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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 vérifiablesFear 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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Antunes, Raquel A. G. "Neural mechanisms of stimulus generalization in auditory fear conditioning." Doctoral thesis, Universidade Nova de Lisboa. Instituto de Tecnologia Química e Biológica, 2011. http://hdl.handle.net/10362/6175.
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Dissertation presented to obtain the Ph.D degree in Neuroscience Instituto de Tecnologia Química e Biológica, Universidade Nova de LisboaFear is a physiological trait with a strong weight on survival and adaptation. Great progress has been made to understand the mechanisms of fear learning, mainly using auditory fear conditioning (AFC). In this behavioral paradigm, an initial neutral tone (conditioned stimulus, CS) acquires aversive predictive properties after successive pairings with a footshock (unconditioned stimulus, US) and comes to elicit responses characteristically elicited by threatening stimuli. In this behavioral paradigm, the amygdala has been identified has a key neural substrate for associative fear learning, and the site where unconditioned stimuli (US) and conditioned (CS) auditory stimuli come to be associated. Auditory information may reach the amygdala either directly from the auditory thalamus or indirectly via thalamo-cortico-amygdala projections. The “high route/low route” hypothesis has thus been proposed, which claims that the cortical pathway (“high route”) is crucial for discrimination between fearful and neutral sounds, while the direct thalamic pathway (“low route”) provides a rapid but less accurate relay of auditory information to the amygdala. This hypothesis relies on the assumption that more complex processing requires cortical activity and that thalamic relay is faster then cortical transmission to the amygdala. The present work essentially aims at putting to test this largely accepted hypothesis.Auditory fear conditioning was used as the behavioral paradigm to unravel the possible functional explanation for the coexistence of two parallel auditory pathways converging into the amygdala, and the high route/low route hypothesis was the working model for the identification of neuronal substrates of auditory discrimination.(...)
This work was supported by Fundação para a Ciência e a Tecnologia (Grant SFRH/BD/27500/2006).
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Ryan, Katherine M. "Methodological differences in Pavlovian fear learning, extinction and return of fear." Thesis, Griffith University, 2021. http://hdl.handle.net/10072/410147.
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Examining methodological differences in fear conditioning and extinction studies is a growing area of research, inspired by the recent ‘replication crisis’ in psychological research. Determining whether methodological differences of fear conditioning and extinction paradigms contribute to inconsistent findings is important in terms of the translational value of this paradigm as an experimental analogue of exposure-based cognitive behavioural therapy. The aim of this thesis was to improve the experimental methodology of fear conditioning and extinction studies, by addressing three key questions: 1) Are there parameters of fear conditioning and extinction tasks that differentiate successful from unsuccessful extinction in studies with children and youth; 2) Do different types and combinations of within-phase subjective measures affect within-phase physiological and between-phase measures of fear conditioning and extinction; and 3) Does behavioural memory reconsolidation in the form of cue reactivation with versus without instructions differentially impact extinction and return of fear?
Question one was addressed by conducting a systematic review of 35 fear conditioning and extinction studies conducted with children and adolescents (Chapter 2, Ryan et al., 2019). This review revealed that successful extinction was observed in studies that used fear irrelevant shapes (CS) and tones (US) (recommended for all youth) or fear relevant faces (CS) and screams (US) (recommended only for adolescents) as well as those studies that used 8 – 12 CS trials per acquisition and extinction phase. The most commonly used and effective dependent measures were skin conductance responses (SCRs) and subjective ratings of CS valence, fearfulness and arousal. Fear potentiated startle (FPS) was also effective, however less commonly used with children. It was suggested that standard measures be adopted for subjective ratings
scales to assist in comparisons across studies. It was recommended that both physiological measures of SCRs and/or FPS be assessed, as well as within-phase subjective measures of US expectancy ratings and CS evaluations and between-phase measures of CS valence, CS arousal and subjective anxiety. Also, additional measures of contingency awareness and US intensity and pleasantness after the conditioning phase was recommended. The review identified unresolved issues and directions for future research to further clarify the most effective designs and measures.
The first experimental study (Chapter 3, Ryan et al., 2021) aimed to address one of the issues identified in Ryan et al. (2019) relating to whether different combinations of within-phase subjective measures of US expectancy and CS evaluations would influence skin conductance responses and between-phase subjective ratings of CS valence, CS arousal and subjective anxiety. The fear conditioning and extinction study involved 88 participants aged between 17- 25 years recruited from first year university psychology students. The Control condition (N =22) included the assessment of SCRs and between-phase ratings. Relative to the Control condition, the US Expectancy condition (N= 21) additionally included within-phase US expectancy ratings throughout each phase, the CS Evaluation condition (N = 21) additionally included within-phase CS evaluations, and the All Measures condition (N = 23) additionally included both within-phase US expectancy and CS evaluations. Within-phase subjective measures influenced learning by changes in arousal measured by SCRs, however they did not influence between-phase ratings. Rating the within-phase US expectancy alone resulted in successful conditioning, extinction and extinction retention of differential SCRs. Providing the within-phase CS evaluation alone resulted in successful conditioning but no extinction of differential SCRs although extinction did occur at the end of the test phase. For the control condition (no within-phase measures), there was also no extinction of SCRs that remained until the end of the test phase. Rating both within-
phase measures resulted in successful conditioning and extinction of differential SCRs; however, the arousal was elevated compared to other conditions. The All measures condition also had a return of differential SCRs during the test phase. It was concluded that researchers need to consider the aims and objectives of their study because different types and combinations of within-phase subjective ratings may influence the outcomes.
The second experimental study (Chapter 4, Ryan et al., under review) investigated a notable methodological difference in behavioural memory reconsolidation studies, in which some studies but not others include instructions before the cue reactivation manipulation. The goal was to determine whether instructions influence extinction and the return of differential fear responses. Participants were recruited from first year university psychology students (N = 109) with an age range of 17 - 40 years. Four conditions tested the role of instructions on cue reactivation by presenting the cue with (CS+ Instruct) and without instructions (CS+ Only) relative to two conditions that controlled for the role of instructions alone (Instruct Only) and no cue or instructions (Control). Participants completed acquisition, extinction and test phases within a single session, using fear relevant dog pictures and an aversive auditory unconditional stimulus (US). Measures included skin conductance responses (SCRs), within-phase US expectancy, between-phase CS evaluations and subjective anxiety. No condition differences were found - all conditions demonstrated extinction retention of SCRs in the test phase. There were also no condition differences in US expectancy ratings within-phase and CS evaluations between-phase. Subjective anxiety ratings also showed no differences between conditions, although fear reduced after extinction for all conditions. The findings found no support for instructions before cue reactivation and no support for behavioural memory reconsolidation.
Three general conclusions were drawn from the results of the systematic review and the two experimental studies: 1) Parameters of fear conditioning and extinction tasks can differentiate successful from unsuccessful extinction; 2) Different types and combinations of within-phase subjective measures affect physiological measures of fear conditioning and extinction studies; and 3) Cue reactivation with or without instructions during behavioural memory consolidation does not impact extinction and the return of fear. Future research implications and recommendations are discussed. The findings from the current PhD program of research have methodological implications for future fear conditioning and extinction studies and add to the literature focused on improving scientific rigour and the replication crisis in psychological research.Thesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Applied Psychology
Griffith Health
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Conceição, Luiz Henrique Santana. "Sleep modifications after contextual fear conditioning and extinction in rats." reponame:Repositório Institucional da UFABC, 2016.
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Orientadora: Profa. Dra. Paula Ayako TibaDissertação (mestrado) - Universidade Federal do ABC, Programa de Pós-Graduação em Neurociência e Cognição, 2016.
Memórias de extinção são um produto das variações nas condições de condicionamento e na quantidade de tempo e sessões de extinção. Aumentos de sono paradoxal após a exposição a sessões de extinção foram descritas anteriormente, contudo trabalhos anteriores não testaram mais de um dia de extinção e tão pouco testaram se a modificação do sono após a extinção dependeria do intervalo de tempo entre condicionamento e extinção. Nós exploramos modificações da arquitetura do sono em diferentes condições de aprendizagem a extinção do medo condicionado. Em primeiro lugar, usamos uma tarefa de condicionamento de medo ao contexto (CMC) a fim de explorar o efeito de um evento aversivo (o choque elétrico) e um possível efeito do intervalo de tempo entre a sessão condicionamento e a sessão de extinção no sono e comportamento. O primeiro grupo, chamado Extinção Múltipla recebeu um treino de CMC com uma apresentação de choque único seguido por cinco sessões de extinção. O segundo grupo, chamado extinção única, foi treinado no CMC e expostos à extinção sete dias após este treino. O terceiro grupo - chamado choque imediato - recebeu uma sessão de treinamento com um único choque aplicado imediatamente depois de entrar na caixa de condicionamento e seguiu o mesmo protocolo de extinção que o grupo de extinção múltipla. A resposta de congelamento foi o parâmetro comportamental analisado. Informações sobre sono-vigília foram registradas através da coleta de dados de ECOG e EMG e classificado entre três fases: vigília, sono de ondas lentas e sono paradoxal. Os resultados mostraram aumento do sono de ondas lentas após CMC e aumento do sono paradoxal depois de CMC e extinção entre os grupos T-múltipla e T-única. Nossas descobertas apoiam achados anteriores sobre a relação entre sono paradoxal e aprendizagem da extinção e sugerem que modificações de sono de ondas lentas para extinção antecipada sejam dependentes do tempo.
Extinction memory is a product of variations in fear conditioning and fear extinction procedure and the amount of time and sessions of extinction. Increases in paradoxical sleep (PS) after exposure to extinction sessions was previously described; however, previous works did not test more than one day of extinction and did not test whether sleep modifications after extinction are dependent upon the time interval between conditioning and extinction. We explored sleep architecture modifications on different conditions of conditioned fear extinction learning. We first adapted a contextual fear-conditioning task in order to explore the effect of an aversive event (the electric shock) and a possible effect of time interval between conditioning and extinction session on sleep and behaviour. The first group, named Multiple Extinction (T-10 Multiple) received a contextual fear conditioning (CFC) training with a single shock presentation followed by five sessions of extinction. The second group, named single extinction (T-Single), was trained in the same CFC procedure and exposed to one single extinction session, seven days after training. The third group ¿ named immediate shock ¿ received a training 1session with a single shock applied immediately after entering the conditioning box following the same protocol of extinction as the T-Multiple group. The freezing response was the behavioural parameter analysed. Sleep-wake information was recorded by collecting electrocorticogram (ECOG) and electromyogram (EMG) data and scored as one between three phases: awake, slow wave sleep (SWS) and PS. Results showed that SWS increased after CFC, and it also showed that PS increased after CFC and extinction for either T-Multiple and T- Single group. Our findings support previous findings on PS relation with extinction learning and suggest some time-dependent SWS modification for early extinction re-exposure. The discovery of the participation of PS in contextual fear extinction and SWS role on nuances of extinction procedure expands the understanding of behaviour and sleep relations and, at the same time, offer a behavioural model to study sleep dependent stressful memory related to PTSD or HPA axis without the unconditioned behavioural and physiological effects of ES.
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Cullen, Patrick Kennedy. "NEUROBIOLOGICAL MECHANISMS OF FEAR GENERALIZATION." Kent State University / OhioLINK, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=kent1374536919.
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Kunkel, Rebecca Ann. "Can Positive Reinforcement Overcome Fear? An Investigation of Competing Contingencies." Thesis, University of North Texas, 2011. https://digital.library.unt.edu/ark:/67531/metadc84232/.
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Escape maintained behavior in dogs is generally displayed by one of two behaviors-fleeing or aggression. Once aggression is negatively reinforced by the removal of the aversive stimulus, it is very difficult to eliminate from the organism's repertoire. Counterconditioning is the process of pairing a positive reinforcer with an aversive stimulus in the attempts that an organism will no longer exhibit fear responses in its presence. This process must be done gradually with small approximations. Many organisms have been trained to tolerate the presence of aversive stimuli via counterconditioning. However, this process can be time consuming and has inconsistent results. The purpose of this experiment was to monitor the effects of counter conditioning around an aversive stimulus while simultaneously training an identical behavior in the presence of a neutral stimulus. The results demonstrated that even though counterconditioning produced approach to the aversive stimulus the subject still exhibited numerous fear responses when results were compared to the control condition.
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Lewis, Michael. "Fear Conditioning as an Intermediate Phenotype: An RDoC Inspired Methodological Analysis." Thesis, Virginia Tech, 2018. http://hdl.handle.net/10919/83837.
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Due to difficulties in elucidating neurobiological aspects of psychological disorders, the National Institute of Mental Health (NIMH) created the Research Domain Criteria (RDoC), which encourages novel conceptualizations of the relationship between neurobiological circuitry and clinical difficulties. This approach is markedly different from the Diagnostic and Statistical Manual of Mental Disorders (DSM) based approach that has dominated clinical research to date. Thus, RDoC necessitates exploration of novel experimental and statistical approaches. Fear learning paradigms represent a promising methodology for elucidating connections between acute threat (“fear”) circuitry and fear-related clinical difficulties. However, traditional analytical approaches rely on central tendency statistics, which are tethered to a priori categories and assume homogeneity within groups. Growth Mixture Modeling (GMM) methods such as Latent Class Growth Analysis (LCGA) may be uniquely suited for examining fear learning phenotypes. However, just three extant studies have applied GMM to fear learning and only one did so in a human population. Thus, the degree to which classes identified in known studies represent characteristics of the general population and to which GMM methodology is applicable across populations and paradigms is unclear. This preliminary study applied LCGA to a fear learning lab study in an attempt to identify heterogeneity in fear learning patterns based on a posteriori classification. The findings of this investigation may inform efforts to move toward a trans-diagnostic conceptualization of fear learning. Consistent with the goals laid out in RDoC, explication of fear learning phenotypes may eventually provide critical information needed to spur innovation in psychotherapeutic and psychopharmacological treatment.Master of Science
To date, most clinical psychology research has been based on the Diagnostic and Statistical Manual of Mental Disorders (DSM), which is a catalog of mental health disorders that was originally designed to facilitate communication among clinicians. Many experts contend that this approach has hampered progress in the field of biological clinical psychology research. Thus, the National Institute of Mental Health (NIMH) created a new template for biological clinical psychology research called the Research Domain Criteria (RDoC). Since RDoC calls for a complete overhaul in the conceptualization of clinical dysfunction, this approach requires statistical and experimental innovation. One traditional experimental approach that may be helpful in understanding the RDoC topic of acute threat (“fear”) is called Pavlovian Fear Learning (PFL). However, traditional PFL studies have utilized statistical methods that are based on comparing group averages and require researchers to determine groups of interest based on theory before the study begins. This is problematic because RDoC calls for research that begins with evidence rather than theory. Growth Mixture Modeling (GMM) is a statistical methodology that may allow researchers to analyze fear learning data without having to begin with theoretically determined categories such as DSM disorders. However, little research has tested how well this approach would work. This study is just the second to apply a GMM approach to a human PFL study. The findings from this investigation may inform efforts to develop a statistical technique that is well suited for RDoCian research and may also spur innovation in psychotherapeutic and psychopharmacological treatment.
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Kochli, Daniel. "The amygdala is critical for trace, delay, and contextual fear conditioning." Miami University / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=miami1406560508.
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Isaacs, Sofie. "The Roles of the Amygdala and the Hippocampus in Fear Conditioning." Thesis, Högskolan i Skövde, Institutionen för biovetenskap, 2015. http://urn.kb.se/resolve?urn=urn:nbn:se:his:diva-11284.
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The amygdala, a small structure located deep bilaterally in the medial temporal lobe, is the key structure for the emotional processing and storage of memories associated with emotional events, especially fear. The structure has also been shown to enable humans and animals to detect and respond to environmental threats. Fear conditioning became the main model to examine the neural substrates of emotional learning in mammals and specifically in rats’. With the fear conditioning method, researchers can tests rats’, responses to aversive stimuli during the delivery of a cue and then measure how the responses change after learning of the association between the stimuli and the cue. After learning of the two stimuli, the delivery of a cue alone will prompt a fear response in the rats. The fear response can also be elicited by placing the rats in the same chamber in which the aversive stimuli has previously been experienced, which depends on both the amygdala and the hippocampus. Where the amygdala stores the memories of stimulus related to fear, the hippocampus seems to hold all the fear memories in relation to contextual information about the stimulus. The aim of this paper will be to make a comprehensive overview of internal neural processes of both the amygdala and hippocampus and the interaction between the two structures during fear conditioning, to see how the structures separately work to overlap emotion and memory processes.
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Iberico, Carlos, Debora Vansteenwegen, Bram Vervliet, and Dirk Hermans. "The effect of (un)predictability on contextual fear: A replication of the basic findings." Pontificia Universidad Católica del Perú, 2012. http://repositorio.pucp.edu.pe/index/handle/123456789/102314.
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The aim of this experiment was to study the role of (un)predictability in a fear conditioning paradigm: analyzing the differences in both cue and context conditioning. For this reason, we manipulated the presentation of the unconditional stimulus (US) using two conditions: a paired presentation of the US-CS (predictable) and an unpaired presentation of the US (unpredictable). We manipulated the context using the lightning of the experimental room: dark and light conditions. Our dependent variables were the skin conductance response (SCR) and the startle reflex measurement. Participants were 65 students from the University of Leuven. Results showed more context conditioning in the unpaired block (unpredictable) compared to the paired one and cue conditioning in the paired block (predictable).El objetivo de este estudio fue investigar el rol de la (im)predictabilidad en el paradigma de condicionamiento de miedo, al analizar las diferencias tanto en el condicionamiento específico (cue) como en el contextual. Por consiguiente, se manipuló la presentación del estímulo incondicionado (EI) utilizando dos condiciones: una presentación apareada del EI con el estímulo condicionado —EC en adelante— (predecible) y una presentación no apareada del EI (impredecible). Se manipuló el contexto utilizando la luz central del cuarto experimental: condiciones de oscuridad y claridad. Las variables independientes fueron la respuesta de conductancia de la piel y la medición de la respuesta de sobresalto. Los participantes fueron 65 alumnos de primer año de psicología. Los resultados muestran más condicionamiento contextual en el bloque no apareado (impredecible) comparado con el apareado, y condicionamiento específico en el bloque apareado (predecible).
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Björkstrand, Johannes. "The Amygdala, Fear and Reconsolidation : Neural and Behavioral Effects of Retrieval-Extinction in Fear Conditioning and Spider Phobia." Doctoral thesis, Uppsala universitet, Institutionen för psykologi, 2017. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-317866.
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The amygdala is crucially involved in the acquisition and retention of fear memories. Experimental research on fear conditioning has shown that memory retrieval shortly followed by pharmacological manipulations or extinction, thereby interfering with memory reconsolidation, decreases later fear expression. Fear memory reconsolidation depends on synaptic plasticity in the amygdala, which has been demonstrated in rodents using both pharmacological manipulations and retrieval-extinction procedures. The retrieval-extinction procedure decreases fear expression also in humans, but the underlying neural mechanism have not been studied. Interfering with reconsolidation is held to alter the original fear memory representation, resulting in long-term reductions in fear responses, and might therefore be used in the treatment of anxiety disorders, but few studies have directly investigated this question. The aim of this thesis was to examine the effects of the retrieval-extinction procedure on amygdala activity and behavioral fear expression in humans. The work presented here also investigated whether findings from studies on recent fear memories, established through fear conditioning, extends to naturally occurring long-term phobic fears. Study I, combining fear conditioning and a retrieval-extinction procedure with functional magnetic resonance imaging (fMRI), demonstrated that memory retrieval shortly followed by extinction reduces later amygdala activity and fear expression in healthy subjects. In Study II, these subjects were re-tested 18 months later. The results showed that the effects on fear expression were still present and that initial amygdala activity predicted long-term fear expression. Using an adapted version of the retrieval-extinction procedure, Study III showed that memory retrieval shortly followed by exposure to spider pictures, attenuates subsequent amygdala activity and increases approach behavior in subjects with life-long fear of spiders. In Study IV, these subjects were re-tested 6 months later, and the results showed that effects on amygdala activity as well as approach behavior were maintained. In summation, retrieval-extinction leads to long-lasting reductions in amygdala activity and fear expression. These findings are consistent with the hypothesis that retrieval-extinction alters an amygdala dependent fear memory. Retrieval-extinction can also attenuate long-term phobic fears, indicating that this manipulation could be used to enhance exposure-based treatments for anxiety disorders.
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Ray, Madelyn. "TheRole of the Nucleus Accumbens Core in Scaling Fear to Degree of Threat:." Thesis, Boston College, 2021. http://hdl.handle.net/2345/bc-ir:109068.
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Thesis advisor: Michael A. McDannaldIdentifying the neural circuits underlying adaptive fear is fundamental to understanding and developing more effective treatments for anxiety disorders. Adaptive behavior requires fear to scale to the level of threat and dysfunction in this capacity is a hallmark of fear-related anxiety disorders. Identifying the neural circuits underlying adaptive fear is fundamental to understanding anxiety disorders and propelling more effective treatments for patients. Fear is adaptive when the level of the response rapidly scales to degree of threat. Using a discrimination procedure consisting of danger, uncertainty, and safety cues, our laboratory has found rapid fear scaling (within 2 s of cue presentation). However, the neural underpinnings of this behavior are unknown. The overarching goal of this dissertation is to examine a role for the nucleus accumbens core (NAcc) in scaling fear to degree of threat. In three experiments I used neurotoxic lesions, optogenetic inhibition, and in vivo electrophysiology combined with an intricate fear learning procedure to elucidate a role for the NAcc in both general and rapid scaling of fear. Permanent NAcc dysfunction, via neurotoxic lesion, generally disrupted the ability to scale fear to degree of threat and specifically impaired one component of scaling: rapid discrimination of uncertain threat and safety. Reversible NAcc dysfunction, via optogenetic inhibition, specifically impaired rapid discrimination of uncertain threat and safety. Further, I demonstrated that NAcc activity is threat responsive and exhibits heterogeneity in the timing and specific nature of threat firing. The results reveal that the NAcc is essential to scale fear to degree of threat and responds to threat cues across both rapid and general timescales. Taken together, the results reveal a novel role for the NAcc in scaling fear and identify it as a plausible source of dysfunction in stress and anxiety disorders. Identifying the brain regions underlying adaptive fear is fundamental to understanding and developing more effective treatments for anxiety disorders
Thesis (PhD) — Boston College, 2021
Submitted to: Boston College. Graduate School of Arts and Sciences
Discipline: Psychology
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Ågren, Thomas. "Erasing Fear : Effect of Disrupting Fear Memory Reconsolidation on Central and Peripheral Nervous System Activity." Doctoral thesis, Uppsala universitet, Institutionen för psykologi, 2012. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-180202.
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Fear memories, here defined as learned associations between a stimulus and a physiological fear reaction, are formed through fear conditioning. In animals, fear memories, present in the lateral amygdala, undergo reconsolidation after recall. Moreover, this reconsolidation process can be disrupted both pharmacologically and behaviourally, resulting in a reduced fear response to the stimulus. This thesis examines the attenuation of fear memories by disrupting reconsolidation in humans, using measures of both the central and peripheral nervous system activity. Serotonergic and dopaminergic genes have previously been tied to both fear conditioning and anxiety disorders, where fear conditioning mechanisms are important. In order to evaluate the possible role of fear memory reconsolidation mechanims in the effect on fear and anxiety by these genes, this thesis also compare the reconsolidation disruption effect between different serotonergic and dopaminergic genotypes. Study I examined the attentuation of fear memories by disrupting reconsolidation in humans using reacquisition as a measure of the return of fear. Moreover, study I investigated the impact of differences in serotonergic and dopaminergic alleles on this process. Study II examined the attentuation of fear memories by disrupting reconsolidation in humans using reinstatement as a measure of the return of fear. Study II also investigated the impact of differences in serotonergic and dopaminergic alleles on the process of fear memory reconsolidation. Study III used psychophysiology and fMRI to localize the functional neural activity mediating the fear memory reconsolidation disruption effect. In summary, this thesis provides evidence that fear memories are attenuated by reconsolidation disruption in humans and that serotonergic and dopaminergic alleles influence this process. Moreover, this thesis support that human fear memory reconsolidation is amygdala-dependent, suggesting an evolutionary shared memory mechanism.
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Leung, Hiu Tin Psychology Faculty of Science UNSW. "Spontaneous recovery in Pavlovian fear extinction and latent inhibition." Publisher:University of New South Wales. Psychology, 2009. http://handle.unsw.edu.au/1959.4/43701.
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The experiments reported in the present thesis examined the behavioural processes of Pavlovian fear extinction and latent inhibition. The first series of experiments studied the reacquisition of extinguished fear responses following different amounts of extinction training. Rapid reacquisition occurred when rats were reconditioned after moderate extinction, showing that the original learning remained intact across this extinction. In contrast, when reconditioning was given after massive extinction, reconditioned responding was first depressed but then spontaneously recovered over time. This suggests that massive extinction produces a relatively permanent loss of the originally learned responding, while additionally imposes on the extinguished CS a transient latent inhibitory process that prevented the immediate but not the delayed expression of reconditioning. The second series of experiments studied the impact of spontaneous recovery of extinguished fear responses on their additional extinction. These experiments demonstrated that a CS that had time to show spontaneous recovery underwent greater response loss across additional extinction than one lacking recovery. They also showed that an excitor extinguished in compound with a CS showing recovery suffered greater response loss than an excitor extinguished in compound with a CS lacking recovery. Further, extinction of a compound composed of two CSs, one showing recovery and a second lacking recovery, produced greater extinction to the CS that showed recovery. These results show that spontaneous recovery of extinguished responses deepens their extinction through an error-correction mechanism regulated by both common and individual error terms. The third series of experiments studied the spontaneous recovery of latently inhibited and extinguished fear responses in within-subject designs. Using a compound test procedure, a CS that had received extensive preexposure or extensive extinction was found to have undergone greater spontaneous recovery relative to a CS just moderately preexposed or moderately extinguished. A CS given a mixed history of preexposure and extinction also underwent greater recovery relative to a CS just preexposed or just extinguished. These results suggest that both latent inhibition and extinction share a transient depressive process, and that the resulting recovery of responding is proportional to the amount of this depression.
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Top, Jr David Nicholas. "A fMRI of Fear Conditioning and Auditory Looming in Autism Spectrum Disorder." BYU ScholarsArchive, 2020. https://scholarsarchive.byu.edu/etd/8599.
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Many autistic adults experience debilitating anxiety that interferes with their daily functioning. Atypical sensory processing and intolerance of uncertainty are cognitive processes linked to atypical limbic system functioning and impaired fear conditioning as potential mediators of anxiety in autism. A previous fear conditioning study using fMRI found atypical amygdala functioning in autism when the threat stimulus was only partially reinforced. The first aim of this dissertation is a multimethod examination of brain and psychophysiological response in autistic and in neurotypical adults during a fear conditioning/extinction task with the threat stimulus reinforced 100% percent of the time. We were also interested in the responses of autistic and neurotypical adults during an auditory looming task that requires no learning contingencies. We used fMRI, pupillometry, and skin conductance response as the dependent measures. Results demonstrated a significant main effect for insula activation, but not amygdala activation, during the 100%-reinforcement fear conditioning task with no between-group differences or group x condition interactions. There were likewise no condition differences (Safe vs Threat) for amygdala in the auditory looming task. However, the autism group demonstrated increased insula response to both Threat and Safe auditory conditions of the looming task, suggesting the autism group utilized alternative cognitive resources than the neurotypical group. Results indicate intact fear conditioning and extinction in autism for more certain conditions and suggests that behavioral (exposure) anxiety treatments for phobias could be useful under certain conditions. Results of this study are inconsistent with the atypical/hyperactive amygdala hypotheses of anxiety with autism and inconsistent with the portion of the South & Rodgers (2017) anxiety model regarding the importance of intolerance of uncertainty in autism samples.
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Ulmen, Adam Richard. "The NMDA receptor antagonist MK-801 renders pavlovian fear conditioning state-dependent." Kent State University / OhioLINK, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=kent1430140456.
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Bellafiore, Amber. "Fear Conditioning: Using the Scream of a Woman's Voice: A Pilot Study." Thesis, The University of Arizona, 2011. http://hdl.handle.net/10150/144176.
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Diggs, Herman Augustus. "EFFECTS OF ACUTE THC ADMINISTRATION ON EXTINCTION OF CONDITIONED FEAR RESPONSES IN HUMANS: A FUNCTIONAL ANALYSIS OF HIGH DENSITY EEG." OpenSIUC, 2014. https://opensiuc.lib.siu.edu/dissertations/947.
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High density electroencephalographic (EEG) measures were used to assess the effects of acute delta 9-tetrahyrdrocannabidol (THC) administration on extinction of conditioned fear responses. Fear conditioning was initiated using a differential classical conditioning paradigm that paired an aversive unconditioned stimulus (shock) with a signaling stimulus (CS+), whereas another stimulus served as a safety signal (CS-). Evoked potentials, induced event-related spectral perturbations (ERSP), and associated intertrial coherence (ITC) measures were used to quantify the acquisition and extinction of conditioned fear responses. Participants (N = 10 males) exhibited conditioning to the CS+ across fear acquisition training, as reflected by greater late positive (posterior sites) and late negative (anterior sites) potential amplitude to the CS+ relative to the CS-. Acute administration of THC facilitated extinction of the conditioned response to the CS+ relative to placebo, as reflected by greater LPP and LNP amplitude to the CS+ relative to the CS- in the placebo, but not THC condition. ERSP analyses suggest the lack of difference between CS+ and CS- ERP amplitude may be partially explained by a shifting of attention from external stimuli to internal processing in the THC condition. However, relative to placebo, THC administration also increased the amplitude of some measures of the conditioned response (LNP) to the CS-, suggesting a generalization of fear or lack of discrimination in this condition.
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Walker, Rachel Ann. "Neural Mechanisms of Aversive Prediction Errors:." Thesis, Boston College, 2020. http://hdl.handle.net/2345/bc-ir:109027.
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Thesis advisor: Michael McDannaldUncertainty is a pervasive facet of life, and responding appropriately and proportionally to uncertain threats is critical for adaptive behavior. Aversive prediction errors are signals that allow for appropriate fear responses, especially in the face of uncertainty, and provide a critical updating mechanism to adapt to change. Positive prediction errors (+PE) are generated when an actual outcome of an event is worse than the predicted outcome and increase fear upon future encounters with the related predictive cue. Negative prediction errors (-PE) are generated when the predicted outcome is worse than the actual outcome and decrease fear upon future encounters with the related predictive cue. While some regions have been offered as the neural source of positive and negative prediction errors, no causal evidence has been able to identify their sources of generation. The objective of this dissertation was to causally identify the neural basis of aversive prediction error signaling. Using precise neural manipulations paired with a robust behavioral fear discrimination task, I present causal evidence for vlPAG generation of +PEs and for a ventrolateral periaqueductal grey (vlPAG) to medial central amygdala (CeM) pathway to carry out +PE fear updating. Further, I demonstrate that while dorsal raphe serotonergic neurons are not the source of -PE generation, they appear to receive and utilize this signal. Understanding the neural network responsible for aversive prediction error signaling will not only inform understanding of the neurological basis of fear but also may provide insights into disorders, such as PTSD and anxiety disorders, that are characterized by excessive/inappropriate fear responses
Thesis (PhD) — Boston College, 2020
Submitted to: Boston College. Graduate School of Arts and Sciences
Discipline: Psychology
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Levillain, Mary Elizabeth. "Nicotine Facilitates Trace Fear Conditioning in Normal and FASD Rats Tested as Adolescents." W&M ScholarWorks, 2008. https://scholarworks.wm.edu/etd/1539626575.
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Chaaya, Nicholas. "Investigation of cellular and molecular mechanisms involved in contextual fear memory encoding." Thesis, Queensland University of Technology, 2019. https://eprints.qut.edu.au/134258/1/Nicholas_Chaaya_Thesis.pdf.
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This thesis examined the role of three distinct brain regions following the formation or maintenance of contextual fear memories (e.g. fear memories to particular rooms or environments). The results of this thesis demonstrated how neuronal activity and neuronal plasticity alter following minor changes to the context via addition of simple stimuli, such as auditory tones. This indicates that the manner in which a fear memory is obtained alters where and how it is stored within the brain. This has implications for individuals with fear-based disorders, such as post-traumatic stress disorder.
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Rantavuori, K. (Kari). "Aspects and determinants of children’s dental fear." Doctoral thesis, University of Oulu, 2008. http://urn.fi/urn:isbn:9789514289439.
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Abstract The aims of this study were to explore different aspects of dental fear and their determinants among children at different ages. The study samples comprised 378 children from the Veneto region of Italy aged 3–13 years and 1474 children from Jyväskylä and Kuopio, Finland, aged 3, 6, 9, 12 and 15 years. In the Italian study, the child’s age, first dental visit, number of subsequent visits and dental fear, and the parent’s dental fear were asked in a questionnaire. In the Finnish study, a questionnaire was used that contained 11 dental fear-related questions and family member’s dental fear and questions on oral health habits and family characteristics. Dental status was determined clinically and information on treatment procedures from three preceding years was collected from patient records. A total of 21 to 36% of Finnish children were quite or very afraid of something in dental treatment. The prevalence of dental fear among Finnish children was not lower among older children but rather fluctuated among different ages. The characteristics of dental fear differed among children at different ages. Among Finnish children, four aspects of dental fear were revealed from the questionnaire, i.e. ‘Treatment of dental decay’, ‘Attending dentist’, ‘Peak value for dental fear’ and ‘Fear of dental treatment in general’. Correlations between the four abovementioned aspects, the differences between age groups separately for the above mentioned aspects, and the determinants of dental fear were studied. At younger ages, the dental fear was abstract, commonly related to attending dentist. At older ages, dental fear was often related to invasive treatment, such as fear of local anaesthesia and drilling. Fear of pain which was common among all age groups. Among Italian children, the first dental experiences were strong determinants of dental fear. Among Finnish children, dental fear among other members of the family was more often found among children with dental fear than among non-fearful children. 15-year-old girls were more likely to be afraid than boys of the same age but gender differences were not found at younger ages. The results indicated that dental fear is not solely based on direct conditioning but rather consists of child, family and environment related determinantsTiivistelmä Tutkimuksen tarkoituksena oli selvittää lasten hammashoitopelon piirteitä ja niihin liittyviä seikkoja eri-ikäisillä lapsilla. Tutkimuksessa käytettiin havaintoaineistoa, joka koostui 378:sta 3–13-vuotiaasta italialaisesta lapsesta Veneton maakunnan alueelta sekä 1474:stä 3-, 6-, 9-, 12- ja 15-vuotiaasta lapsesta Jyväskylästä ja Kuopiosta. Tutkimuksessa italialaisilla lapsilla vanhempi täytti kyselylomakkeen, joka sisälsi kysymyksiä lapsen iästä, hammashoitopelosta, ensimmäisestä hammashoitokäynnistä ja seuraavien hoitokäyntien lukumäärästä sekä vanhemman omasta hammashoitopelosta. Suomalaisilla lapsilla tutkimustiedot kerättiin kyselylomakkeella, joka sisälsi 11 kysymystä lapsen hammashoitopelosta ja kysymyksiä lapsen suun terveystottumuksista sekä perheeseen liittyvistä seikoista, kuten perheenjäsenten hammashoitopelosta. Hampaiden senhetkinen kliininen tila sekä kolmen tarkastusta edeltävän vuoden hoitokäynnit ja tuolloin tehdyt toimenpiteet otettiin mukaan tutkimukseen. Suomalaisista lapsista 21–36 % pelkäsi jonkin verran tai paljon jotain asiaa hammashoidossa. Suomalaisten lasten hammashoitopelko ei ollut alempi nuoremmilla lapsilla vaan vaihteli ikäryhmien välillä. Myös hammashoitopelon luonne vaihteli ikäluokittain. Suomalaisesta kyselystä löydettiin neljä pelon osa-aluetta: paikkaushoitoon liittyvä pelko, hammaslääkärissä käymiseen liittyvä pelko, yleinen hammashoitopelko sekä voimakkaimmaksi koettu hammashoitoon liittyvä yksittäinen pelko. Tutkimuksessa tutkittiin pelon osa-alueiden välisiä korrelaatioita ikäryhmittäin, erikseen yksittäisen pelon osa-alueen vaihtelua ikäryhmien välillä sekä hammashoitopelon liittyviä seikkoja ikäryhmittäin. Nuoremmilla lapsilla hammashoitopelko oli useammin abstraktia, yleensä hammashoidossa käymiseen liittyvää pelkoa. Vanhemmilla lapsilla hammashoitopelko oli usein hammashoitotoimenpiteisiin liittyvää pelkoa, esimerkiksi puudutuksen ja porauksen pelkoa. Kivun pelko oli yleistä kaikissa ikäryhmissä. Ensimmäiset hammashoitokokemukset olivat voimakkaita hammashoitopelon selittäjiä italialaisilla lapsilla. Suomalaisten lasten hammashoitopelko oli vahvasti yhteydessä muiden perheenjäsenten hammashoitopelkoon. 15-vuotiaat tytöt pelkäsivät hammashoitoa enemmän kuin pojat, mutta sukupuolten välisiä eroja ei havaittu nuoremmissa ikäryhmissä. Tutkimus osoittaa, että lasten hammashoitopelko ei ole ainoastaan seurausta suorasta ehdollistumisesta hammashoitokokemusten kautta vaan siihen vaikuttavat enemmänkin lapseen, perheeseen ja ympäristöön liittyvät seikat
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Diggs, Herman Augustus. "EFFECTS OF ACUTE THC ADMINISTRATION ON EXTINCTION OF CONDITIONED FEAR RESPONSES IN HUMANS." OpenSIUC, 2010. https://opensiuc.lib.siu.edu/theses/305.
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Skin conductance responses were used to assess the effects of THC on conditioned fear response amplitude and extinction using a fear conditioning and extinction paradigm that paired an aversive unconditioned stimulus (shock) with a conditioned stimulus (angry face). Participants (N = 10 males) exhibited conditioning to the CS+, as indicated by a larger CR to the CS+ than to the CS-. THC did not have a significant effect on extinction of the CR across trials, but there was a significant interaction of social anxiety with drug that suggests that THC may facilitate extinction of CR to fear-conditioned stimuli in more socially anxious individuals. These results provide support for the hypothesis that THC may act as an anxiolytic in fear-eliciting situations. The current study was limited by a small sample size and a potential confound that may have influenced the SCL during conditioned responding.
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Kircher, Tilo, Volker Arolt, Andreas Jansen, Martin Pyka, Isabelle Reinhardt, Thilo Kellermann, Carsten Konrad, et al. "Effect of Cognitive-Behavioral Therapy on Neural Correlates of Fear Conditioning in Panic Disorder." Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2013. http://nbn-resolving.de/urn:nbn:de:bsz:14-qucosa-120091.
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Background: Learning by conditioning is a key ability of animals and humans for acquiring novel behavior necessary for survival in a changing environment. Aberrant conditioning has been considered a crucial factor in the etiology and maintenance of panic disorder with agoraphobia (PD/A). Cognitive-behavioral therapy (CBT) is an effective treatment for PD/A. However, the neural mechanisms underlying the effects of CBT on conditioning processes in PD/A are unknown.
Methods: In a randomized, controlled, multicenter clinical trial in medication-free patients with PD/A who were treated with 12 sessions of manualized CBT, functional magnetic resonance imaging (fMRI) was used during fear conditioning before and after CBT. Quality-controlled fMRI data from 42 patients and 42 healthy subjects were obtained.
Results: After CBT, patients compared to control subjects revealed reduced activation for the conditioned response (CS+ > CS–) in the left inferior frontal gyrus (IFG). This activation reduction was correlated with reduction in agoraphobic symptoms from t1 to t2. Patients compared to control subjects also demonstrated increased connectivity between the IFG and regions of the “fear network” (amygdalae, insulae, anterior cingulate cortex) across time.
Conclusions: This study demonstrates the link between cerebral correlates of cognitive (IFG) and emotional (“fear network”) processing during symptom improvement across time in PD/A. Further research along this line has promising potential to support the development and further optimization of targeted treatments.
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Rands, Gabriella. "The effect of executive function on the conditioning and counter-coditioning of children's fear." Thesis, University of East Anglia, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.521023.
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Introduction: Fear and anxiety disorders have a high prevalence in the general population. Childhood fears are a normal part of development, but in some cases these persist over longer periods and can cause considerable distress. The role of direct and indirect conditioning processes in anxiety development is well established. Recent research has considered the role of individual difference factors in the fear acquisition, and there is evidence to suggest that executive functioning is relevant to fear learning. Aims: This study investigates the hypotheses that individual differences in the form of executive functions kills and temperamental factors will be associated with the effectiveness of conditioning and counter-conditioning of childhood fear. Method: A sample of non-clinical children (n = 70), aged between 7 and 9 years, and their parents was recruited from local schools. This study used an observational design with a within-subjects experimental component. Parents completed the Behavioural Rating Inventory of Executive Function (BRIEF; Gioa et al., 2000) and the Children's Behaviour Questionnaire - very short form (CBQ; CBQ-VST; Putnam & Rothbart, 2006). Children completed the six-part test from the Behavioural Assessment of Dysexecutive Syndrome for children (BADS-C; Emslie et al., 2003), the Spence Children's Anxiety Scale (SCAS; Spence, 1994), and a go/nogo task. An experimental procedure manipulated children's fear beliefs and behavioural avoidance through provision of negative information or modelling. Fear levels were reduced using positive information and modelling. Results: Neither executive function nor temperamental elements were able to significantly predict the effectiveness of fear conditioning or counter-conditioning. Tentative evidence for a relationship between these individual difference factors and fear measures was identified when the sample was split by conditioning method. Conclusions: There was no evidence that individual difference factors influenced fear acquisition, or the reduction of fear following counter-conditioning. Group differences in results are discussed, and the findings are considered in relation to previous research. Clinical and theoretical implications outlined and directions for future research are identified.
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Kim, Jee Hyun Psychology Faculty of Science UNSW. "Extinction of conditioned fear in the developing rat." Publisher:University of New South Wales. Psychology, 2008. http://handle.unsw.edu.au/1959.4/41106.
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The present thesis examined extinction of conditioned fear in the developing rat. In the adult rat, the hippocampus is thought to be important for the context-specificity of extinction. Because the hippocampus is a late-maturing structure, it was hypothesised that context-modulation of extinction may be different across development. The first series of experiments investigated reinstatement of extinguished fear in the developing rat (Chapter 2). The results showed that P24 rats exhibited context-specific reinstatement. On the other hand, P17 rats did not exhibit reinstatement of extinguished fear following a US reminder treatment. The failure to see reinstatement in P17 rats was not due to the reminder treatment being ineffective in these rats because the same treatment alleviated spontaneous forgetting in rat this age. The second series of experiments then examined the renewal effect and GABAergic involvement in extinction in P24 and P17 rats (Chapter 3). It was observed that P24 rats displayed renewal whereas P17 rats did not. Also, pre-test injection of FG7142 recovered extinguished fear in P24 rats but not in P17 rats, even across a range of doses. This failure to see any FG7142 effect on extinction in P17 rats was not due to the lack of responsiveness to this drug in these rats because FG7142 was found to be effective in alleviating spontaneous forgetting in rats this age. The third series of experiments then examined the effect of temporary inactivation of the amygdala on extinction and re-extinction in the developing rat (Chapter 4). It was observed that extinction retention is impaired in both P24 and P17 rats if the amygdala is inactivated during extinction training. Interestingly, when a CS that had been previously extinguished and then re-trained was re-extinguished, re-extinction was amygdala-independent if initial extinction occurred at 24 days of age but amygdala-dependent if initial extinction occurred at 17 days of age. That is, amygdala involvement in re-extinction was dissociated across development. Taken together, these experiments provide strong evidence for fundamental differences in mechanisms underlying fear extinction across development. The implications of the findings were discussed in light of the theoretical and neural models of extinction.
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Dalrymple, Savannah. "Development of Ethologically-Based Inhibitory Avoidance Models of Fear Memory." Scholar Commons, 2017. http://scholarcommons.usf.edu/etd/6823.
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Translational research provides a unique opportunity to investigate innate and conditioned fear to develop an integrated understanding of anxiety disorders, ultimately improving treatment for those afflicted. Many fear conditioning paradigms use physically aversive stimuli to induce fear but ethological stimuli may better represent psychological disorders from a translational standpoint. Natural predators and immobilization have been successful in inducing both innate and contextually conditioned fear in rodents but an inhibitory avoidance paradigm that uses ethologically relevant stimuli has yet to be developed. To expand the use of these stimuli into inhibitory avoidance conditioning, an inhibitory avoidance paradigm was developed to include a range of ethologically relevant psychologically (predator exposure, physical restraint) and physically aversive stimuli (electric shock). Adult male Sprague-Dawley rats were conditioned using a step-through inhibitory avoidance model to associate crossing between two compartments with the presentation of an aversive stimulus. Subjects were assessed for conditioned fear measured by crossing latency, freezing behavior and defecation during conditioning and a contextual memory test. Freezing behavior within the conditioning chamber remained constant throughout conditioning regardless of stimulus but all groups conditioned with an aversive stimulus showed significant increases in crossing latency both overtime and during the retention test compared to subjects that received no aversive stimulus after crossing, indicating that inhibitory avoidance conditioning was achieved. Significant increases in defecation were also observed for footshock and predator exposed animals and this effect was intensified by predator exposure, but only after repeated exposures. With this, both predator based and restraint-based variations of the inhibitory avoidance model (PBIA and RBIA, respectively) have been successfully established and have been shown to induce evidence of emotionality similar to those seen in traditional shock-based inhibitory avoidance (SBIA) models. Successful development of PBIA and RBIA expands the range of stimuli that can be used with conventional inhibitory avoidance models, allowing for investigation into topics that have yet to be addressed in inhibitory avoidance conditioning.
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Raybuck, Jonathan Dennis. "SPECIFIC EFFECTS OF NICOTINE AND NICOTINIC ANTAGONISTS ON TRACE AND CONTEXTUAL FEAR CONDITIONING IN C57BL/6 MICE: A ROLE FOR NICOTINIC ACETYLCHOLINERGIC SIGNALING IN THE DORSAL HIPPOCAMPUS, VENTRAL HIPPOCAMPUS, AND MEDIAL PREFRONTAL CORTEX IN TRACE FEAR CONDITIONING." Diss., Temple University Libraries, 2009. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/59884.
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PsychologyPh.D.
Nicotine has been shown to enhance multiple forms of learning and memory. However the substrates through which these effects occur are not well understood. To examine the specific substrates of nicotine's acute effects on trace fear conditioning, I infused nicotine into areas thought to support trace fear conditioning, the dorsal hippocampus, ventral hippocampus and medial prefrontal cortex. Additionally, we investigated the contributions of nicotinic acetylcholinergic signaling to trace fear conditioning by infusing the nicotinic antagonists dihydro-beta-erythroidine (DHbE) and methyllycaconitine (MLA) into these areas. Nicotine had different effects on both trace and contextual fear conditioning depending on dose and brain region, as did the nicotinic antagonists. In the dorsal hippocampus nicotine infusion enhanced both trace and contextual conditioning, although these effects were dissociable by dose and training protocol. Additionally, the high-affinity nicotinic antagonist DHbE produced selective deficits in trace conditioning, suggesting that while enhancement of nicotinic signaling can affect both contextual and trace learning, nicotinic activity in the dorsal hippocampus is critically involved in trace but not contextual conditioning. In the ventral hippocampus nicotine infusion produced deficits in both trace and contextual fear conditioning, without affecting delay conditioning, while the antagonists had no effect. This finding suggests that altered nicotinic signaling in the ventral hippocampus can suppress hippocampus dependent learning. In the mPFC nicotine selectively enhanced trace conditioning though both antagonists also enhanced trace fear conditioning. Unlike in the mPFC or dorsal hippocampus, where nicotine and antagonist induced effects occurred during training, effects in the ventral hippocampus occurred at both training and testing, suggesting that the ventral hippocampus may be able to modulate acquisition as well as expression of hippocampus dependent learning. Additionally, antagonist infusion into the mPFC during testing produced deficits in expression, suggesting that this area can modulate fear expression. Thus, the substrates of nicotinic acetylcholinergic contributions to trace and contextual fear conditioning are diverse. I put forth a multi-component model of these contributions, where trace fear conditioning is supported by dorsal hippocampus dependent maintenance of the CS during the trace interval, long-term storage in the mPFC and ventral hippocampal mediated acquisition and expression.
Temple University--Theses
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Senn, Verena. "Differential activation of anatomically defined neuronal subpopulations in the amygdala during fear conditioning and extinction /." [S.l.] : [s.n.], 2009. http://edoc.unibas.ch/diss/DissB_8782.
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Halonen, Joshua D. "Predator-Based Fear Conditioning: A Novel Approach to the Study of the Neurobiology of Memory." Scholar Commons, 2012. http://scholarcommons.usf.edu/etd/4062.
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This series of experiments developed novel paradigms involving the integration of conventional and ethologically relevant forms of reinforcement in the study of fear conditioning in rats. Experiment 1 compared the effects of foot shock, immobilization and predator exposure, alone and in combination, on the expression of conditioned fear memory and extinction. The combination of all 3 reinforcers produced a significantly stronger fear memory and greater resistance to extinction, compared to when each reinforcer was administered alone. Furthermore, whereas conditioning with foot shock, alone, resulted in rapid extinction of the fear memory, the combination of immobilization and cat exposure, or all 3 reinforcers together, produced a robust extinction resistant fear memory. Experiment 2 explored the effects of giving extinction trials every two versus every seven days. This experiment demonstrated extinction when the trials were given every 2 days, with no evidence of extinction when trials were given every 7 days. Experiment 3 focused on extending predator-based conditioning to enhance the development of cue-based fear conditioning. Rats were administered multiple predator-based conditioning trials in one session to enhance the formation of both contextual and cue-based fear memories. Experiment 4 tested the hypothesis that hippocampal involvement during learning is necessary for predator-based contextual, but not cued, fear memory. This work provided support for this hypothesis with the finding of impaired contextual memory, with no effect on cued memory, in rats that had a pharmacological suppression of hippocampal activity during fear conditioning. Experiment 5 developed an entirely novel form of inhibitory avoidance conditioning. This work demonstrated that rats learned to avoid entering a place which was paired with immobilization and predator exposure. Experiment 6 investigated the effects of sleep deprivation occurring prior to fear conditioning on the expression of fear memory. This experiment showed that pre-training sleep deprivation blocked the development of contextual (hippocampal-dependent), but not cue (hippocampal-independent), fear memory. Overall, this series of experiments established the groundwork to use ethologically relevant stimuli, including predator exposure, in conjunction with conventional reinforcers, such as foot shock and immobilization, to advance our understanding of the neurobiology of emotional memory.
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Pierson, Jamie L. "DORSAL HIPPOCAMPUS INFUSIONS OF CNQX INTO THE DENTATE GYRUS DISRUPT EXPRESSION OF TRACE FEAR CONDITIONING." Miami University / OhioLINK, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=miami1355165370.
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Lueken, U., B. Straube, I. Reinhardt, N. I. Maslowski, H. U. Wittchen, A. Ströhle, A. Wittmann, et al. "Altered top-down and bottom-up processing of fear conditioning in panic disorder with agoraphobia." Cambridge University Press, 2014. https://tud.qucosa.de/id/qucosa%3A39007.
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Background: Although several neurophysiological models have been proposed for panic disorder with agoraphobia (PD/AG), there is limited evidence from functional magnetic resonance imaging (fMRI) studies on key neural networks in PD/AG. Fear conditioning has been proposed to represent a central pathway for the development and maintenance of this disorder; however, its neural substrates remain elusive. The present study aimed to investigate the neural correlates of fear conditioning in PD/AG patients.
Method: The blood oxygen level-dependent (BOLD) response was measured using fMRI during a fear conditioning task. Indicators of differential conditioning, simple conditioning and safety signal processing were investigated in 60 PD/AG patients and 60 matched healthy controls.
Results: Differential conditioning was associated with enhanced activation of the bilateral dorsal inferior frontal gyrus (IFG) whereas simple conditioning and safety signal processing were related to increased midbrain activation in PD/AG patients versus controls. Anxiety sensitivity was associated positively with the magnitude of midbrain activation.
Conclusions: The results suggest changes in top-down and bottom-up processes during fear conditioning in PD/AG that can be interpreted within a neural framework of defensive reactions mediating threat through distal (forebrain) versus proximal (midbrain) brain structures. Evidence is accumulating that this network plays a key role in the aetiopathogenesis of panic disorder.
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Schmeltzer, Sarah N. "The Role of Forebrain Neuropeptide Y in the Regulation and Development of PTSD-like Behaviors." University of Cincinnati / OhioLINK, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1479820132199223.
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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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Ganev, Jennifer. "The Role of the Amygdala and Other Forebrain Structures in the Immediate Fear Arousal Produced by Footshock Exposure." Thesis, University of Canterbury. Psychology, 2007. http://hdl.handle.net/10092/1503.
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When a human or animal is threatened or confronted with a stimuli signalling danger, internal defence mechanisms are activated that evoke feelings of fear and anxiety. These emotional responses promote the behaviour patterns necessary for an organism's survival. Animal research seeks to understand how these emotions affect behaviour both physiologically and neurologically in order to develop effective treatment for those suffering from severe anxiety disorders. The aim of this thesis was to examine the role of the amygdala, and dorsal and ventral hippocampus in relation to immediate fear arousal brought on by footshock. This was assessed by examining whether muscimol would interfere with the acoustic startle response before or after footshock presentation, and then comparing these reactions to a control group that received saline infusions. The results of this research are extremely important because they identify various brain structures involved in the fear-arousing effects of footshock as measured by the shock sensitization of acoustic startle. Laboratory rats received muscimol (0.1ug and 0.01ug) infusions into the basolateral amygdala, dorsal and ventral hippocampus. These three brain regions have been identified as playing a prominent role in fear neurocircuitry. The results demonstrated that the GABA A receptor agonist muscimol in doses of 0.1ug and 0.01ug reliably blocked shock sensitization of the acoustic startle response. The muscimol doses did not alter the shock reactivity amplitudes therefore indicating a normal perception of the fear arousing properties of footshock. Therefore, the present study's results suggest that a decrease of GABA activity in the amygdala, dorsal and ventral hippocampus may be essential for the neuronal basis of fear acquisition and expression of unconditioned and conditioned stimuli.
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Kitamura, Haruka. "Boundary conditions of acquisition and post-retrieval extinction in fear conditioning: Individual differences and methodological factors." Thesis, Queensland University of Technology, 2021. https://eprints.qut.edu.au/207826/2/Haruka%20Kitamura%20Thesis.pdf.
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This thesis examined a range of potential reasons as to why people differ in how well the fear associated with a memory can be reduced. These reasons included the strength of the initial fear memory and individual differences such as the level of female hormones, strength of stress reaction, type of emotion regulation used, optimistic and neurotic personalities, and mood. The thesis revealed that stronger initial fear memories did not prevent the effective treatment of a fearful memory. It was also found that pessimism and hormonal contraception use prevent the effective reduction of the fear associated with memories.
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Coffman, Marika Cerie. "Common and Distinct Neural Mechanisms of Fear Acquisition and Reversal in comorbid Autism with Social Anxiety and Social Anxiety Disorder uncomplicated by Autism." Diss., Virginia Tech, 2019. http://hdl.handle.net/10919/102409.
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Social Anxiety (SAD) increases in prevalence as children enter adolescence. Adolescents with Autism Spectrum Disorder (ASD) are diagnosed with comorbid SAD at higher rates than these individuals are diagnosed with other clinical disorders, including depression and other anxiety disorders. However, there is little research on whether the presentation and neural underpinning of comorbid SAD within the context of ASD is the same as SAD alone. Individual and diagnostic differences exist in neural and biological mechanisms of fear conditioning. Characterization of whether neural mechanisms of fear are different within ASD with comorbid SAD and SAD alone may better inform clinical treatments. Accordingly, the present study characterizes neural responses during a fear-inducing experiment, as measured by fMRI. Fifty-seven adolescents participated in this study, with adolescents with ASD and SAD (n=17), SAD alone (n=20), and typically developing adolescents (n=20). All participants completed two fear conditioning and reversal paradigms while completing an fMRI scan. The paradigm consisted of a Social condition and Nonsocial condition. An ANOVA for fear conditioning was conducted. Results revealed significant activation in the Inferior Temporal Gyrus (ITG) during fear conditioning. No between group differences were observed, but within-group differences indicated differential modulation of the ITG in the ASD with SAD group in the Social condition compared to the Nonsocial condition. The SAD group demonstrated differential activation between conditioning stimuli in the Nonsocial condition, but not in the Social condition. Results indicate that adolescents with ASD and SAD may display different neural mechanisms for acquiring fear compared to typically developing peers. Results have potential to inform treatment approaches.Doctor of Philosophy
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Vurbic, Drina. "Mechanisms of Secondary Extinction." ScholarWorks @ UVM, 2010. http://scholarworks.uvm.edu/graddis/237.
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Pavlov (1927) first reported that following appetitive conditioning of multiple stimuli, extinction of one CS attenuated responding to others which had not undergone direct extinction. Four experiments with rat subjects investigated potential mechanisms of this secondary extinction effect. Experiment 1 assessed whether secondary extinction would be more likely to occur with target CSs that have themselves undergone some prior extinction. Two CSs were initially paired with shock. One CS was subsequently extinguished before the second CS was tested. The target CS was partially extinguished for half the rats and not extinguished CS for the other half. A robust secondary extinction effect was obtained with the non-extinguished target CS. Experiment 2 investigated whether secondary extinction occurs if the target CS is tested outside the context where the first CS is extinguished. Despite the context switch secondary extinction was observed. Extinction of one CS was also found to thwart renewal of suppression to a second CS when it was tested in a neutral context. Experiment 3 examined whether secondary extinction can be attributed to mediated generalization caused by association of the CSs with a common US during conditioning. Rats received conditioning with three CSs and then extinction with one of them. Secondary extinction was observed with a shock-associated CS when the extinguished CS had been associated with either food pellets or shock, suggesting that secondary extinction is not US-specific and is thus not explained by this mediated generalization mechanism. Experiment 4 examined whether intermixing trials with the two stimuli during conditioning is necessary for secondary extinction to occur. Rats were either conditioned with intermixed trials as in Experiments 1-3, or with blocked trials of each CS presented in conditioning sessions separated by a day. Secondary extinction was observed only in the former condition. The results are consistent with the hypothesis that CSs must be associated with a common temporal context for secondary extinction to occur.
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Santos, Teresa P. G. "Tone-evoked Fos labeling in the central auditory pathway : effects of stimulus intensity and auditory fear conditioning." Thesis, Massachusetts Institute of Technology, 2006. http://hdl.handle.net/1721.1/37905.
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Thesis (Ph. D.)--Harvard-MIT Division of Health Sciences and Technology, 2006.Includes bibliographical references.
Understanding intensity coding and auditory learning are basic concerns of research on the auditory central pathway. There is no unifying model of intensity coding but several mechanisms have been proposed to play a role. The first aim of this thesis was to determine the mechanisms of intensity coding in the central auditory pathway from the cochlear nucleus to the auditory cortex. The Fos labeling method was used to assess neuronal activation in the central auditory system. This technique allows one to study large regions of the brain in awake animals. Increasing sound pressure level led to: (1) spreading of labeling towards neurons with higher best frequencies; (2) spread of labeling orthogonal to the tonotopic axis; (3) and increased density of labeling within the tonotopic band. In addition to encoding the physical features of a stimulus, it is fundamental for survival that we learn about the meaning of sounds and put them in a behavioral context. The second aim of this thesis was to study how learning, in particular auditory fear conditioning, changes the pattern of neuronal activation of neurons, as measured with Fos labeling, in the central nervous system. Conditioning led to an increase in Fos labeling in central auditory nuclei.
(cont.) This increase in labeling was similar to the effects of increasing sound intensity. The present results support the idea that auditory fear memories are stored in the auditory pathway.
by Teresa P.G. Santos.
Ph.D.
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Portugal, George Sussman. "Strain-dependent and age-dependent effects of acute, chronic, and withdrawal from chronic nicotine on fear conditioning." Diss., Temple University Libraries, 2010. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/111566.
Full textAbstract:
PsychologyPh.D.
Research in both humans and animals demonstrates that nicotine addiction is a complex disorder that can be influenced by several factors. For instance, individual differences in genetics can impact sensitivity to nicotine and can modulate the severity of nicotine withdrawal. Although nicotine alters cognitive processes such as learning and memory, it remains unknown whether genetic variability modulates the effects of nicotine on these cognitive functions. Thus, the present study characterized the effects of acute, chronic, and withdrawal from chronic nicotine administration on fear conditioning in 8 strains of inbred mice. Furthermore, nicotine withdrawal-related changes in somatic signs and the elevated plus maze were examined because nicotine withdrawal consists of multiple symptoms that can include increased somatic signs and increased anxiety. Strain-dependent effects of acute nicotine and nicotine withdrawal on contextual fear conditioning were observed in several inbred strains. However, the effects of acute nicotine on contextual fear conditioning were not associated with the effects of nicotine withdrawal, suggesting that different genetic substrates may mediate these two effects. Nicotine withdrawal produced few changes in somatic signs and exploration in the elevated plus maze. Overall, these data demonstrate that genetics contribute to variability in the effects of acute nicotine and withdrawal from chronic nicotine treatment on contextual fear conditioning. The identification of genes that may alter the effects of nicotine on cognition may lead to more efficacious treatments for nicotine addiction. The age during which nicotine use begins is a second factor that may influence the severity of nicotine addiction. Pre-adolescence and adolescence are periods of development that have an increased risk for developing addiction to nicotine. Nicotine alters contextual learning, but it remains unknown whether these effects are age-dependent. Therefore, the present study examined the effects of acute, chronic, and withdrawal from chronic nicotine on fear conditioning in pre-adolescent, adolescent, and adult mice. In addition, we investigated whether exposure to chronic nicotine during pre-adolescence or adolescence has long-lasting effects on contextual learning that occurs during adulthood. Pre-adolescent mice were more sensitive to the effects of acute nicotine than adolescents and adults, showed enhanced contextual learning when treated with high doses of chronic nicotine, and were less sensitive than adolescents and adults to nicotine withdrawal-related deficits in contextual learning. In contrast, adolescent mice were less sensitive to the effects of acute nicotine on contextual learning than pre-adolescents and adults and were more sensitive to nicotine withdrawal-related deficits in contextual learning relative to pre-adolescents and adults. Chronic nicotine exposure during pre-adolescence or adolescence also produced long-lasting impairments in contextual learning that were observed during adulthood, whereas adult chronic nicotine exposure had no effect on fear conditioning. Together, these data suggest that pre-adolescent and adolescent nicotine exposure has both short-term and long-term effects on contextual learning that may play an important role in the development and maintenance of nicotine addiction.
Temple University--Theses
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Blechert, Jens. "The psychophysiology of posttraumatic stress disorder and panic disorder : fear conditioning, autonomous underpinnings and issues of measurement /." Basel : [s.n.], 2006. http://edoc.unibas.ch/diss/DissB_7853.
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