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Books on the topic 'Fear conditioning'

Author: Grafiati

Published: 4 June 2021

Last updated: 20 February 2023

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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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Ho, Ping Yun Ivan. The role of the medial geniculate body: Medial nucleus (MGm) and posterior intralaminar nucleus (PIN) in auditory fear conditioning. 2006.

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Morinobu, Shigeru, Shigeto Yamamoto, and Manabu Fuchikami. Translational Research from Animals to Humans. Edited by Israel Liberzon and Kerry J. Ressler. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190215422.003.0017.

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To elucidate the pathophysiology of post-traumatic stress disorder (PTSD), the establishment of an appropriate animal model is necessary. In a series of studies, the authors validated single prolonged stress (SPS) as a model for PTSD. SPS-treated rats mimic the pathophysiological abnormalities and behavioral characteristics of PTSD, such as enhanced anxiety-like behavior, glucocorticoid negative feedback, and analgesia. In addition, the authors demonstrated enhanced freezing in response to contextual fear conditioning, and impaired extinction of fear memory, which was alleviated by D-cycloserine (DCS). In parallel, there was a decrease in extracellular glycine mediated by an increase in glycine transporter 1 in the hippocampus of SPS-treated rats after fear conditioning, which suggested that activation of N-methyl-D-asparate receptor by DCS during fear extinction training might alleviate the impaired fear extinction. This chapter summarizes PTSD-like symptoms in SPS and evaluates the validity of SPS as an animal model of PTSD.

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Karpova, Nina N. Pharmacological Adjuncts and Evidence-Supported Treatments for Trauma. Edited by Sara Maltzman. Oxford University Press, 2016. http://dx.doi.org/10.1093/oxfordhb/9780199739134.013.32.

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A large proportion of humans experienced a traumatic event in their lifetime, with more than 10% developing posttraumatic stress disorder (PTSD), panic disorder, phobias, and other fear/anxiety disorders. The neural circuitry of fear responses is highly conserved in humans as well as rodents, and this allows for translational research using animal models of fear. Fear/anxiety disorders in humans are most efficiently treated by exposure-based psychotherapy (i.e., cognitive behavioral therapy; CBT), the main aspects of which are closely modeled by extinction training in Pavlovian fear conditioning and extinction paradigms in rodents. To improve the efficacy of psychotherapy, pharmacological agents potent for enhancing learning and memory consolidation processing should be developed to combine with exposure-based therapy. The purpose of these adjunctive pharmacological agents is to promote fear memory erasure and the consolidation of extinction memories, thus providing a combined treatment of increased effectiveness. This review discusses established pharmacological adjuncts to behavioral therapeutic interventions for fear/anxiety disorders. The mechanisms of action of these adjuncts, as well as the evidence for and against the pharmacological treatment strategies and their limitations are discussed.

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Heller, Aaron S. Functional Brain Imaging and PTSD. Edited by Charles B. Nemeroff and Charles R. Marmar. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190259440.003.0018.

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Post-traumatic stress disorder (PTSD) is associated with a host of neurobiological changes, including abnormalities in subcortical and cortical structure and function. The majority of neuroimaging studies have been motivated by a fear conditioning and extinction perspective to examine neural changes associated with PTSD. Several studies have found alterations in amygdala, hippocampal, and ventromedial prefrontal cortex. However, not all studies have replicated these findings. This suggests that more nuanced models of PTSD may be needed to account for the pathophysiology of the disorder. This chapter reviews neuroimaging findings related to this fear model and discusses additional considerations, including trauma type, age of trauma, and affective neurodynamics, that may help to account for the lack of consistent replications. Explicit consideration of these factors may facilitate greater coherence among studies going forward and advance our understanding of the neurobiological alterations associated with PTSD.

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Jovanovic, Tanja, and Seth Davin Norrholm. Human Psychophysiology and PTSD. Edited by Israel Liberzon and Kerry J. Ressler. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190215422.003.0015.

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Psychophysiological measures provide useful tools for investigating neurobiological mechanisms of trauma-related sequalae. In addition, they can serve as objective biological assessments of symptom severity in clinical research. This chapter describes the methods for collection of psychophysiological measures. These include muscle contractions (startle), electrodermal skin conductance, heart rate, and heart rate variability (HRV) at baseline, under stress, and following Pavlovian fear conditioning. These approaches are important both for understanding biology as well as for providing objective biomarkers that can be compared translationally from animals to humans. It also reviews the literature that has used these measures in PTSD. The evidence to date strongly suggests that these data provide robust correlates of PTSD severity.

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Carrión, Victor G., John A. Turner, and Carl F. Weems. Emotion Processing. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190201968.003.0003.

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Prolonged difficulty identifying and regulating emotions is another essential symptom of PTSD, and has been associated with hormonal dysregulation, social and academic difficulties, and structural and functional brain deficits in youth and adults. Individual subject variance in personality, disposition, sex, and genotype has been shown to uniquely modulate the prefrontal and limbic brain regions associated with emotion processing. The current chapter examines how the component processes of emotion regulation, such as fear conditioning, can be dysregulated by the experience of traumatic stress, by which the brain centers that manage reactions to emotionally charged stimuli are over- or underactivated. The preclinical literature that serves as the basis for our understanding of these systems is reviewed, as well as studies of adults and children who have experienced trauma. Future directions, such as clinical care based on neuroendocrine research, are also discussed.

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Miu, Andrei C., Judith R. Homberg, and Klaus-Peter Lesch, eds. Genes, brain, and emotions. Oxford University Press, 2019. http://dx.doi.org/10.1093/oso/9780198793014.001.0001.

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With the advent of methods from behavioral genetics, molecular biology, and cognitive neuroscience, affective science has recently started to approach genetic influences on emotion, and the underlying intermediate neural mechanisms through which genes and experience shape emotion. The aim of this volume is to offer a comprehensive account of current research in the genetics of emotion, written by leading researchers, with extensive sections focused on methods, intermediate phenotypes, and clinical and translational work. Major methodological approaches are reviewed in the first section, including the two traditional “workhorses” in the field, twin studies and gene–environment interaction studies, and the more recently developed epigenetic modification assays, genome-wide association studies, and optogenetic methods. Parts 2 and 3 focus on a variety of psychological (e.g. fear conditioning, emotional action control, emotion regulation, emotional memory, decision-making) and biological (e.g. neural activity assessed using functional neuroimaging, electroencephalography, and psychophysiological methods; telomere length) mechanisms, respectively, that may be viewed as intermediate phenotypes in the pathways between genes and emotional experience. Part 4 concentrates on the genetics of emotional dysregulation in neuropsychiatric disorders (e.g. post-traumatic stress disorder, eating disorders, obsessive–compulsive disorder, Tourette’s syndrome), including factors contributing to the risk and persistence of these disorders (e.g. child maltreatment, personality, emotional resilience, impulsivity). In addition, two chapters in Part 4 review genetic influences on the response to psychotherapy (i.e. therapygenetics) and pharmacological interventions (i.e. pharmacogenetics) in anxiety and affective disorders.

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Davey, Graham. Classical conditioning and the acquisition of human fears and phobias: A review and synthesis of the literature. 1992.

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