doi.org/10.21236/ada547601.

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Rosen, Jeff. Oxytocin and Social Support as Synergistic Inhibitors of Aversive Fear Conditioning and Fear-Potentiated Startle in Male Rats. Fort Belvoir, VA: Defense Technical Information Center, May 2011. http://dx.doi.org/10.21236/ada554060.

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Rosen, Jeffrey B. Oxytocin and Social Support as Synergistic Inhibitors of Aversive Fear Conditioning and Fear-Potentiated Startle in Male Rats. Fort Belvoir, VA: Defense Technical Information Center, September 2010. http://dx.doi.org/10.21236/ada555016.

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Drummond, Sean P. Role of Sleep Deprivation in Fear Conditioning and Extinction: Implications for Treatment of PTSD. Fort Belvoir, VA: Defense Technical Information Center, October 2014. http://dx.doi.org/10.21236/ada613608.

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Drummond, Sean P. Role of Sleep Deprivation in Fear Conditioning and Extinction: Implications for Treatment of PTSD. Fort Belvoir, VA: Defense Technical Information Center, October 2012. http://dx.doi.org/10.21236/ada570524.

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Drummond, Sean P. Role of Sleep Deprivation in Fear Conditioning and Extinction: Implications for Treatment of PTSD. Fort Belvoir, VA: Defense Technical Information Center, October 2013. http://dx.doi.org/10.21236/ada590493.

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