Tesis sobre el tema "Conditioned fear"
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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.
Texto completoUrcelay, Gonzalo Pablo. "Potentiation and overshadowing in Pavlovian fear conditioning". Diss., Online access via UMI:, 2008.
Buscar texto completoUgland, Carina C. O. "Resistance to extinction in human fear learning, an ERP investigation of procedural and fear relevance effects on conditioned responding". Thesis, University of Sussex, 2011. http://sro.sussex.ac.uk/id/eprint/6960/.
Texto completoGriffin, William C. "Prenatal stress alters fear-conditioned behaviors and the response to serotonergic drugs". Morgantown, W. Va. : [West Virginia University Libraries], 2001. http://etd.wvu.edu/templates/showETD.cfm?recnum=2171.
Texto completoTitle from document title page. Document formatted into pages; contains xii, 150 p. : ill. Vita. Includes abstract. Includes bibliographical references (p. 131-150).
Tarpley, Jason William. "Molecules, neuronal firing, and circuits for the learning and expression of conditioned fear". Diss., Restricted to subscribing institutions, 2008. http://proquest.umi.com/pqdweb?did=1679374151&sid=1&Fmt=2&clientId=1564&RQT=309&VName=PQD.
Texto completoDiggs, Herman Augustus. "EFFECTS OF ACUTE THC ADMINISTRATION ON EXTINCTION OF CONDITIONED FEAR RESPONSES IN HUMANS". OpenSIUC, 2010. https://opensiuc.lib.siu.edu/theses/305.
Texto completoHolahan, Matthew R. "Memory modulation produced by post-training exposure to an aversive conditioned stimulus". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp03/MQ64370.pdf.
Texto completoDiggs, 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.
Texto completoBarnett, Scott Thomas Charles. "Glutamate receptors in the ventral tegmental area : a potential mechanism involved in long term potentiation : a thesis submitted in partial fulfilment of the requirements of the degree of Masters of Science in Psychology at the University of Canterbury /". Thesis, University of Canterbury. Psychology, 2006. http://hdl.handle.net/10092/1358.
Texto completoMasugi, Miwako. "Metabotropic Glutamate Receptor Subtype 7 Ablation Causes Deficit in Fear Response and Conditioned Taste Aversion". Kyoto University, 1999. http://hdl.handle.net/2433/181694.
Texto completoTaylor, Amanda Lee. "Elucidating the fear - maintaining properties of the Ventral Tegmental Area". Thesis, University of Canterbury. Psychology, 2008. http://hdl.handle.net/10092/2853.
Texto completoLi, Chun-I. "Distinct roles of the medial and central nucleus of the amygdala in unconditioned and conditioned fear". Thesis, University of Hawaii at Manoa, 2003. http://hdl.handle.net/10125/7108.
Texto completovii, 40 leaves
Ludlum, Madonna L. "A Multimodal Investigation of Renewal of Human Avoidance, Perceived Threat, and Emotion". Thesis, University of North Texas, 2015. https://digital.library.unt.edu/ark:/67531/metadc801907/.
Texto completoVurbic, Drina. "Mechanisms of Secondary Extinction". ScholarWorks @ UVM, 2010. http://scholarworks.uvm.edu/graddis/237.
Texto completoWood, Melissa Allison. "A psychological analysis of the effects of memory retrieval prior to extinction on the reacquisition of a conditioned fear association". Thesis, University of Cambridge, 2010. https://www.repository.cam.ac.uk/handle/1810/237034.
Texto completoCourtin, Julien. "Role of cortical parvalbumin interneurons in fear behaviour". Thesis, Bordeaux 2, 2013. http://www.theses.fr/2013BOR22045/document.
Texto completoLearning and memory processes are controlled by specific neuronal circuits and elements. Numerous recent reports highlighted the important role of cortical circuits in the regulation of fear behaviour, however, the anatomical and functional characteristics of their neuronal components remain largely unknown. During my thesis, we used single unit recordings and optogenetic manipulations of specific neuronal elements in behaving mice, to show that both the auditory cortex and the medial prefrontal cortex contain a disinhibitory microcircuit required respectively for the acquisition and the expression of conditioned fear memory. In both cases, parvalbumin-expressing interneurons constitute the central element of the circuit and are phasically inhibited during the presentation of the conditioned tone. From a functional point of view, we demonstrated that this inhibition induced the disinhibition of cortical pyramidal neurons by releasing the ongoing perisomatic inhibition mediated by parvalbumin-expressing interneurons onto pyramidal neurons. Thereby, this disinhibition allows the precise temporal regulation of pyramidal neurons excitability. In particular, we showed that the acquisition of associative fear memories depend on the recruitment of a disinhibitory microcircuit in the auditory cortex. Fear-conditioning-associated disinhibition in auditory cortex is driven by foot-shock-mediated inhibition of parvalbumin-expressing interneurons. Importantly, pharmacological or optogenetic blockade of pyramidal neuron disinhibition abolishes fear learning. Together, these data suggest that disinhibition is an important mechanism underlying learning and information processing in cortical circuits. Secondly, in the medial prefrontal cortex, we demonstrated that expression of fear behaviour is causally related to the phasic inhibition of prefrontal parvalbumin-expressing interneurons. Inhibition of parvalbumin-expressing interneuron activity disinhibits prefrontal pyramidal neurons and synchronizes their firing by resetting local theta oscillations, leading to fear expression. These results identify two complementary neuronal mechanisms both mediated by prefrontal parvalbumin-expressing interneurons that precisely coordinate and enhance the neuronal efficiency of prefrontal pyramidal neurons to drive fear expression. Together these data highlighted the important role played by neuronal disinhibition in fear behaviour by binding behavioural relevant information, selecting specific circuit elements and orchestrating pyramidal neurons activity
Erasmus, Madeleine Monique. "An investigation into the role of noradrenergic receptors in conditioned fear : relevance for posttraumatic stress disorder / Erasmus M.M". Thesis, North-West University, 2011. http://hdl.handle.net/10394/7334.
Texto completoThesis (M.Sc. (Pharmacology))--North-West University, Potchefstroom Campus, 2012.
Dutta, Sohini. "Dissociable Roles of the Nucleus Accumbens Core and Shell Subregions in the Expression and Extinction of Conditioned Fear". Kent State University / OhioLINK, 2021. http://rave.ohiolink.edu/etdc/view?acc_num=kent1618493518479902.
Texto completoYap, Carol Sue Lynn Psychology Faculty of Science UNSW. "An analysis of late-developing learning and memory systems in rats: fear-potentiated startle and context-specific latent inhibition and extinction". Awarded by:University of New South Wales. Psychology, 2006. http://handle.unsw.edu.au/1959.4/24374.
Texto completoBergstrom, Hadley C. "Lateralized dendritic correlates of enhanced conditioned fear retrieval following cessation from chronic nicotine exposure in adolescent and adult rats". Fairfax, VA : George Mason University, 2009. http://hdl.handle.net/1920/4511.
Texto completoVita: p. 118. Thesis director: Robert F. Smith. Submitted in partial fulfillment of the requirements for the degree of Doctor of Philosophy in Psychology. Title from PDF t.p. (viewed June 10, 2009\). Includes bibliographical references (p. 101-117). Also issued in print.
Chaudun, Fabrice. "Involvement of dorsomedial prefrontal projections pathways to the basolateral amygdala and ventrolateral periaqueductal grey matter in conditioned fear expression". Thesis, Bordeaux, 2016. http://www.theses.fr/2016BORD0118/document.
Texto completoA central endeavour of modern neuroscience is to understand the neural basis of learningand how the selection of dedicated circuits modulates experience-dependent changes inbehaviour. Decades of research allowed a global understanding of the computations occurring inhard-wired networks during associative learning, in particular fear behaviour. However, brainfunctions are not only derived from hard-wired circuits, but also depend on modulation of circuitfunction. It is therefore realistic to consider that brain areas contain multiple potential circuitswhich selection is based on environmental context and internal state. Whereas the role of entirebrain areas such as the amygdala (AMG), the dorsal medial prefrontal cortex (dmPFC) or theperiaqueductal grey matter (PAG) in fear behaviour is reasonably well understood at themolecular and synaptic levels, there is a big gap in our knowledge of how fear behaviour iscontrolled at the level of defined circuits within these brain areas. More particularly, whereas thedmPFC densely project to both the basolateral amygdala (BLA) and PAG, the contributions ofthese two projections pathway during fear behaviour are largely unknown. Beside theinvolvement of these neuronal pathways in the transmission of fear related-information, theneuronal mechanisms involved in the encoding of fear behaviour within these pathways are alsovirtually unknown. In this context, the present thesis work had two main objectives. First,evaluate the contribution of the dmPFC-BLA and dmPFC-vlPAG pathways in the regulation offear behaviour, and second, identify the neuronal mechanisms controlling fear expression in thesecircuits. To achieve these goals, we used a combination of single unit and local field potentialrecordings coupled to optogenetic approaches in behaving animals submitted to a discriminativefear conditioning paradigm. Our results first, identified a novel neuronal mechanism of fear expression based on the development of 4 H oscillations within dmPFC-BLA circuits thatdetermine the dynamics of freezing behaviour and allows the long-range synchronization offiring activities to drive fear behaviour. Secondly, our results identified the precise circuitry at thelevel of the dmPFC and vlPAG that causally regulate fear behaviour. Together these data provideimportant insights into the neuronal circuits and mechanisms of fear behaviour. Ultimately thesefindings will eventually lead to a refinement of actual therapeutic strategies for pathological conditions such as anxiety disorders
Reinhardt, Emily K. "The NR2B subunit and differential rearing: the role of the amygdala and hippocampus in the acquisition of Pavlovian conditioned fear". Thesis, Kansas State University, 2015. http://hdl.handle.net/2097/20335.
Texto completoDepartment of Psychological Sciences
Mary Cain
Research has demonstrated that an enriched rearing environment improves learning in many tasks. However, growing evidence suggests that an enriched environment may not provide the same benefits during a fear conditioning paradigm. In fact, it appears that an isolated rearing environment may facilitate acquisition of fear to an aversive stimulus. The neural mechanisms responsible for this disparity in fear learning among differentially reared animals are currently unknown. The NR2B subunit of the NMDA receptor has been shown to be involved in the acquisition of fear and influenced by differential rearing, making it a prime candidate to begin investigating these underlying neural mechanisms. Therefore, this study assessed the expression of the NR2B subunit in brain regions important for the acquisition of fear (amygdala and hippocampus) among differentially reared rats. Rats were reared in an enriched, an isolated, or a standard condition for 30 days. They received four tone-footshock pairings, after which their brains were removed and expression of the NR2B subunit was quantified in the basolateral amygdala (BLA), central nucleus of the amygdala (ACe), and the CA3 region of the hippocampus. Analyses found that the isolated rats began to acquire fear to the aversive stimulus faster than the enriched and standard housed rats. However, the isolated rats showed the least amount of NR2B expression in the BLA while there were no rearing differences in expression within the ACe or the CA3. The results from this study provide further insight to the importance of the rearing environment in learning and memory, especially the learning of fear, and its central neural basis.
Lawless, Caroline. "The Role of Basal Forebrain Cholinergic Projections to the Anterior Cingulate Cortex in Cued and Contextual Fear Conditioned Suppression Paradigms". Thesis, University of Delaware, 2018. http://pqdtopen.proquest.com/#viewpdf?dispub=10744544.
Texto completoBasal forebrain corticopetal cholinergic neurons are critical for contextual and cued fear memory in the conditioned suppression paradigm, but neural mechanisms that alter these neurons in fear memory remain unknown. Interestingly, basal forebrain cholinergic lesions have no effect on behavioral performance in commonly-studied fear conditioning paradigms like Pavlovian conditioned freezing or fear-potentiated startle, yet impair fear memory in the conditioned suppression paradigm. Many studies conducted have experimented with lesions of cell bodies of corticopetal cholinergic neurons in the nucleus basalis magnocellularis (NBM), but there is a void in the literature defining which specific projections may be responsible for their discrepant role in different fear memory paradigms. The basal forebrain projects to the anterior cingulate cortex (ACC), a subregion of the medial prefrontal cortex. The ACC is a well-established portion of the fear circuit across all fear conditioning paradigms and has a clear role in decision-making in the conditioned suppression paradigm. Given the role in choice conflict that the ACC plays in operant tasks involved in the conditioned suppression paradigm, it is plausible that it may be a region that allows basal forebrain cholinergic neurons to alter a fear memory in the conditioned suppression paradigm. The goal of this study is to examine the specific roles that basal forebrain cholinergic projections to the ACC play in fear memory, specifically in the conditioned suppression paradigm. These lesions may target specific cholinergic input to the ACC from the NBM in the basal forebrain and this may isolate a specific fear circuit involved in fear memory in the conditioned suppression paradigm. Data have suggested that ACC lesioned animals demonstrate less fear-conditioned suppression over sham animals, but further experiments and cohorts of animals are required. If ACC cholinergic lesions are shown to produce deficits in fear memory in the conditioned suppression paradigm, it may suggest that the presence of the appetitive task, which only occurs in the conditioned suppression paradigm and not in any of the other commonly studied fear paradigms, may be able to elicit changes in functional connectivity to incorporate this projection from the NBM to the ACC to the fear circuit. Discrepancies in fear memory between fear conditioning paradigms demand to be addressed because assumptions about functional connectivity across different paradigms are assumed to be similar in the literature. If the notion of paradigmdependent functional connectivity presented here is true, deductions about this functional connectivity may only be made in the context of one fear paradigm and may not necessarily be applicable across paradigms. In other words, to say that Pavlovian fear conditioning and fear-potentiated startle are indicative of the broad neurobiology of fear memory would only be looking at a fraction of the reality behind how fear circuitry operates. In order to further the literature to propose holistic circuits, molecular processes and constructs that apply to all fear memory regardless of protocol or paradigm, it is necessary to investigate neural involvement across alternative fear paradigms, like conditioned suppression. This study supports the novel idea that neural circuitry that supports fear can expand with new learning tasks or events and therefore, may be more susceptible to change than previously considered, but future studies are required
BALLESTEROS, CAROLINA IRURITA. "ROLE OF DORSAL AND VENTRAL HIPPOCAMPUS ON CONDITIONED AND UNCONDITIONED FEAR ELICITED BY DORSAL PERIAQUEDUCTAL GREY MATTER ELECTRICAL STIMULATION IN RATS". PONTIFÍCIA UNIVERSIDADE CATÓLICA DO RIO DE JANEIRO, 2012. http://www.maxwell.vrac.puc-rio.br/Busca_etds.php?strSecao=resultado&nrSeq=19918@1.
Texto completoEste estudo investiga o papel do hipocampo no comportamento de defesa condicionado e incondicionado examinando o efeito de lesões eletrolíticas pré-treino no hipocampo dorsal e ventral de ratos expostos a dois tipos de estímulos aversivos: estimulação elétrica da matéria cinzenta periaquedutal dorsal e choque nas patas. A lesão na parte dorsal e ventral diminuiu significativamente o comportamento defensivo condicionado. No comportamento defensivo incondicionado, a lesão ventral alterou significativamente o congelamento pré-fuga e a fuga. Os resultados sugerem um papel específico da parte dorsal e ventral do hipocampo na modulação de defesa através da utilização do modelo animal de ataque de pânico e TAG.
This study investigates the role of the hippocampus in both unconditioned and conditioned defense behavior by examining the effects of pre-training electrolytic lesions to the dorsal and ventral hippocampus in male rats exposed to two types of threat stimuli: electrical stimulation of the DPAG and footshock. Our results indicate that ventral and dorsal lesions significantly attenuated conditioned defensive behavior. During unconditioned trials, ventral hippocampal lesion altered threshold needed for escape and pre-escape freezing. These results suggest a specific role of the ventral and dorsal hippocampus in modulating GAD and panic-attack like behaviors in certain animal model of defense.
Ray, Colleen Andrea. "THE EFFECT OF ENGAGEMENT IN COGNITIVE REAPPRAISAL IN RESPONSE TO PREVIOUSLY CONDITIONED STIMULI ON ONLINE AND LONG-TERM EXPECTANCY RATINGS AND EMOTION INDICES". Diss., The University of Arizona, 2009. http://hdl.handle.net/10150/194432.
Texto completoSissons, Heather T. "Overexpectation and trial massing". Diss., Online access via UMI:, 2008.
Buscar texto completoLaborda, Mario A. "An associative account for the etiology of phobias without recall of original trauma S-R associations, their extinction, and recovery /". Diss., Online access via UMI:, 2009.
Buscar texto completoOrtiz, Vanderhoof Samantha. "The Paradox of Corticosterone Treatment Ameliorating the Effects of Preadolescent Stress into Adulthood: Enhanced Maintenance of Long-Term Associative Memories". Kent State University / OhioLINK, 2021. http://rave.ohiolink.edu/etdc/view?acc_num=kent1624536916105986.
Texto completoStegmann, Yannik [Verfasser], Matthias J. [Gutachter] Wieser, Paul [Gutachter] Pauli, Matthias [Gutachter] Gamer y Erhard [Gutachter] Wischmeyer. "Electrocortical mechanisms of sustained attention during the acquisition and interaction of conditioned fear and anxiety / Yannik Stegmann ; Gutachter: Matthias J. Wieser, Paul Pauli, Matthias Gamer, Erhard Wischmeyer". Würzburg : Universität Würzburg, 2021. http://d-nb.info/1234391511/34.
Texto completoD'Amico, Davide 1983. "Fear memories in TgNTRK3 mice, a model of panic disorder : definition of mechanism and search for new therapeutic targets". Doctoral thesis, Universitat Pompeu Fabra, 2013. http://hdl.handle.net/10803/292366.
Texto completoThe neurotrophin tyrosine kinase receptor type 3 (NTRK3) gene has been proposed to contribute to the pathological phenotype of panic disorder (PAND), an anxiety disorder characterized by perturbed and exaggerated fear. In this thesis we hypothesized that PAND could be related to abnormal associative fear learning processes, underlined by a deregulated functioning of the hippocampus – amygdala – medial prefrontal cortex fear circuit. We addressed this hypothesis, by using the unique validated genetic mouse model of PAND, the TgNTRK3, overexpressing the human NTRK3 gene, encoding for TrkC. We found that overexpression of NTRK3 in mice leads to: i) enhanced and extinction resistant hippocampal-dependent fear memories; ii) an aberrant activation of the fear circuit during learning and storage of fear-related information. The underlying mechanisms are possibly related to hippocampal overexcitability. Our study confirmed the role of the NTRK3 gene on pathological fear memories and suggests potential effective therapeutical strategies targeting the excitatory/ inhibitory system and the NT3-TrkC pathway to block exaggerated fear in PAND.
Dubreucq, Sarah. "Rôle tonique du récepteur CB1 dans les conséquences émotionnelles de l'exercice physique et du stress répété". Thesis, Bordeaux 2, 2011. http://www.theses.fr/2011BOR21889/document.
Texto completoThe endocannabinoid system regulates a plethora of physiological functions. In the central nervoussystem, such a regulation is mainly achieved through the stimulation of CB1 receptors. Thus, these receptors exert a key control over excitatory and inhibitory transmissions, including in brain areas ubserving emotional processes. The data gathered so far have provided evidence for a tonic controlof several dimensions of emotionality (e.g. anxiety, fear) by CB1 receptors, but the role played by these receptors in the emotional consequences of the repeated exposure to positive or to negative stimuli has been poorly addressed. Thus, the aims of this work were to examine the role of CB1 receptors (i) in voluntary exercise (wheel running) performance, and in several emotional effects of(ii) repeated voluntary exercise and (iii) repeated social stress in mice. This task was mainly achievedthrough the use of genetic (constitutive and conditional CB1 receptor mutants) and, albeit to a lowerextent, pharmacological (CB1 receptor antagonists) tools.The aforementioned tools allowed us to assign to CB1 receptors located on ventral tegmental area GABAergic neurons a tonic stimulatory influence on voluntary running performance. Moreover, behavioural experiments led us to conclude that CB1 receptors located on cortical glutamatergic neurons are involved in the anxiety and fear extinction patterns observed in animals given repeatedaccess to exercise. Lastly, a series of studies allowed us to distinguish between the respective impacts of housing enrichment and exercise in the consequences of wheel running on emotional behaviours and hippocampal neurogenesis.A second set of experiments defined the respective roles played by distinct neuronal CB1 receptor populations in the psychoneuroendocrine effects of repeated social stress. Thus, this work presentedevidence for a tonic role exerted by CB1 receptors located on central serotonergic neurones in stresselicited changes in body weight growth and hedonia for sucrose. Besides, CB1 receptors located on cortical glutamatergic neurons or on Sim1-expressing neurons (which are mainly present in the paraventricular hypothalamus) were found to exert major roles in the extinction of cued fear memory in unstressed and/or stressed animals
Vianna, Daniel Machado Luiz. "Organização do sistema neural mesencefálico responsável pela resposta de congelamento". Universidade de São Paulo, 2003. http://www.teses.usp.br/teses/disponiveis/59/59134/tde-25042003-203921/.
Texto completoFreezing to a context previously associated to footshock is attenuated by ventrolateral periaqueductal gray (vlPAG) lesion. Moreover, electrical stimulation or microinfusion of compounds that interfere with GABA neurotransmission in the dorsolateral periaqueductal gray (dlPAG) provoke freezing and escape. The present study examined the possibility of this freezing being the result of an indirect activation of vlPAG through dlPAG stimulation. Rats bearing vlPAG or sham lesions were electrically stimulated at dlPAG sites to have their freezing and escape threshold currents measured. The same animals were also submitted to a contextual fear-conditioning paradigm through footshock to validate our experimental setting. A second group of vlPAG- and sham-lesion rats received infusions of semicarbazide, a GABA-synthesis blocker, in the MCPdl. The results obtained show that vlPAG lesions do attenuate conditioned freezing, but are ineffective against dlPAG-stimulation freezing and escape. The vlPAG is the main PAG target to central nucleus of amygdala projections, while the dlPAG receives afferents primarily from hypothalamic nuclei related to defense. This evidence is coherent with vlPAG mediating responses to potential danger, while dlPAG would be more related to immediate danger.
Oliveira, Amanda Ribeiro de. "Mecanismos dopaminérgicos na aquisição e expressão do medo condicionado: envolvimento de receptores D1 e D2". Universidade de São Paulo, 2006. http://www.teses.usp.br/teses/disponiveis/59/59134/tde-30032006-144132/.
Texto completoThe increase in the startle reflex in the presence of a stimulus that has been previously paired to footshock is taken as an index of fear and named fear potentiated startle (FPS). Freezing behavior, a cessation of all observable movements, except those associated with respiration, has also been used as an index of fear in rats. A growing body of evidence has suggested that dopaminergic mechanisms are implicated in different aspects of affective memory, namely its formation, expression or retrieval. However, the results of studies that have examined how, and through which receptors, dopaminergic mechanisms influence fear have been inconsistent. This work is aimed at examining the involvement of dopaminergic receptors in the acquisition and expression of conditioned fear to ligth-CS. We evaluated the effects of systemic administration of the D1 antagonist, SCH 23390, the D1 agonist, SKF 38393, the D2 antagonist, sulpiride, and the D2 agonist, quinpirole before and after conditioning on FPS and freezing. The motor activity of the animals was also evaluated in an open field test. SCH 23390, SKF 38393, sulpiride and quinpirole, injected before conditioning sessions, did not produce any effect on FPS, but SCH 23390 decreased freezing. Injections of SCH 23390, SKF 38393 and sulpiride before testing session did not produce any effect on FPS or freezing. Quinpirole, injected at doses acting at presynaptic level, caused significant reduction in FPS and freezing, when injected before testing. Drugs action was not due to nonspecific effects since they had no effect in the open field test. Our findings indicate that DA mechanisms are involved in the acquisition and expression of conditioned fear using light-CS. Dopaminergic mechanisms mediated by postsynaptic D1 receptors seem to be involved in the acquisition of conditioned freezing to light-CS, but not in FPS. On the other hand, dopaminergic mechanisms mediated by presynaptic D2 receptors seem to be involved in the expression of conditioned fear to light-CS.
Oliveira, Amanda Ribeiro de. "Envolvimento de receptores dopaminérgicos da área tegmental ventral e do complexo basolateral da amígdala na aquisição e na expressão do medo condicionado". Universidade de São Paulo, 2010. http://www.teses.usp.br/teses/disponiveis/59/59134/tde-18022010-093027/.
Texto completoOLIVEIRA, A.R. Involvement of dopaminergic receptors of ventral tegmental area and basolateral amygdala in the acquisition and expression of conditioned fear. 2010. 93 p. Thesis (Doctoral) Faculdade de Filosofia, Ciências e Letras de Ribeirão Preto, Universidade de São Paulo. The Pavlovian fear conditioning is one of the most used paradigms to study the biological basis of emotion, as well as of learning and memory. Dopamine (DA) is one of the most important neurotransmitters involved in mechanisms underlying states of fear and anxiety. A growing body of evidence supports the hypothesis that excitation of the mesocorticolimbic pathway, originating from DA neurons in the ventral tegmental area (VTA), is particularly sensitive to fear-arousing stimuli. Among the forebrain regions innervated by this pathway, the basolateral amygdala (BLA) is an essential component of the neural circuitry of conditioned fear. The present study explored the involvement of VTA and BLA DA receptors, using DA agonists and antagonists, in the acquisition and expression of conditioned fear to a light conditioned stimulus (CS). None of the drugs used produced significant effects on fear-potentiated startle (FPS) when injected in VTA before conditioning, indicating that VTA DA receptors are not involved in the acquisition of conditioned fear to a light-CS. In contrast, when injected before the test session, intra-VTA quinpirole (D2 agonist) significantly reduced FPS, whereas the other drugs had no effect. Intra-BLA SCH 23390 (D1 antagonist) did not produce significant effects on FPS, indicating that BLA D1 receptors do not appear to be involved in the expression of FPS. On the other hand, intra-BLA sulpiride (D2 antagonist) inhibited FPS produced by light-CS previously paired with footshocks. Also, conditioned fear was associated with increased freezing and DA levels in the BLA, both inhibited by intra-VTA quinpirole. Quinpirole\'s ability to decrease FPS and conditioned freezing may be the result of an action on VTA D2 presynaptic autoreceptors. The activation of those receptors decreases dopamine levels in terminal fields of the mesocorticolimbic pathway. Sulpirides results stress the importance of BLA D2 receptors in the fear-activating effects of the Pavlovian conditioning.
Reimer, Adriano Edgar. "Envolvimento de mecanismos glutamatérgicos da substância cinzenta periaquedutal dorsal e do hipotálamo medial no medo condicionado à luz". Universidade de São Paulo, 2012. http://www.teses.usp.br/teses/disponiveis/59/59134/tde-27112012-140923/.
Texto completoThe dorsal periaqueductal gray matter (dPAG) and the medial hypothalamus (MH) are two brain structures that are involved in the elaboration of aversive states and expression of defensive responses. Electrical stimulation of the dPAG or MH produces a series of behavioral responses that resemble those defensive responses triggered in the presence of a predator. These same behaviors can be elicited with the local microinjection of glutamate agonists into these structures, indicating the involvement of excitatory amino acids in the expression of unconditioned fear responses. Nevertheless, the involvement of these structures in fear conditioning is still unknown. The objective of this study was to evaluate the involvement of glutamatergic mediation of the dPAG and MH nuclei anterior nucleus (AH) and dorsal pre-mammillary nucleus (PMd) in the expression of conditioned fear to the light. Thus, we evaluated the effects of glutamatergic agonists and antagonists (AMPA/Kainate and NMDA) administered into these structures in fear potentiated startle (FPS) and conditioned freezing responses to the light. Male Wistar rats with guide-cannulae implanted in the dPAG, AH or PMd were subjected to aversive conditioning (light+shock pairings). Twenty-four hours later, the animals were injected intra-dPAG, AH or PMd with NMDA or kainic acid (NMDA and AMPA/Kainate agonists, respectively) or AP7 or NBQX (NMDA and AMPA/Kainate antagonists, respectively) and were subjected to the FPS test. The conditioned freezing response was measured in the same session. Potential motor effects were evaluated with the open-field test. The administration of glutamate agonists into the dPAG promoted pro-aversive effects in the FPS and conditioned freezing. NBQX produced no significant effect per se, whereas AP7 only decreased conditioned freezing. Both antagonists blocked the effects of the respective agonist. On the other hand, the administration of glutamatergic agonists and antagonists into AH and PMd, in doses that did not affect motor activity, produced no significant effects on conditioned fear responses. The present results suggest the involvement of mechanisms mediated by excitatory amino acids of the dPAG, but not of the MH, in the expression of conditioned fear responses to light.
Metna-Laurent, Mathilde. "Cell Type-Specific Control of Memory Functions by CB1 Cannabinoid Receptors". Thesis, Bordeaux 2, 2012. http://www.theses.fr/2012BOR21928/document.
Texto completoThe endocannabinoid system is an important regulator of physiological functions. In the brain, this control is mainly exerted through the type-1-cannabinoid (CB1) receptors. CB1 receptors are abundant at excitatory glutamatergic and inhibitory GABAergic neuron terminals where their stimulation inhibits neurotransmitter release. The activity of CB1 receptors on astrocytes has been recently proposed as facilitating excitatory transmission. Through this general control on brain neurotransmission, CB1 receptors mediate distinct forms of synaptic plasticity that are associated with memory processing. Indeed, CB1 receptors control memory functions. In particular, the exogenous stimulation of CB1 receptors impairs working memory. Moreover, the endogenous CB1 receptor signalling ensures the adaptation of learned fear responses. However, the brain mechanisms of this CB1-mediated control of memory functions are poorly characterized. The goals of this research work were to dissect the cellular mechanisms by which CB1 receptors control both working memory and learned fear responses. We used constitutive and conditional mutagenesis in mice to address the roles of CB1 receptors on particular cell types in these functions. We first showed that exogenous cannabinoids, including Δ9-tetrahydocannabinol (THC, the main psychoactive constituent of cannabis), impairs spatial working memory through the stimulation of astroglial CB1 receptors. Cannabinoids also induce a form of in vivo long-term depression in the hippocampus that shares several cellular mechanisms with the cannabinoid-induced working memory impairments. These results suggest that cannabinoids disrupt spatial working memory by altering hippocampal synaptic plasticity through astroglial CB1 receptor stimulation. We then showed that CB1 receptors expressed on GABAergic and glutamatergic neurons oppositely control fear coping strategies in the presence of fear conditioned stimuli. The selective and local re-expression of CB1 receptors in the amygdala of constitutive CB1 mutant mice allowed to precise the involvement of this brain structure in the regulation of conditioned fear responses by CB1 receptors. Altogether, these studies indicate that the endocannabinoid system differentially controls memory functions through its distinct modulation of the activity of specific brain cells. The involvement of astrocytes in the effects of cannabinoids on memory highlights their key roles in cognitive processes and further suggests that astroglial CB1 receptors might play a role in other high order brain functions. Our results also point the importance of performing thorough behavioral analyses in the experimental models of fear adaptation
Figueiredo, Rebeca Machado de. "Diferenças associadas ao ciclo estral na reatividade emocional de ratas a estímulos incondicionados e condicionados de medo". Universidade de São Paulo, 2016. http://www.teses.usp.br/teses/disponiveis/59/59134/tde-07112016-124538/.
Texto completoDysfunctional emotional regulation has been implicated as a potential mechanism underlying anxiety and mood disorders. Changes in hormonal secretion during the different phases of the estrous cycle may underlie changes in emotional reactivity to stressful events in female animals. Previous behavioral studies of sex differences in emotion processing in females have yielded conflicting results. This may be due to the range of different behavioral tests used and difficulties in selecting the best animal models to test for estrous cycle-linked differences in responsiveness. Furthermore, the commonly used behavioral tests were developed in male animals and it may not be appropriate to translate directly the protocols from males to females. In the present study we have attempted to address these problems by using different animal models of anxiety based on tests for unconditioned or conditioned fear. We compared the performance of male rats and female rats at four stages of the estrous cycle defined by differences in vaginal cytology. To test for unconditioned fear, we used two tests: a light switch- off test, in which rats escape to the other compartment of a shuttle-box to turn off an aversive light and recordings of 22 kHz ultrasound vocalizations (USVs) during acute restraint stress. For the conditioned fear paradigm, we used fear potentiated startle in an aversive context and conditioned freezing using an aversive context as the conditioned stimulus. In both tests of conditioned fear there were no gender or estrous cycle-linked differences in emotional reactivity. However, with respect to unconditioned fear, female rats in late diestrus showed greater emotional reactivity expressed as switch-off responses to a light environment and USVs in response to restraint compared to other phases of the cycle. These findings suggest that the hormonal profile during the late diestrous phase may predispose to up-regulated emotional reactivity in rats facing emotional challenges to unconditioned, but not conditioned fear- inducing stimuli.
Reis, Fernando Midea Cuccovia Vasconcelos. "Mediação do medo condicionado contextual por glicocorticóides e mecanismos glutamatérgicos no córtex pré-frontal medial". Universidade de São Paulo, 2015. http://www.teses.usp.br/teses/disponiveis/59/59134/tde-06122015-142707/.
Texto completoChanges in the glutamatergic system and in the functioning of the medial prefrontal cortex (mPFC) have been associated with different psychiatric disorders, including anxiety. It is also recognized that changes in circulating levels of glucocorticoids can induce changes in glutamatergic synapses and circuits and therefore alter the emotional reactivity of animals. Although is known that glucocorticoids can influence the release of glutamate in the mPFC, the interaction between mineralocorticoid receptors (MR) and glucocorticoid receptors (GR) activation and the glutamatergic activity on the expression of conditioned fear response is not yet elucidated. The aims of the present study were to investigate (i) the influence of glucocorticoids on the expression of contextual conditioned fear and its effects in the activity of the mPFC in rats, (ii) the role of MR and GR in the prelimbic cortex (PrL) on expression of conditioned freezing response and (iii) a possible interaction between the effects mediated by the glucocorticoids and the glutamatergic system, via NMDA receptors on the expression of this response. Male Wistar rats were treated with vehicle or metyrapone, a corticosterone synthesis blocker, and exposed to a context previously paired with footshock. The time of contextual fear (freezing behavior) and Fos protein expression in different regions of mPFC were evaluated. The results showed that exposure to the aversive context induced a significant increase in freezing and Fos protein expression in the PrL, in the anterior cingulate cortex, areas 1 and 2 (Cg1 and Cg2), but not in the infralimbic cortex. The administration of metyrapone induced a decrease on the expression of freezing and Fos in PrL, Cg1 and Cg2. Bilateral administration of spironolactone (a MR antagonist) in PrL before the test, decreased conditioned fear response and the pretreatment with RU38486 (a GR antagonist) abolished this effect. The results also showed that the decrease of freezing response induced by intra-PrL corticosterone injections was abolished by prior administration of RU38486, but not by spironolactone, indicating that corticosterone recruits preferentially GR to produce the observed effects. Prior administration of the NMDA receptor antagonist also prevented the effects induced by corticosterone treatment in the PrL, suggesting that part of rapid effects of glucocorticoids on the expression of conditioned fear occurs by an interaction with the glutamatergic system. Additionally, NMDA administration in the PrL prior to the test induced similar effects to corticosterone treatment in this region. Overall, the results suggest that the release of corticosterone during the presentation of a conditioned aversive stimulus influences the mPFC activity so that a change in the balance of the activities mediated by MR and GR through an increase in GR activity interacts with the glutamatergic system by increasing the activity of NMDA receptors influencing the expression of contextual fear conditioning response. It is suggested that the reduction in the expression of conditioned fear observed after local administration of corticosterone in the PrL is also due to changes in the balance between MR and GR towards an increase in the actions mediated by GR, as well as an increase in the release of glutamate and a greater NMDA receptor activity in this region.
Caetano, Kátia Alessandra de Souza. "Envolvimento de mecanismos dopaminérgicos na expressão do medo condicionado contextual em ratos". Universidade de São Paulo, 2012. http://www.teses.usp.br/teses/disponiveis/59/59134/tde-14052012-182651/.
Texto completoIt is well established that experiences that generate fear reactions are practically unforgettable and that aversive conditioning raises several defensive responses such as freezing, which is an index of fear in rodents. Several studies have pointed to the existence of a relationship between changes in dopaminergic neurotransmission and aversive states. However, there are conflicting results in the literature with the use of dopaminergic drugs in different animal models of anxiety. Thus, further investigations should be conducted to evaluate the importance of dopaminergic modulation of aversive states. The aim of the present study was to evaluate the involvement of dopaminergic neurotransmission in the expression of contextual conditioned fear in rats. Initially, we evaluated the effects of intraperitoneal injections of D1 and D2 receptors agonists (SKF 38393 and quinpirole) and antagonists (SCH 23390 and sulpiride) in the expression of contextual conditioned fear by measuring the time of freezing response of the animals. The motor activity was evaluated in the open field test. The results indicate that the D2 receptors, but not D1 receptors, are involved in the expression of contextual conditioned fear, since administration of quinpirole and sulpiride, but not SCH 23390 and SKF 38393, decreased conditioned freezing to the context. There were no changes in motor activity of animals. Based on these results it was hypothesized that quinpirole and sulpiride probably acted on presynaptic and postsynaptic D2 receptors, respectively, leading to a decrease of dopaminergic neurotransmission in both cases. To test this hypothesis, microinjections of quinpirole were performed into the ventral tegmental area (VTA). The results show a decrease in the expression of conditioned freezing, indicating that the effects obtained with the intraperitoneal administration of the dopamine D2 receptor agonist is probably due to its action in the VTA. Therefore, dopaminergic mechanisms in the VTA seem to be important in the modulation of conditioned fear responses and activation of this structure appears to take place during the fear memory following the context aversive conditioning.
Ferreira, Renata. "A expressão do medo condicionado em ratos com fenótipos de baixa e alta reatividade emocional: modulação serotoninérgica cortical e subcortical sobre as diferenças de gênero". Universidade de São Paulo, 2014. http://www.teses.usp.br/teses/disponiveis/59/59134/tde-05092014-110344/.
Texto completoExtensive data in the literature have signaled the importance of serotonin (5-HT) on the modulation of fear and anxiety-like behaviors in rodents. In the present study, we have analyzed the influence of peripheral and central 5-HT neurotransmission on the expression of the conditioned and unconditioned fear, and on the fear-potentiated startle in male and female rats previously selected as low- (LA) or high-anxiety (HA). For this purpose, we used the fear-potentiated startle (FPS) test. The global and central influence of 5-HT was evaluated by using the acute systemic or intraventricular administration of the irreversible tryptophan hydroxylase inhibitor PCPA (p-chlorophenylalanine - 200 mg/mL i.p., or 200 µg/5 µL i.v.). Local effects were evaluated through local infusions of 5-HT itself (10 nmol/0.2 µL) or the selective 5-HT1A receptors agonist 8-hydroxy-2-(di-n-propylamino)-tetralin (8-OH-DPAT 0.3 µg/0.2 µL) in the prelimbic cortex (PrL), basolateral amygdala (BLA) or the dorsal periaqueductal gray (DPAG). These brain regions were chosen for the present study based on their great importance in the modulation and expression of conditioned and unconditioned fear. Dependent variables recorded were the amplitude and latency of unconditioned and conditioned fear, and fear-potentiated startle (FPS).
Saunier, Gaëlle. "Etude expérimentale du fractionnement isotopique du fer aux conditions hydrothermales". Phd thesis, Université Paul Sabatier - Toulouse III, 2011. http://tel.archives-ouvertes.fr/tel-00572866.
Texto completoHurst, Vicky Louise. "Can Rachman's indirect pathways be used to counter-condition fear? : the effect of positive verbal information and modelling a non-anxious response on fear beliefs and behavioural avoidance in children". Thesis, University of East Anglia, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.442542.
Texto completoAngelhuber, Martin. "The neural circuitry of fear conditioning : a theoretical account". Thesis, Strasbourg, 2016. http://www.theses.fr/2016STRAJ082/document.
Texto completoFear 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
Green-Armytage, Miriam. "Are disgust, contamination fear and health anxiety associated with desire to avoid contact with people with facial dermatological conditions?" Thesis, University of Surrey, 2016. http://epubs.surrey.ac.uk/812229/.
Texto completoCodina, Olivier. "De fer et de laine : économie et société des vallées andorranes de 1575 à 1875". Perpignan, 2003. http://books.openedition.org/pupvd/31042.
Texto completoFrom the end of the XVI century until the XIX century the different transformations suffered by the Principality of Andorra, modified the structure of the society. The detailed analysis of the several evolutions affecting the land market, sheep cattle, trade, mule trade and the iron and steel works, highlighted an extensive system open to the outside and swiftly adapted to the circumstances. The multiple sources that have been used provide a sharp sight leading from the private to the political sphere. The development of the pastoral companies, followed by the forge repercuted on the increase of the market wages. The growing influence of the families controlling these economic sectors was combined with a progressive hoard of the collective resources, of arising their prominent position acquired within the different councils. From integration to exclusion, this evolution carried out a major inner crisis at the same time that the glance of neighbouring countries of the Principality was modified. In the "nation-state" century, Andorra had become anachronistic and consequently, the existence of the Principality was questioned
Matsuzaki, Tadanobu. "Hes1 expression in mature neurons in the adult mouse brain is required for normal behaviors". Kyoto University, 2020. http://hdl.handle.net/2433/253154.
Texto completoSkidmore, Monique. "Flying through a skyful of lies : survival strategies and the politics of fear in urban Myanmar (Burma)". Thesis, McGill University, 1999. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=35670.
Texto completoAn important culturally constructed strategy of survival in Myanmar entails the detaching of agency from the body while the mind "flies" to freedom. This strategy has a long history not only in Burmese, but also in other Southeast Asian histories, myths, and legends. Just as Burmese wizards fly to a mythical landscape in the foothills of the Himalayas when released from their physical bodies, so too do heroin addicts, prostitutes, psychiatric patients, and the urban poor flee to Burmese fantasylands to escape the domination of the military regime. This strategy, one of many adopted by urban residents, denies the State the final prize it so desperately craves: the willing participation of Burmans in a military society, the complete internalization of totalitarian ideology such that no other ideologies can exist and no space is left for their creation and negotiation. In the conclusion I argue that the regime is aware that it has faded in this task.
I also examine the possibility that the existence of multiple Burmese worlds or realities, in conjunction with a strong belief in the miraculous may offer new ground for research into the trauma of survivors of violence and terror. The construction of madness, death, and reanimation in Burmese culture, grounds particular survival strategies in logical, hopeful, and perhaps curative, rationalities.
Schusler, Ralph Willard Jr. "Depictions of Fear in Lev Tolstoy's Sevastopol Sketches and Stephen Crane's The Red Badge of Courage". FIU Digital Commons, 2017. http://digitalcommons.fiu.edu/etd/3180.
Texto completoRamey, Guillemette. "L' hepcidine, l'hormone du fer : activité et mode de régulation en conditions physiopathologiques". Paris 5, 2009. http://www.theses.fr/2009PA05T012.
Texto completoThe laboratory which welcomed me in thesis identified the regulator of the iron homeostasis, hepcidin. The production of hepcidin is modulated according to the iron demands of the body : in the presence of iron, the synthesis of hepcidin is increased to avoid the excess of the metal which is toxic, and, on the contrary, hepcidin is decreased to allow an effective mobilization of the metal. I participated in the characterization of the phenotype of mouse KO HEPC1 which present a multivisceral iron overload with a particularly important hepatic and pancreatic accumulation of iron. In this murin model, I tried to establish the link between the iron metabolism and the glucose metabolism. I studied the mechanisms of physiopathological regulation of the hepcidin by the iron in a system of primary culture of hepatocytes. This system of culture of hepatocytes allowed me to study ferroportin, the iron excarrier and the mechanisms of mobilization of the iron of the hepatocyte
Mengou, Nguema Samuel. "L'impact du chemin de fer transgabonais sur l'aménagement et les modifications de l'environnement de Booue (Gabon)". Montpellier 3, 1988. http://www.theses.fr/1988MON30031.
Texto completoThe transgabonese is a railway which has benefited from the modern techology, but its total cost is excessively stiff. It is a railway infrastructure which will be useful for the evacuation towards libreville-owendo port of ore abstracted from franceville area, also for the evaluation of the forst working production from the crossed areas, till then without reliable roads and insufficiently peopled. So it is desirable that the gabonese state showld put a presmium on a supervised immigation policy of the africain rural workers alongside the railway particularly in the environs of the fat booue in forest farming. Those rew farmers will alsabe able to contribute to the agriculture development, for it is obvious that the gabonese development goes by the development of its agriculture which only can assure the alimony self sufficiency of the state in the transgabonese geographical context