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1
Li, 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.
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Pre-clinical and clinical data suggest that the amygdala plays a role in the detection of emotional events and in the production of fear responses. The amygdala is composed of distinct nuclei that may serve different functional roles in the modulation of fear. The present study examined the roles of the medial (MeA) and central (CeA) nucleus of the amygdala in unconditioned and conditioned fear. Following bilateral ibotenic acid lesions of the MeA or CeA, rats were exposed to cat odor, an unconditioned fear stimulus. In comparison with sham-operated controls, rats with MeA lesions exhibited significant deficits in cat odor-induced unconditioned fear as indicated by a significant reduction in the duration of freezing and avoidance and an increase in the frequency of contact with the cat odor stimulus. In contrast, excitotoxic lesions of the CeA had no significant effects on cat odor-induced unconditioned fear. To examine the role of the MeA and CeA in conditioned fear, rats with similar fiber-sparing lesions of the MeA and CeA were exposed to foot-shock. Conditioned freezing was measured in the immediate post-shock period and a retention test administered after 24-h. Results indicated that MeA lesions had no reliable effects on contextual fear conditioning as indicated by no significant differences in freezing between lesion and control groups in the immediate post-shock period and in the retention test. In contrast, CeA lesions produced significant deficits in freezing occurring in the post-Shock interval and in the retention test. Together, these results suggest that the MeA, but not the CeA, plays a role in the mediation of predator odor-induced unconditioned fear. In contrast, the CeA, but not the MeA, appears to playa role in fear conditioning to a context paired with electric foot-shock.<br>vii, 40 leaves
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Barnett, 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.
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In the present study, footshock, which produces a powerful aversive emotional response was used in a Pavlovian conditioning experiment as an unconditioned stimulis (UCS), and was paired with the presentation of a light used as a conditioned stimulis (CS). There is an accumulation of evidence that supports the assertion that dopaminergic (DA) neurons within the ventral tegmental area (VTA) are active in processes that contribute to the amygdala-based circuitry involved in regulating emotionally salient responses. To build upon findings implicating VTA DA, excitatory glutamate (Glu), NMDA and AMPA receptors, were examined with respect to their role in Pavlovian conditioned fear responding. Fear potentiated startle (FPS) was used to assess the effects of intra-VTA infused AP5, and intra-VTA infused CNQX on conditioned fear responding in laboratory rats. The administration of the NMDA receptor antagonist AP5 (at 1.0, 2.5, and 5.0ug doses), blocked the ability of a conditioned stimulus (CS) previously paired with footshock to become conditioned to the UCS. Similarly, administration of the AMPA receptor antagonist CNQX (at 1.0, 2.5, 5.0ug doses), inhibited the ability of the CS to become conditioned to the UCS. The results of this study indicate the VTA is an important site for synaptic modifications associated with fear learning, and that activation of excitatory Glutamatergic receptors in the VTA play a necessary part of the processing underlying fear conditioning. Measures of shock reactivity demonstrated that the infusion of AP5 and CNQX into the VTA did not inhibit baseline startle amplitudes. The administration of AP5 and CNQX did not suppress the perception of footshock as an aversive stimulus. This study provides further definition to established knowledge surrounding the neural processes whereby neutral environmental cues gain negative emotional salience as occurs in fear conditioning. It was hypothesised that the action of excitatory glutamatergic transmission within the VTA acts on NMDA and AMPA receptors is to assist in the acquisition of Pavlovian conditioned fear, possibly through the same synaptic mechanisms that govern LTP.
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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.
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PONTIFÍCIA UNIVERSIDADE CATÓLICA DO RIO DE JANEIRO<br>Este 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.<br>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.
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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/.
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O desequilíbrio da homeostase emocional tem sido considerado como um mecanismo subjacente aos transtornos de ansiedade e humor. Em fêmeas, as alterações na secreção hormonal durante as diferentes fases do ciclo estral podem ser a base das alterações na reatividade emocional a eventos estressantes. Estudos comportamentais sobre diferenças sexuais no processamento das emoções mostram resultados conflitantes em fêmeas devido às dificuldades na seleção dos melhores modelos animais para testar as diferenças associadas ao ciclo estral. Uma vez que os testes comportamentais foram desenvolvidos em animais do sexo masculino, eles podem não ser apropriados para fêmeas. O presente estudo foi desenvolvido para contribuir nessa linha de pesquisa usando diferentes modelos de animais de medo incondicionado e condicionado, considerando as diferentes fases do ciclo estral das ratas. Comparou-se o desempenho de machos e fêmeas nas quatro fases do ciclo estral em dois testes de medo incondicionado: o switch-off, em que ratos cruzam uma caixa vai-e-vem para desligar uma luz aversiva, e o registro de vocalizações ultrassônicas (VUSs) a 22 kHz emitidos por animais sob o estresse agudo de restrição. Nos testes de medo condicionado, registrou-se o sobressalto potencializado pelo medo e a resposta decongelamento a um contexto aversivo. Em ambos os testes de medo condicionado, a reatividade emocional não se mostrou diferente entre os sexos. No entanto, no que diz respeito ao medo incondicionado, ratas em diestro tardio apresentaram maior reatividade emocional em desligar a luz intensa e maior emissão de VUSs em resposta à restrição em relação a outras fases do ciclo. Estes achados sugerem que o perfil hormonal durante a fase do diestro 2 pode aumentar a reatividade emocional de ratas frente a estímulos inatos, porém não àqueles aprendidos.<br>Dysfunctional 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.
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Burns, Melissa Leah. "Effects of conditioned, unconditioned, and contextual stimuli on the direction of conditioned responding /." Digital version accessible at:, 1999. http://wwwlib.umi.com/cr/utexas/main.
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Vargo, Kristina K. "An Evaluation of Resistance to Change with Unconditioned and Conditioned Reinforcers." OpenSIUC, 2013. https://opensiuc.lib.siu.edu/dissertations/746.
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Several variables have been shown to influence resistance to change including rate, magnitude, and delay to reinforcement (Nevin, 1974). One variable that has not been studied with humans concerns the evaluation of resistance to change with unconditioned and conditioned reinforcers. In Experiment 1 (Resistance to Extinction Assessment), 5 participants' behaviors were reinforced during a baseline phase on a mult VI 30 s VI 30 s schedule with either a conditioned (i.e., token) or unconditioned reinforcer (i.e., food). Following equal reinforcement rates across components, extinction was introduced as a disruptor. All participants showed greater resistance to extinction in the component associated with conditioned reinforcers than unconditioned reinforcers. In Experiment 2 (Varied Distractors Assessment), 4 participants experienced a baseline phase the same as Experiment 1 (i.e., mult VI 30 s VI 30 s). Each participant was then exposed to prefeeding and distraction as disruptors in separate analyses. Results showed that behaviors were more resistant to distraction with conditioned than unconditioned reinforcers, similar to Experiment 1. However, when prefeeding disrupted responding, greater resistance to change was observed with unconditioned reinforcers than conditioned reinforcers. Implications of the results are discussed.
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Lee, Jennifer Elizabeth. "Comparison of Auditory Thresholds Obtained with a Conditioned and an Unconditioned Response." University of Toledo / OhioLINK, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=toledo1325738685.
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Davison, Ian. "The effects of temporal relationships on the associability of both conditioned and unconditioned stimuli." Thesis, University of St Andrews, 1988. http://hdl.handle.net/10023/15083.
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Several models of animal associative learning are described. The evidence for the concept of associability is reviewed. The review contains a detailed account of blocking, including the Mackintosh, Bygrave and Picton (1977) experiment. It is shown that the two major associability models need to be modified, mathematically, to simulate the results of this experiment. A general, simple framework for investigating putative associability changes is suggested. A review of stimulus pre-exposure effects is put into this framework, and indicates a suitable direction for research. The experiments looked for associability changes of both conditioned and unconditioned stimuli. Sometimes the stimulus was a predictor of subsequent events; if not, it was predicted by another stimulus. A variety of procedures was employed. Experiments 1, 2, and 3 tried to replicate and extend previous work with a conditioned stimulus predicting subsequent events, but they were unsuccessful. Experiments 4, 5, 6, 7, and 8 investigated whether conditioned and unconditioned stimuli would change in associability when they were well predicted. Unfortunately, the data were difficult to interpret. An appetitive-aversive transfer paradigm was used in Experiments 9, 10, and 11; there was some evidence that a tone could change in associability, both when it was acting as a predictor, and when it was being predicted. Alternative Interpretations were also discussed. In Experiments 12 and 13, a shock was used to predict the occurrence of food; and there was no evidence that the associability of the shock could be increased in this way.
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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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Duke, Marcus Alan. "The effects of kappa opioid and dopamine agonists on unconditioned behaviors and fos immunoreactivity in preweanling and adult rats." CSUSB ScholarWorks, 1996. https://scholarworks.lib.csusb.edu/etd-project/1209.
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Griffin, 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.
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Thesis (Ph. D.)--West Virginia University, 2001.<br>Title from document title page. Document formatted into pages; contains xii, 150 p. : ill. Vita. Includes abstract. Includes bibliographical references (p. 131-150).
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Urcelay, Gonzalo Pablo. "Potentiation and overshadowing in Pavlovian fear conditioning." Diss., Online access via UMI:, 2008.
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Ugland, 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/.
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In human fear conditioning 'resistance to extinction' occurs when the removal of the aversive outcome fails to produce a reduction in conditioned responding. This phenomenon is important to understanding the persistence of anxiety disorders such as phobias. The research presented in this thesis examines factors that promote the acquisition and maintenance of learned fear response and attempts to differentiate between different explanations of the resistance to extinction phenomenon. To investigate the impact of different conditioning procedures (evaluative or classical conditioning) on the durability of the conditioned response (CR), event-related potential (ERP) methodology was employed. In addition, the role of the fear-relevance of the conditioned stimulus (CS), in supporting the acquisition and resistance to extinction of the CR, was explored. Evidence suggested that extinction effects are likely to reflect procedural differences in conditioning rather than different underlying learning processes. Extinction effects were dissociable across procedures, supporting the role of the type of unconditioned stimulus (US) in explaining past demonstrations of extinction when responses were indexed by physiological measures. Verbally transmitted, threat information heightened aversive US-expectancies and fear beliefs without the need for conditioning. Additionally, fear-beliefs were reduced without the need for extinction training when positive information was provided. Contrary to Davey's (1997) expectancy bias model, the results do not support the hypothesis that verbal information interacts with direct contingency experience to create fear responses; instead, information appears to be a direct pathway to fear. ERP measures for fear responses did not echo the effects of verbal information and contingency on fear-beliefs. However, the comparability of our ERP data, to other research using physiological measures of response, is discussed regarding the number of trials required to calculate the average ERP response. Due to averaging over a large number of trials the ERP measure may not be sensitive to fluctuations in response that may be dependent on information or contingency manipulations. In conclusion our data suggests the importance of verbal information as a pathway to fear and the role of cognitive factors in the prevention and treatment of fears.
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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.
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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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Holahan, 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.
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de, Groot Marleen H. M. "Classical conditioning of the circadian system of rodents, effects of conditioned and unconditioned stimuli on behaviour and immediate-early gene expression." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp03/MQ36428.pdf.
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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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Lorenz, Kristina, Pia Nicolaides, and Kristina Lorenz. "Hud konduktans Rädslobetingning och Psykopatiska Personlighetsdrag En Tvilling studie." Thesis, Örebro universitet, Institutionen för juridik, psykologi och socialt arbete, 2014. http://urn.kb.se/resolve?urn=urn:nbn:se:oru:diva-42722.
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Tidigare studier har visat på sambandet mellan oräddhet, psykopati, aggressivitet och antisocialt beteende. Denna studie undersökte fenotypiska och genetiska relationer mellan komponenter i the skin conductance fear conditioning task och i psykopatiska personlighetsdrag. Data hämtades från den longitudinella studien; Tvillingstudie om riskfaktorer för antisocialt beteende (RFAB) vid University of Southern California och data från pågående tillfälle 5 inkluderades i studien. Resultatet visade på betydelsen av både genetiska och icke-gemensamma miljö influenser förklarade variansen i obetingad respons. I överensstämmelse med tidigare forskning visade resultaten att individer som visade på högre nivåer av manipulativt och svekfullt beteende också uppvisade större brister i rädslobetingelser.<br>Previous studies have shown a relationship among fearlessness, psychopathy, aggression and antisocial behavior. This study examined the phenotypic and genetic relationships among components of the skin conductance fear conditioning task and psychopathic personality traits. Data were retrieved from a longitudinal study; the Twin Study of Risk Factor for Antisocial Behavior at the University of Southern California. The present study included data from the ongoing Wave 5. Results indicated the importance of both genetic and non-shared environmental influences in explaining the variance in the unconditioned response. Consistent with previous research, the results showed that individuals who displayed higher levels of manipulative and deceitful traits also showed deficits in fear conditioning.
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Masugi, 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.
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Horsley, Rachel. "Stimulus salience and dopamine : effects of systemic amphetamine and electrolytic lesions of the nucleus accumbens on conditioned and unconditioned behaviour in the rat." Thesis, University of Nottingham, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.431256.
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Taylor, Amanda Lee. "Elucidating the fear - maintaining properties of the Ventral Tegmental Area." Thesis, University of Canterbury. Psychology, 2008. http://hdl.handle.net/10092/2853.
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The ventral tegmental area (VTA) and its dopaminergic (DA) mesocorticolimbic projections are thought to be essential in the brain’s reward neurocircuitry. In humans and animal experimental subjects, mild electrical VTA stimulation increases dopamine levels and can induce euphoria. Paradoxically, aversive stimuli activate VTA neurons and forebrain DA activity, and excessive electrical stimulation of the VTA exaggerates fearfulness. Research suggests that experimental manipulation of either the amygdala or the VTA has similar effects on the acquisition and expression of Pavlovian conditioned fear. Recently it was demonstrated that electrical stimulation of the amygdala produced fear extinction deficits in rats. Fear extinction involves the progressive dissipation of conditioned fear responses by repeated non-reinforced exposure to a conditioned stimulus (CS). Maladaptive states of fear in fear-related anxiety disorders, such as post-traumatic stress disorders (PTSD) or specific phobias are thought to reflect fear extinction learning deficits. The primary purpose of the present study was to examine the effects of intra-VTA stimulation on fear extinction learning. Using fear-potentiated startle as a behavioural index of conditioned fear, it was found that 120 VTA stimulations paired or unpaired with non-reinforced CS presentations impaired the extinction of conditioned fear. This effect was not apparent in rats that received electrical stimulation of the substantia nigra (SN), suggesting that not all midbrain regions respond similarly. Electrical stimulation parameters did not have aversive affects because rats failed to show fear conditioning when electrical VTA stimulation was used as the unconditioned stimulus. Also, VTA stimulation did not alter conditioned fear expression in non-extinguished animals. Based on the results it is suggested that VTA activation disinhibited conditioned fear responding. Therefore, VTA neuronal excitation by aversive stimuli may play a role in fear-related anxiety disorders thought to reflect extinction learning deficits.
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Tanabe, Juichiro. "Buddhist philosophy and the epistemological foundations of conflict resolution." Thesis, University of Bradford, 2010. http://hdl.handle.net/10454/4910.
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The aim of this research is to expand the framework of contemporary conflict resolution by constructing a complementary relationship between Western epistemologies and a Buddhist epistemology. Despite its evolution and development through self-reflexivity and self-critique, contemporary conflict resolution established upon Western epistemologies has confined the understanding of human mind to social/cultural orientations and left a comprehensive and qualitative analysis of the potential of individual human mind underdeveloped. Buddhist epistemology, the central theme of which is to address human suffering that is mainly psychological and subjective, makes a critical analysis of human subjectivity in terms of how it can be become a root cause of suffering including conflict and how it can be addressed by gaining an insight into the social/cultural construction of human subjectivity. The argument of the thesis is that when a socially/culturally-oriented view of human mind and a deeper and more profound view of human mind are combined together, we can engage in a qualitatively richer and deeper analysis of the psychological and subjective dynamics of conflict resolution.
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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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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/.
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Many people who receive exposure-based treatments for anxiety disorders exhibit a return of fear and avoidance which is often referred to as renewal or relapse. Human and nonhuman research on fear conditioning and renewal has been instrumental in helping understand relapse in anxiety disorders. The purpose of this investigation was to examine renewal of human avoidance and assess whether avoidance may aid in sustaining renewal of fear responses. We adopted a multimodal measurement approach consisting of an approach-avoidance task along with ratings of perceived threat and fear and measures of skin-conductance, a widely used physiological measure of fear. A traditional, single-subject research design was used with six healthy adults. All tasks employed a discrete trial procedure. Experimental conditions included Pavlovian fear conditioning in which increased probability of money loss was paired with a “threat” meter in Context A and later followed extinction in Context B. Fear and avoidance increased to higher threat levels in Context A but not Context B. Renewal testing involved presenting the threat meter on a return to Context A to determine if it evoked fear and avoidance (i.e., relapse). As predicted, renewal testing in Context A showed that increased threat was associated with increased avoidance, ratings of perceived threat and fear, and higher skin-conductance. Moreover, results showed that renewal maintained over six blocks of trials. This is the first investigation of renewal of threat and avoidance in humans that highlights avoidance as a mechanism that may contribute to maintaining fear in anxiety pathology.
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Wood, 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.
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The successful reduction of fear is the aim of clinicians treating people with anxiety disorders such as post-traumatic stress disorder or phobias. Existing treatments for these conditions, however, require many treatment sessions and are prone to relapse. A new technique, first demonstrated in rats by Monfils, Cowansage, Klann, & LeDoux (2009) and later shown to be effective in humans (Schiller et al., 2010), provides a method of efficiently reducing fear in a manner which is resistant to various known triggers of relapse. This procedure involves a single presentation of the fear-inducing stimulus one hour prior to extinction training. This procedure produces extinction learning that is resistant to the return of fear resulting from a change of context, the passage of time, exposure to the unconditioned stimulus, and even further conditioning of the stimulus with an aversive stimulus. This dissertation focuses on one particular property of this procedure: that a stimulus extinguished using this procedure is resistant to subsequent retraining of the fear association. The first four experiments presented here are aimed at replicating this phenomenon and determining whether prediction error at retrieval is necessary for the effect to occur. Following on from these studies, the next chapter presents three experiments which investigate whether trial spacing effects could explain the enhanced extinction and highlights conditions under which the effect is weakened, or possibly reversed. The next three experiments compare the properties of a stimulus extinguished under these conditions with a stimulus extinguished under normal conditions. These studies focus on explanations involving inhibition, inattention and the disruption of stimulus representations. In the final three experiments, the possibility of reversing the effect is investigated. These studies look at the effect of memory retrieval prior to retraining of the stimulus to determine the conditions under which the stimulus can again come to elicit a fear response.
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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.
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Posttraumatic stress disorder is a debilitating anxiety disorder that can develop in
the aftermath of a traumatic or life–threatening event involving extreme horror,
intense fear or bodily harm. The disorder is typified by a symptom triad consisting
of re–experiencing, hyperarousal and avoidance symptoms. Approximately 15–25%
of trauma–exposed individuals go on to develop PTSD, depending on the nature
and severity of the trauma. Although dysfunctional adaptive responses exist in
multiple neurobiological pathways in the disorder, e.g. glutamate, GABA,
glucocortocoids and serotonin, the noradrenergic system is particularly prominent
and represents an important pharmacological target in attempts at preventing the
development of PTSD posttrauma. However, current literature shows opposing and
conflicting results regarding the effect of selective noradrenergic agents in memory
processing, and the effect of modulation of selective noradrenergic receptors are
spread over diverse protocols and paradigms of learning and fear also employing
different strains of animals.
Fear conditioning is a behavioural paradigm that uses associative learning to study
the neural mechanisms underlying learning, memory and fear. It is useful in
investigating the underpinnings of disorders associated with maladaptive fear
responses. Performing fear conditioning experiments with the aim of applying it to
an animal model of PTSD, and relating these behavioural responses to a defined
neural mechanism, will assist both in the elucidation of the underlying pathology of
the disease, as well as the development of more effective treatment. This project
has set about to re–examine the diverse and complex role of noradrenergic
receptors in the conditioned fear response with relevance to PTSD. To the best of
my knowledge, this study represents the first attempt at studying a range of
noradrenergic compounds with diverse actions and their ability to modify
conditioned fear in a single animal model. This work thus introduces greater
consistency and comparative relevance not currently available in the literature, and
will also provide much needed pre–clinical evidence in support of treatment
strategies targeting the noradrenergic system in the prevention of PTSD
posttrauma.
The first objective of this study was to set up and validate a passive avoidance fear
conditioning protocol under our laboratory conditions using the Gemini
Avoidance System. The noradrenergic system plays a prominent role in memory
consolidation and fear conditioning, while administration of –adrenergic blockers,
such as propranolol, have been shown to abolish learning and fear conditioning in
both humans and animals. Propranolol has also demonstrated clinical value in
preventing the progression of acute traumatic stress syndrome immediately
posttrauma to full–blown PTSD. To confer predictive validity to our model, the
centrally active –adrenergic antagonist, propranolol, and the non–centrally acting –adrenergic antagonist, nadolol, were administered to Wistar rats after passive
avoidance fear conditioning training in the Gemini Avoidance System. Wistar rats
were used because of their recognised enhanced sensitivity to stress. Evidence
from this pilot study confirmed that propranolol 10 mg/kg significantly inhibits the
consolidation of learned fear in rats, whereas nadolol is ineffective. This effectively
validated our protocol and the apparatus for further application in this study and
also confirmed the importance of a central mechanism of action for –adrenoceptor
blockade in the possible application of these drugs in preventing the development
of PTSD posttrauma.
The second objective of this study was to investigate the role of 1–, 2–, 1–, and 2–receptors in a conditioned fear passive avoidance paradigm. This was done in
order to investigate how selective pharmacological modulation of these receptors
may modify the conditioned fear response, and whether any of these receptor
systems might exert opposing effects in passive fear conditioning. Various centrally
active noradrenergic agents were employed over a 3–tiered dose response design,
including the 1–antagonist, prazosin, the 2–agonist, guanfacine, the 2–antagonist,
yohimbine, the 1–antagonist, betaxolol and the 2–antagonist ICI 118551. The
effect of post–exposure administration of these drugs on conditioned fear was
compared to that of propranolol 10 mg/kg. Selected doses of betaxolol (10 mg/kg)
and ICI 118551 (1 mg/kg) attenuated fear conditioning to an extent comparable to
propranolol, as did prazosin (0.1 mg/kg). Yohimbine tended to boster fear learning
at all doses tested, albeit not significantly, while guanfacine did not produce any
significant effect on memory retention at any of the doses studied. This latter
observation was surprising since yohimbine tended to bolster fear conditioning
while earlier studies indicate that 2–agonism impairs conditioned fear.
Concluding, this study has conferred validity to our passive avoidance model and
has provided greater insight into the separate roles of noradrenergic receptors in
contextual conditioned fear learning. The study has provided supportive evidence
for a key role for both 1– and 2–antagonism, as well as 1–antagonism, in
inhibiting fear memory consolidation and hence as viable secondary treatment
options to prevent the development of PTSD posttrauma. However, further study is
required to delineate the precise role of the 2–receptor in this regard.<br>Thesis (M.Sc. (Pharmacology))--North-West University, Potchefstroom Campus, 2012.
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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.
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Yap, 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.
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Eleven experiments examined two late-developing learning and memory systems in rats: fear-potentiated startle (FPS) and the contextual regulation of latent inhibition and extinction. The first study was based on three previous developmental findings on FPS: (1) FPS to an odour CS emerges at postnatal day (PN) 23; Rats conditioned at PN16 to an odour CS express freezing but not FPS when tested at PN23, and (3) FPS to an odour CS trained at PN16 is activated if rats are also trained to a difference odour at PN23 (Yap, Stapinski, & Richardson, 2005). Yap et al. (2005) hypothesised that the activation effect only occurs if rats are given training to the second odour at an age when FPS has emerged. Study 1 assessed this hypothesis and trained the second odour CS at either PN23 or PN20. Contrary to expectations, the results of this study showed the activation effect for both groups of rats. Surprisingly, the results also revealed a significant FPS effect to the odour CS trained at PN20. Subsequent experiments examined this unexpected result, and found that learning to odour 1 at PN16 facilitated the age of onset for FPS at PN20. The results of Study 1 are discussed in relation to past findings on enrichment, cumulative learning, and neurobiological models of conditioned fear. The second section of this thesis (Studies 2 and 3) examined the context-specificity of two memory interference paradigms, latent inhibition and extinction, in developing rats. The studies found that both phenomena were context-specific at PN23-25 but not at PN16-18. Moreover, the results suggest that the context-specificity of both latent inhibition depended on the age of the rat during the second phase of training, but not their age during the first phase of training or their age at test. The implications of these findings for theoretical and neural models of learning, as well as the occurrence of latent inhibition and extinction during development are discussed.
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Bergstrom, 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.
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Thesis (Ph.D.)--George Mason University, 2009.<br>Vita: 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.
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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.
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A l’heure actuelle, une des principales questions des neurosciences comportementales est de comprendre les bases neurales des apprentissages et de comprendre comment des modifications au sein de circuits neuronaux spécifiques contrôlent les changements comportementaux liés à une expérience particulière. De nombreuses études ont récemment mis en évidence le rôle important des circuits neuronaux dans les phénomènes d’apprentissages associatifs, et notamment dans la régulation des comportements de peur. Cependant, leurs caractéristiques anatomiques et fonctionnelles restent encore largement inconnues. L’une des principales fonctions des circuits neuronaux est leur capacité à adapter le comportement en fonction de la nature des informations internes ou environnementales disponibles. Malgré de nombreux progrès réalisés sur la compréhension des substrats et mécanismes neuronaux sous tendant le conditionnement de peur au sein de structures telles que l'amygdale (AMG), le cortex préfrontal dorso-médian (dmPFC) et la substance grise periaqueducale (PAG), les mécanismes neuronaux gouvernant les interactions inter-structure ainsi que le contrôle local de ces différents circuits neuronaux restent encore largement inconnus. Dans ce contexte, ce travail de thèse a eupour objectifs principaux, d’évaluer la contribution des voies de projections dmPFC-BLA et dmPFC-vlPAG dans la régulation des comportements de peur, et, d’identifier les mécanismes neuronaux sous-jacent contrôlant l'expression de la peur. Afin de répondre à ces questions, nous avons utilisé conjointement des enregistrements électrophysiologiques unitaires et de potentiels de champs couplés à des approches optogénétiques au cours de l’expression de la peur conditionnée. Nous avons pu mettre en évidence un nouveau mécanisme neuronal basé sur une oscillation cérébrale à 4 Hz entre le dmPFC et le BLA impliqué dans la synchronisation neuronale des neurones de ces deux structures nécessaire à l’expression de la peur. Nous avons aussi démontré que le dmPFC via ses projections sur le vlPAG contrôle directement l’expression de la peur. Ensemble, nos données contribuent à une meilleure compréhension des circuits neuronaux ainsi que des mécanismes du comportement de peur qui dans le futur pourront aider à une amélioration thérapeutique des troubles anxieux<br>A 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
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Courtin, Julien. "Role of cortical parvalbumin interneurons in fear behaviour." Thesis, Bordeaux 2, 2013. http://www.theses.fr/2013BOR22045/document.
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Les processus d'apprentissage et de mémoire sont contrôlés par des circuits et éléments neuronaux spécifiques. De nombreuses études ont récemment mis en évidence que les circuits corticaux jouent un rôle important dans la régulation des comportements de peur, cependant, leurs caractéristiques anatomiques et fonctionnelles restent encore largement inconnues. Au cours de ma thèse, en utilisant des enregistrements unitaires et des approches optogénétiques chez la souris libre de se comporter, nous avons pu montrer que les interneurones inhibiteurs du cortex auditif et du cortex préfrontal médian forment un microcircuit désinhibiteur permettant respectivement l'acquisition et l'expression de la mémoire de peur conditionnée. Dans les deux cas, les interneurones parvalbuminergiques constituent l'élément central du circuit et sont inhibés de façon phasique. D’un point de vue fonctionnel, nous avons démontré que cette inhibition était associée à la désinhibition des neurones pyramidaux par un mécanisme de réduction de l'inhibition continue exercée par les interneurones parvalbuminergiques. Ainsi, les interneurones parvalbuminergiques peuvent contrôler temporellement l'excitabilité des neurones pyramidaux. En particulier, nous avons montré que l'acquisition de la mémoire de peur conditionnée dépend du recrutement d'un microcircuit désinhibiteur localisé dans le cortex auditif. En effet, au cours du conditionnement de peur, la présentation du choc électrique induit l'inhibition des interneurones parvalbuminergiques, ce qui a pour conséquence de désinhiber les neurones pyramidaux du cortex auditif et de permettre l’apprentissage du conditionnement de peur. Dans leur ensemble, ces données suggèrent que la désinhibition est un mécanisme important dans l'apprentissage et le traitement de l'information dans les circuits corticaux. Dans un second temps, nous avons montré que l'expression de la peur conditionnée requière l'inhibition phasique des interneurones parvalbuminergiques du cortex préfrontal médian. En effet, leur inhibition désinhibe les cellules pyramidales préfrontales et synchronise leur activité en réinitialisant les oscillations thêta locales. Ces résultats mettent en évidence deux mécanismes neuronaux complémentaires induits par les interneurones parvalbuminergiques qui coordonnent et organisent avec précision l’activité neuronale des neurones pyramidaux du cortex préfrontal pour contrôler l'expression de la peur conditionnée. Ensemble, nos données montrent que la désinhibition joue un rôle important dans les comportements de peur en permettant l’association entre des informations comportementalement pertinentes, en sélectionnant les éléments spécifiques du circuit et en orchestrant l'activité neuronale des cellules pyramidales<br>Learning 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
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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.
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Master of Science<br>Department of Psychological Sciences<br>Mary Cain<br>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.
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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.
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<p> Basal 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</p><p>
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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.
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Previous research has shown that cognitive reappraisal, an emotion regulation strategy, has beneficial effects on emotion experience during strategy engagement. The present study extends this work by investigating whether cognitive reappraisal impacts the anticipation of an aversive event during, and five days following, strategy engagement. Emotion profiles, including psychophysiological and self-report indices, were also examined to assess whether reappraisal inhibits affective responses. Participants underwent habituation and simple discriminatory fear conditioning. Stimuli were pictures of a snake and a spider. Two days later participants returned to the laboratory and were either i) cued to engage in cognitive reappraisal while imagining the stimuli ii) exposed to the stimuli with no reappraisal instructions iii) exposed to the stimuli while engaging in cognitive reappraisal or iv) had an experience unrelated to the stimuli (control condition). Participants returned to the lab five days later and were exposed to both pictures paralleling initial habituation and conditioning protocols. It was found that cognitive reappraisal during exposure reduced expectancy of the UCS faster than exposure alone and resulted in lower mean skin conductance response (SCR) for those low, but not high, in fear of snakes. Five days later participants in the intervention conditions, compared to the control condition, demonstrated less anticipation of the UCS and smaller emotion-modulated startle magnitudes to the UCS. These findings suggest that cognitive reappraisal may be an effective tool for reducing anticipation of an aversive event and can result in enduring fear inhibition. This may have important implications for the treatment of individuals with anxiety disorders. The present study also examined the relationship between cardiac vagal control, indexed by respiratory sinus arrhythmia (RSA), and subsequent sympathetic arousal during fear conditioning, indexed by SCR. Results demonstrate that participants with low, compared to high, resting RSA had larger SCRs during habituation and conditioning trials. In addition, participants with lower RSA showed greater SCR reactivity following UCS presentation to both conditioned stimuli, suggesting that those with the lower RSA initially differentiated less between the UCS paired and unpaired images. These findings are consistent with theories that associate faster recovery from emotionally demanding situations with greater cardiac vagal control.
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Sissons, Heather T. "Overexpectation and trial massing." Diss., Online access via UMI:, 2008.
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Laborda, 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.
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Reimer, Adriano Edgar. "Envolvimento de mecanismos GABAérgicos da substância cinzenta periaquedutal dorsal e do colículo inferior no medo condicionado e incondicionado." Universidade de São Paulo, 2008. http://www.teses.usp.br/teses/disponiveis/59/59134/tde-08092013-014529/.
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A substância cinzenta periaquedutal dorsal (SCPd) e o colículo inferior (CI) são duas estruturas do teto mesencefálico que, juntamente com a amígdala, o hipotálamo dorsomedial e o colículo superior, estão envolvidas na modulação da expressão comportamental dos estados de medo. A estimulação química ou elétrica destas estruturas produz uma série de respostas comportamentais defensivas. Além disso, dados comportamentais com modelos animais de ansiedade têm fornecido evidências da existência de uma regulação inibitória tônica GABAérgica na SCPd e CI. Neste estudo investigamos o envolvimento da neurotransmissão GABAérgica na expressão do medo condicionado e do medo incondicionado. Para isso, os efeitos da administração de muscimol (agonista GABA-A) e semicarbazida (inibidor da descarboxilase do ácido glutâmico) na SCPd e CI foram analisados no teste do sobressalto potencializado pelo medo, na resposta de congelamento condicionada, nos limiares de congelamento e fuga determinados por estimulação elétrica dessas estruturas e no congelamento pós-estimulação. No modelo de medo incondicionado, microinjeções de muscimol intra-SCPd reduziram a aversividade da estimulação elétrica, mas não o congelamento pós-estimulação, ao passo que a semicarbazida produziu efeitos pró-aversivos em ambas as condições. O muscimol também causou redução significativa no sobressalto potencializado pelo medo e congelamento condicionado, enquanto que a semicarbazida não alterou essas respostas. Já a microinjeção de ambas as drogas no CI não produziu efeitos no modelo condicionado, mas no teste incondicionado, o muscimol reduziu a aversividade da estimulação elétrica. Esses dados mostram uma participação diferencial de mecanismos GABAérgicos no medo condicionado e incondicionado. Estes mecanismos na SCPd parecem estar envolvidos tanto no medo condicionado quanto no incondicionado, enquanto que no CI eles parecem participar somente do medo incondicionado.<br>The dorsal periqueductal gray (dPAG) and inferior colliculus (IC) are two structures of the midbrain tectum that, together with amygdala, dorsomedial hypothalamus and superior colliculus, are involved in the modulation of the expression of fear-related behaviors. The chemical or electrical stimulation of these structures produces a series of behavioral defensive responses. Moreover, behavioral data from animal models of anxiety have provided evidences of tonic inhibitory GABAergic regulation in dPAG and IC. This study investigated the involvement of GABAergic neurotransmission in the expression of unconditioned and conditioned fear. To this aim, the effects of intra-dPAG and IC administration of muscimol (GABA-A agonist) and semicarbazide (glutamic acid decarboxylase inhibitor) were examined in the fear potentiated startle test, in conditioned freezing, in the thresholds for freezing and escape determined by electrical stimulation of these structures, and in the post-stimulation freezing. In the unconditioned model, intra-dPAG injections of muscimol reduced the aversiveness of the electrical stimulation but had no effects on the post-stimulation freezing, while semicarbazide produced aversive-like effects in both conditions. Muscimol also caused significant reduction in fear potentiated startle and conditioned freezing, while semicarbazide had no effect in these responses. In contrast, intra-IC injections of both drugs were ineffective in the conditioned model. In the unconditioned model, however, muscimol reduced the aversiveness of the electrical stimulation. These data show a differential participation of GABAergic mechanisms on conditioned and unconditioned fear. These mechanisms in the dPAG seem to be involved in both conditioned and unconditioned fear, while in IC they seem to participate in unconditioned fear only.
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Gore, Sayali Gore. "Behavioral characterization of substituted amphetamines and their synthetic cathinone analogues in the rusty crayfish (Orconectes rusticus)." Bowling Green State University / OhioLINK, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=bgsu1510511175410233.
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Ortiz, 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.
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Broiz, Ana Carolina Garcia. "Envolvimento de receptores 5-HT1A no comportamento defensivo induzido por estimulação elétrica da substãncia cinzenta periaquedutal dorsal de ratos com experiência prévia a eventos estressantes." Universidade de São Paulo, 2007. http://www.teses.usp.br/teses/disponiveis/59/59134/tde-31082007-112429/.
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O comportamento emocional tem sido considerado fundamental para a sobrevivência dos animais, sendo o medo uma se suas mais primitivas e importantes formas. A substância cinzenta periaquedutal dorsal (SCPD) tem-se destacado como uma estrutura importante na organização das respostas defensivas. Estudos usando estimulação elétrica e química da SCPD e microinjeções de drogas agonistas e antagonistas de receptores serotoninérgicos mostraram uma mediação serotoninérgica através dos subtipos de receptores 5-HT1A e 5-HT2A na regulação do comportamento defensivo organizado nesta estrutura. O objetivo deste trabalho foi examinar a mediação serotoninérgica na SCPD através de receptores 5-HT1A nas respostas defensivas de animais sem e com experi~encia aversiva prévia. Para isto, os limiares de congelamento e fuga foram determinados em ratos implantados com uma cânula acoplada a um eletrodo na SCPD, antes e após microinjeção local do agonista 8-OH-DPAT (4 e 8 nmol) e do antagonista WAY100635 (10 nmol). Os efeitos destas drogas injetadas na SCPD foram avaliados também sobre o tempo de congelamento pós-estimulação em animais ingênuos e também em animais colocados em um contexto no qual receberam choques inescapáveis nas patas 24h antes (medo condiconado contextual). O 8-OH-DPAT, de maneira dose dependente, produziu um efeito anti-aversivo sobre os limiares de congelamento e fuga em ratos sem experiência aversiva prévia, mas não nos animais com experiência aversiva prévia quando comparado com seus controles. Por outro lado, este agonista 5-HT1A reduziu o tempo de congelamento contextual. Já o WAY100635 não produziu alterações significativas sobre os limiares aversivos em ratos ingênuos ou com experiência aversiva prévia, mas elevou o tempo de congelamento contextual nestes aniamis (efeito pró-aversivo). Estes resultados estão em concordância com a idéia de uma modulação fásica exercida pela 5-HT sobre os substratos neurais do medo organizado na SCPD. Por outro lado, mecanismos mediados pelos receptores 5-HT1A não são alterados em animais com experiência aversiva prévia. Acreditamos que estes resultados trazem uma contribuição importante para a nossa compreensão sobre a integração de estados aversivos no SNC e, particularmente sobre o funcionamento destes substratos neurais de defesa na SCPD de animais com experiência aversiva prévia.<br>It is well established that 5-HT1 mechanisms modulate the defensive behavior produced by stimulation of the dorsal periaqueductal gray (dPAG). However, in spite of the notion that past stressful experiences play a role in certain types of anxiety only few studies with stimulation of the dPAG of rats without previous aversive experience have been conducted so far. In this study, we examined the mediation of 5-HT1 receptors of the dPAG in rats naive and in rats previously submitted to contextual fear conditionong (CFC). Defensive behaviors induced by activation of the dPAG were assessed by measuring the lowest intensity of electric current applied to this structure (threshold) able to produce freezing and escape responses during testing sessions of CFC, in which animals were placed in a context previously paired to footshocks. The persistence of the freezing behavior after the interruption of the dPAG electrical stimulation was also evaluated. The 5-HT1 function of the dPAG in this condition was evaluated by local injectinos of 8-OH-DPAT (4 and 8 nmol/) and WAY100635 (10nmol), selective agonist and antagonist of 5-HT1 receptors, respectively. In accordance with previous studies, 8-OH-DPAT increased the aversive thresholds (antiaversive effects) and injection of WAY100635 into the dPAG did not produce significant effects in naive rats. On the contrary, both serotonergic drugs 8-OH-DPAT and WAY100635 did not produce any significant effects on the aversive thresholds. Post-stimulation freezing was not affected by any treatment given to animals before or after CFC. However, the contextual conditioned freezing was attenuated or enhanced by intra-dPAG of 8-OH-DPAT and WAY100635, respectively. The present results suggest that 5-HT1 receptor-mediated mechanisms exert a phasic inhibition on the neural substrates of fear in the dPAG in naive rats whereas past stressful experience does not produce significant changes in the synaptic function of 5-HT1 receptors within the dPAG.
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Stegmann, Yannik [Verfasser], Matthias J. [Gutachter] Wieser, Paul [Gutachter] Pauli, Matthias [Gutachter] Gamer, and 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.
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Oliveira, Luciana Chrystine. "Envolvimento de receptores 5-HT2A da substância cinzenta periaquedutal dorsal no medo condicionado e incondicionado de ratos." Universidade de São Paulo, 2007. http://www.teses.usp.br/teses/disponiveis/59/59134/tde-10122007-101529/.
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Sabe-se que o medo condicionado contextual (MCC) pode ativar diversas áreas mesencefálicas, como a Substância Cinzenta Periaquedutal Dorsal (SCPd). Diversos estudos avaliaram como mecanismos serotoninérgicos modulam o comportamento defensivo induzido pela estimulação elétrica da SCPd. Uma função proeminente dos receptores 5-HT2A é regular estados aversivos induzidos pela ativação da SCPd e, apesar de saber que experiências aversivas prévias exercem um importante papel em determinados tipos de ansiedade, somente estudos com estimulação da SCPd de ratos sem experiência aversiva prévia foram conduzidos até o momento. O objetivo do presente estudo foi investigar o papel funcional dos receptores 5-HT2A localizados nos substratos neurais da aversão na SCPd de ratos previamente submetidos ao condicionamento contextual aversivo. Foram avaliadas as respostas de congelamento e fuga obtidas a partir do procedimento de estimulação elétrica da SCPd na sessão teste, realizada 24 horas após o condicionamento, quando os animais foram recolocados no contexto previamente pareado com choques nas patas ou no contexto diferente. A função dos receptores 5-HT2A da SCPd foi avaliada pela injeção local de -metil-serotonina ou cetanserina, agonista e antagonista seletivos de receptores do tipo 5-HT2A, respectivamente. De acordo com estudos anteriores, a -metil-serotonina aumentou os limiares aversivos (efeito antiaversivo) determinados pela estimulação da SCPd em animais ingênuos, enquanto que a injeção de cetanserina não produziu qualquer efeito significativo. No presente estudo, a cetanserina reduziu o limiar de congelamento (efeito proaversivo), enquanto que a -metil-serotonina continuou apresentando efeito antiaversivo em animais com experiência aversiva prévia (choques nas patas). Estes resultados sugerem que experiências aversivas anteriores podem produzir importantes alterações na função sináptica dos receptores 5-HT2A da SCPd, podendo refletir na reatividade da SCPd à sua estimulação aversiva.<br>It has been shown that contextual fear conditioning (CFC) may activate brainstem regions such as the dorsal periaqueductal gray (dPAG). Several studies have been carried out to disclose how 5-HT2 mechanisms modulate the aversive stimulation of the dPAG. One prominent function of 5-HT2 receptors is to regulate the aversive states induced by activation of the dPAG. However, in spite of the notion that past stressful experiences play a crucial role in certain types of anxiety only studies with stimulation of the dPAG of rats without previous aversive experience have been conducted so far. We investigated the mediation of 5-HT2 receptors located in the neural substrates of aversion of the dPAG in rats previously submitted to CFC. Defensive behaviors induced by activation of the dPAG were assessed by measuring the lowest intensity of electric current applied to this structure (threshold) able to produce freezing and escape responses during testing sessions of CFC, in which animals were placed in a context previously paired to footshocks. The 5-HT2 function of the dPAG in this condition was evaluated by local injections of -methyl-5-HT and ketanserin, selective agonist and antagonist of 5-HT2 receptors, respectively. In accordance with previous studies, -methyl-5-HT increased the aversive thresholds (antiaversive effects) determined by stimulation of the dPAG in naive rats and injection of ketanserin into the dPAG did not produce any significant effects. On the other hand, ketanserin decreased the freezing threshold (proaversive effect) determined by the dPAG electrical stimulation while -methyl-5-HT continued to show antiaversive effects in animals with prior experience with foot shocks. The present results suggest that a past stressful experience can produce changes in the synaptic function of 5-HT2 receptors within the dPAG with important impact on the defensive behaviors induced by electrical stimulation of this area.
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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.
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Le système endocannabinoïde régule de nombreuses fonctions physiologiques. Dans le cerveau, cette régulation est exercée principalement par l’activation des récepteurs CB1. En effet, ces derniers jouent un rôle clef dans la régulation des neurotransmissions excitatrices et inhibitrices, y compris dans des régions cérébrales impliquées dans la gestion des processus émotionnels. Les données existantes indiquent que les récepteurs CB1 exercent un contrôle tonique sur certaines dimensions de l’émotion (e.g. anxiété, peur), mais le rôle joué par ces récepteurs dans les conséquences émotionnelles de l’exposition répétée à des stimuli attractifs ou aversifs n’a été que peu analysé. L’objectif de nos travaux a donc été d’examiner chez la souris le rôle des récepteurs CB1 (i) dans l’adhérence à un exercice physique volontaire répété, et dans les impacts émotionnels (ii) de l’exercice volontaire répété, et (iii) du stress par défaites sociales répété. Cet examen a été réalisé principalement à l’aide d’outils génétiques (mutants constitutifs et conditionnels du récepteur CB1) mais également à l’aide d’outils pharmacologiques (antagonistes sélectifs des récepteurs CB1). L’utilisation de ces outils nous a permis d’identifier un rôle spécifique des récepteurs CB1 des neurones GABAergiques de l’aire tegmentale ventrale dans le contrôle des performances d’exercice physique volontaire sur roue chez la souris. De plus, les données comportementales obtenues indiquent que les récepteurs CB1 portés par les neurones glutamatergiques corticaux jouent un rôlecrucial dans les profils d’anxiété et d’extinction de peur observés après un exercice physique volontaire répété. Enfin, une dernière série d’études a permis de distinguer les impacts respectifs del’enrichissement de l’hébergement d’une part, et de la pratique de l’exercice d’autre part, dans les conséquences de l’exercice volontaire sur les comportements émotionnels et la neurogenèse hippocampique.Un second volet de recherche a permis de définir les rôles respectifs des récepteurs CB1 portés pardifférentes populations neuronales dans l’impact psychoneuroendocrinien (comportement, métabolisme, réactivité corticotrope) du stress social par défaites répétées. En particulier, ce travail asouligné l’impact majeur des récepteurs CB1 des neurones sérotonergiques dans les modifications depoids corporel et d’appétence pour le sucre induites par le stress répété. De plus, les résultats obtenus chez des animaux contrôles et des animaux stressés ont mis en avant le rôle des récepteursCB1 des neurones glutamatergiques corticaux et des neurones exprimant le facteur Sim1 (i.e. majoritairement hypothalamiques) dans les processus d’extinction de la mémoire de peur conditionnée au son<br>The 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
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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/.
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O congelamento a um contexto previamente associado ao choque nas patas é atenuado pela lesão da matéria cinzenta periaquedutal ventrolateral (MCPvl). Por outro lado, a estimulação elétrica ou microinjeção de compostos que diminuem a neurotransmissão GABAérgica na matéria cinzenta dorsolateral (MCPdl) provocam congelamento e fuga. O presente estudo examinou a possibilidade deste congelamento provocado pela estimulação da MCPdl ser resultado da ativação indireta da MCPvl. Ratos com lesão da MCPvl ou falsooperados foram eletricamente estimulados na MCPdl para a aferição dos limiares de resposta para o congelamento e a fuga. Os mesmos animais foram também submetidos ao condicionamento aversivo ao contexto através de choque nas patas, visando a validação de nossas condições experimentais. Um segundo grupo de ratos lesados e falso-operados receberam microinjeções de semicarbazida, um bloqueador da síntese do GABA, na MCPdl. Os resultados mostram que a lesão da MCPvl atenua o congelamento condicionado ao contexto, mas é ineficaz em alterar os efeitos da estimulação elétrica ou química da MCPdl sobre o congelamento e a fuga. A MCPvl é o alvo preferencial do núcleo central da amígdala na MCP, enquanto que a MCPdl recebe aferências principalmente dos núcleos do hipotálamo relacionados à defesa. Estas evidências são coerentes com a participação da MCPvl nas respostas de defesa ao perigo potencial, e da MCPdl ao perigo imediato.<br>Freezing 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.
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D'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.
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Estudios genéticos en pacientes sugieren que el gen del receptor tirosina quinasa de la neurotrofina de tipo 3 (NTRK3) podría contribuir en la patología del trastorno de pánico (PAND), un trastorno de ansiedad caracterizado por alteración y exageración del miedo.
En esta tesis, proponemos que PAND podría estar relacionado con procesos anormales de aprendizaje asociativo, subyacentes a una alteración en la regulación del funcionamiento del circuito del miedo hipocampo - amígdala – corteza prefrontal media. Hemos estudiado esta hipótesis utilizando el único modelo genético de ratón validado de PAND, el TgNTRK3, que sobreexpresa el gen humano NTRK3 codificante para el receptor TrkC. Hemos demostrado que la sobreexpresión de NTRK3 en ratones produce: i) un incremento en la memoria de miedo dependiente de hipocampo que es además resistente a extinción; ii) la activación alterada del circuito del miedo durante el aprendizaje y almacenamiento de experiencias emocionales intensas negativas. Nuestros resultados sugieren que los mecanismos responsables están relacionados con una sobre excitabilidad en el hipocampo. Nuestro estudio confirma el papel del gen NTRK3 en la memoria de miedo patológico y sugiere posibles estrategias terapéuticas para bloquear el miedo exagerado en PAND dirigidas al sistema de excitación / inhibición y a la vía de señalización NT3-TrkC.<br>The 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.
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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/.
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O aumento do reflexo de sobressalto na presença de um estímulo que tenha sido previamente pareado a choques nas patas é tomado como índice de medo e nomeado sobressalto potencializado pelo medo (SPM). O congelamento, interrupção de todos os movimentos observáveis, exceto aqueles associados com a respiração, também tem sido utilizado como índice de medo em ratos. Um crescente número de evidências sugere o envolvimento de mecanismos dopaminérgicos em diferentes aspectos da memória afetiva, como sua formação, evocação e expressão. No entanto, resultados sobre como e por meio de quais receptores os mecanismos dopaminérgicos influenciam o medo têm sido inconsistentes. O presente estudo examina o envolvimento dos receptores dopaminérgicos na aquisição e na expressão do medo condicionado à luz. Para isso, foram analisados os efeitos do antagonista D1, SCH 23390, do agonista D1, SKF 38393, do antagonista D2, sulpirida, e do agonista D2, quimpirole, no SPM e no congelamento. A atividade motora dos animais também foi avaliada no teste do campo aberto. SCH 23390, SKF 38393, sulpirida e quimpirole, administrados antes do condicionamento, não produziram efeitos no SPM, mas SCH 23390 diminuiu o congelamento. As administrações de SCH 23390, SKF 38393 e sulpirida antes do teste também não produziram efeitos no SPM e no congelamento. Quimpirole, em doses que agem em receptores pré-sinápticos, causou uma redução significativa no SPM e no congelamento, quando administrado antes do teste. A ação das drogas não foi devida a efeitos não-específicos uma vez que elas não produziram efeitos no teste do campo aberto. Os resultados sugerem que mecanismos dopaminérgicos devem estar envolvidos tanto na aquisição, quanto na expressão do medo condicionado à luz. Receptores D1 pós-sinápticos parecem participar da aquisição do congelamento condicionado à luz-CS, mas não do SPM. Por outro lado, receptores D2 pré-sinápticos parecem estar envolvidos na expressão do medo condicionado à luz-CS.<br>The 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.
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Broiz, Ana Carolina Garcia. "Envolvimento de receptores NK-1 e NK-3 no comportamento defensivo induzido pela estimulação elétrica da substância cinzenta periaquedutal dorsal." Universidade de São Paulo, 2011. http://www.teses.usp.br/teses/disponiveis/59/59134/tde-15122011-150613/.
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A substância cinzenta periaquedutal dorsal (SCPd) é considerada uma das principais estruturas do teto mesencefálico envolvida no substrato neural da aversão a estímulos proximais. GABA e 5-HT são apontados como neurotransmissores envolvidos na modulação das respostas defensivas elaboradas na SCPd. Recentemente, mecanismos neurocininérgicos também têm sido propostos como mediadores das reações de defesa organizadas nessa estrutura. O objetivo do presente estudo foi avaliar o envolvimento dos receptores NK-1 e NK-3 da SCPd no comportamento defensivo induzido pela estimulação elétrica dessa região em ratos com e sem experiência prévia ao condicionamento contextual aversivo. Para isso, os limiares aversivos de congelamento e fuga foram medidos durante a estimulação elétrica da SCPd em ratos ingênuos e em animais submetidos previamente ao procedimento de condicionamento contextual aversivo. A mediação destas repostas defensivas pelos receptores NK-1 e NK-3 foi avaliada pela injeção local de spantide (100 pmol/0,2 L) e SB 222200 (50 e 100 pmol/0,2 L), antagonistas seletivos de receptores NK-1 e NK-3, respectivamente. Os resultados mostraram que a injeção intra-SCPd de spantide aumentou os limiares aversivos determinados pela estimulação elétrica da SCPd em animais ingênuos e com experiência aversiva prévia. Injeções similares de 100 pmol de SB 222200 na SCPd também causaram um aumento nos limiares de congelamento e fuga. Entretanto, esses efeitos devem ser atribuídos a um déficit motor causado por essa dose da droga, uma vez que SB 222200 na dose de 100 pmol, reduziu significativamente a atividade motora dos animais submetidos ao teste do campo aberto. Estes resultados sugerem que receptores NK-1, mas não NK-3, estão envolvidos na mediação do comportamento defensivo induzido pela estimulação elétrica da SCPd.<br>The dorsal periaqueductal gray (dPAG) constitutes the main structure of the neural substrate for the defensive response to proximal aversive stimuli. It is well established that GABA and 5-HT are important neuromediators of the defense reaction at the dPAG level but neurokinin-mediated mechanisms have also been recently implicated in these processes. The aim of the present investigation was to examine the involvement of NK-1 and NK-3 receptors of the dPAG in the unconditioned defensive behaviors induced by electrical stimulation of the dPAG of rats with and without previous experience with contextual fear conditioning. For this, aversive thresholds were measured as the lowest intensity of electric current to produce freezing and escape behaviors using a procedure of gradual increases of the electrical stimulation of the dPAG. These thresholds were also measured in rats previously submitted to a contextual fear conditioning procedure. The mediation of these defensive responses by NK-1 and NK-3 receptors of the dPAG was evaluated by local injections of spantide (100 pmol/0.2 L) and SB 222200 (50 and 100 pmol/0.2 L), selective antagonists of NK-1 and NK-3 receptors, respectively. The present results showed that spantide injections into the dPAG increased the aversive thresholds (anti-aversive effects) determined by stimulation of the dPAG in naive and in animals subjected previously to the contextual fear conditioning. Similar injections of SB 222200 100 pmol into the dPAG increased the freezing and escape thresholds. However, this effect can be attributable to a motor deficit since this dose of SB 222200 decreased the exploratory activity of the animals subjected to the open field test. These results suggest that NK-1 receptors, but not NK-3 receptors, are involved in the mediation of the defensive behaviors induced by electrical stimulation of the dPAG.
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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/.
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OLIVEIRA, A.R. Envolvimento de receptores dopaminérgicos da área tegmental ventral e do complexo basolateral da amígdala na aquisição e na expressão do medo condicionado. 2010. 93 f. Tese (Doutorado) Faculdade de Filosofia, Ciências e Letras de Ribeirão Preto, Universidade de São Paulo. O condicionamento Pavloviano é um dos paradigmas mais utilizados para estudar as bases biológicas das emoções, assim como da aprendizagem e memória. A dopamina (DA) é um dos principais neurotransmissores envolvidos na mediação de estados de medo e ansiedade. Um conjunto crescente de evidências dá suporte à hipótese de que a ativação da via mesocorticolímbica, proveniente de neurônios dopaminérgicos da área tegmental ventral (ATV), é particularmente sensível à estimulação aversiva. Entre as regiões inervadas por esta via, o complexo basolateral da amígdala (BLA) é um componente essencial dos circuitos neurais do medo condicionado. Assim, o presente estudo explorou o envolvimento de mecanismos DA da ATV e do BLA, através do uso de agonistas e antagonistas de receptores DA, na aquisição e expressão do medo condicionado à luz. Não houve efeito das drogas DA no sobressalto potencializado pelo medo (SPM), quando injetadas na ATV antes do condicionamento, indicando que os receptores DA da ATV não participam da aquisição do medo condicionado à luz. Ao contrário, quando injetado na ATV antes do teste, quimpirole (agonista D2) reduziu o SPM, enquanto as demais drogas não tiveram efeito. A administração de SCH 23390 (antagonista D1) no BLA não produziu efeitos no SPM, indicando que os receptores D1 do BLA não parecem envolvidos na expressão do SPM. Já a administração de sulpirida (antagonista D2) no BLA inibiu o SPM produzido pela luz. Além disso, a expressão do medo condicionado foi associada a um aumento do congelamento e dos níveis extracelulares de DA no BLA, ambos inibidos com a administração de quimpirole na ATV. A capacidade do quimpirole em diminuir o SPM e o congelamento condicionado parece ser resultado de sua ação em auto-receptores D2 da ATV. A ativação desses receptores diminui os níveis de dopamina em áreas que recebem terminações da via mesocorticolímbica. Os resultados com a sulpirida realçam a importância dos receptores D2 do BLA na expressão do medo condicionado Pavloviano.<br>OLIVEIRA, 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.
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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/.
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A substância cinzenta periaquedutal dorsal (dPAG) e o hipotálamo medial (MH) são duas estruturas encefálicas que estão envolvidas na elaboração de estados aversivos e expressão de respostas defensivas. A estimulação elétrica da dPAG ou do MH produz uma série de respostas comportamentais que se assemelham às respostas defensivas induzidas pela presença de um predador. Esses mesmos comportamentos podem ser eliciados com a microinjeção local de agonistas glutamatérgicos nessas estruturas, indicando o envolvimento de aminoácidos excitatórios na expressão das respostas defensivas incondicionadas. Apesar disso, a participação destas estruturas no medo condicionado ainda é pouco conhecida. Assim, o objetivo deste estudo foi avaliar o envolvimento da mediação glutamatérgica da dPAG e de núcleos do MH núcleo anterior (AH) e núcleo pré-mamilar dorsal (PMd) na expressão do medo condicionado à luz. Para isso, foram avaliados os efeitos de agonistas e antagonistas glutamatérgicos (AMPA/Cainato e NMDA) administrados nessas estruturas no teste do sobressalto potencializado pelo medo (SPM) e na medida de congelamento condicionado. Ratos Wistar machos com cânulas-guias implantadas na dPAG, AH ou PMd foram submetidos ao condicionamento aversivo (pareamentos luz+choque). Vinte e quatro horas depois, esses animais receberam injeções intra-dPAG, AH ou PMd de NMDA ou ácido caínico (agonistas NMDA e AMPA/Cainato, respectivamente) ou AP7 ou NBQX (antagonistas NMDA e AMPA/Cainato, respectivamente) e foram submetidos ao teste do SPM. A resposta de congelamento condicionado foi avaliada na mesma sessão. Eventuais alterações motoras foram avaliadas no teste do campo aberto. A administração dos agonistas glutamatérgicos na dPAG promoveu efeitos pró-aversivos no SPM e congelamento condicionado. NBQX sozinho não produziu nenhum efeito significativo, ao passo que o AP7 diminuiu somente o congelamento condicionado. Entretanto, ambos os antagonistas bloquearam os efeitos dos respectivos agonistas. Já a administração dos agonistas e antagonistas glutamatérgicos no AH e PMd, em doses que não afetaram a atividade motora, não produziu efeitos significativos na resposta de congelamento condicionado e SPM. Os presentes resultados sugerem a participação de aminoácidos excitatórios da dPAG, mas não do MH, na expressão do medo condicionado à luz.<br>The 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.