Дисертації з теми "Systèmes de récompenses"
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Li, Yansong. "Modulation du système de récompense par le risque et le type de récompenses chez l’homme sain et chez des joueurs pathologiques : une approche intégrative combinant enregistrements intracrâniens, mesures hormonales et IRMf." Thesis, Lyon 1, 2014. http://www.theses.fr/2014LYO10202/document.
How our brain processes reward information and how such processing is influenced by parameters such as reward probability and risk have become key questions in cognitive neuroscience. In addition, recent researches suggest a modulatory effect of a number of hormones on brain and behavior and a dysfunction of the reward system in a number of behavioral addictions, such as gambling disorder. This Ph.D. used intracranial EEG (iEEG) and combined Functional Magnetic Resonance Imaging (fMRI) and endocrinology to perform four studies investigating reward processing in healthy subjects, patients with epilepsy implanted with depth electrodes and individuals with gambling disorder. Together, our series of studies advance our understanding of new aspects concerning reward processing in healthy subjects, patients with epilepsy and individuals with gambling disorder
Dubol, Manon. "Étude en neuro-imagerie multimodale du système dopaminergique et du système de récompense chez des patients psychiatriques." Thesis, Université Paris-Saclay (ComUE), 2017. http://www.theses.fr/2017SACLS477/document.
This work focuses on the study of the neurobiological bases of psychiatric disorders using multimodal imaging, with a particular interest in the dopaminergic pathways and the reward system. Its primary objective is to establish, through Positron Emission Tomography (PET) and Magnetic Resonance Imaging (MRI), a link between the dopaminergic system and the reward system from a functional and structural point of view in humans, and especially in patients with psychiatric disorders such as schizophrenia, cocaine addiction and depression. Numerous studies have demonstrated the concomitant existence of abnormalities affecting dopaminergic function and reward system in several mental disorders. However, understanding of the linkages between dopaminergic dysfunction and dysfunction of the reward circuit in psychiatric disorders remains limited. The main aims of this thesis are to improve knowledge about the pathophysiology of several mental disorders such as schizophrenia, addiction and depression, and to demonstrate the interest of both a dimensional approach and the use of multimodal imaging in psychiatric research, to explore the molecular level of functional neural networks. In perspective, this thesis supports the interest of brain imaging in clinical practice, as it could later clarify the diagnosis, predict response to treatments or follow the course of the disease
Chehade, Imad. "Essais sur l'économie des technologies blockchain et des crypto-monnaies." Electronic Thesis or Diss., Normandie, 2023. http://www.theses.fr/2023NORMR057.
This thesis presents three essays that contribute to determining the opportunities and challenges of blockchain technologies and cryptocurrencies, in order to understand their potential for adoption in the banking system and the economy in general. Firstly, we have demonstrated, through a literature review, practical experiments, and a comparative analysis of different existing DLT platforms, that consortium alternative DLTs are the prototypes likely to predominate in the banking system in the future. Next, we highlighted the resilience and robustness of the main reward systems used by mining pools in the face of Bitcoin halving events. This comparison is complemented by additional calculations that truly enrich the analysis of the decisions and behaviors of miners joining a pool. Finally, we developed a tokenization solution tailored for Lebanon, aimed at ensuring economic recovery, while addressing the country’s tumultuous economic context and examining the challenges of existing digital solutions
David, Vincent. "Opiacés et systèmes centraux de récompense : étude à l'aide d'un modèle d'auto-administration intracérébrale chez la souris." Bordeaux 1, 1997. http://www.theses.fr/1997BOR10538.
Goter, Françoise. "Etude du système de sanctions-récompenses en lien avec la performance des organisations de service public : cas d'expérimentation." Lyon 3, 2005. https://scd-resnum.univ-lyon3.fr/in/theses/2005_in_goter_f.pdf.
Within the framework of their initiatives of modernization, numerous organizations of public service are in search of a model of effective management of their activities and their human resources. This objective notably incites them to look for practices of more stimulating penalties-rewards and favoring a bigger efficiency-efficacy of the actors in their activities. Through the study of the practices of penalties-rewards of the organizations of public service, we try to define the main variables of the system of penalties-rewards and to determine the conditions of development of their efficiency. Our hypothesis is that the identification of individual and collective penalties-rewards of the efficiency of the actors and their development within the framework of a structured and stimulating system are a powerful control lever to lead to more efficient organizations of public service and better insure the survival-development of the public service
Loiodice, Simon. "Altérations du système de récompense dans la maladie de Parkinson : relation entre comportement et signatures moléculaires. : Neuropsychopharmacologie." Thesis, Clermont-Ferrand 1, 2016. http://www.theses.fr/2016CLF1MM10.
In Parkinson’s Disease (PD), the progressive dopaminergic (DA) cell loss mainly affects the substantia nigra pars compacta (SNc). The motor symptoms are classically managed by DA replacement therapies (DRT). Although adding DA agonists to levodopa treatment may contribute to prevent motor complications, it may be associated with drug‑induced changes in reward related pathways. Up to 14% of PD patients under DRT may suffer from ‘addiction‑like’ behavior such as pathological gambling, hypersexuality or DA medication‑induced substance abuse. To date, the only therapeutic answer consists in lowering the DA medications which deteriorates the motor symptoms. Neuroadaptations leading to reward bias in PD patients under DRT are still poorly understood. To address this challenge, we propose a work in which we have assessed the rewarding effect of the D2/D3 agonist pramipexole (ppx) after chronic exposure to L‑dopa in an alpha-synuclein PD rat model. In a first study, we assessed the effect of repeated DA receptors stimulations on sensitization of the reward system in a parkinsonian context. Our findings demonstrated that ppx had a rewarding effect after chronic L-dopa administrations and alpha-synuclein-mediated nigral loss. No transcriptional changes within DA receptors were highlighted. However, we identified an association between the main drug or lesion and transcriptional changes which were potentially related to the context of psychostimulant addiction. This study provides evidences strongly suggesting that PD-like lesion and L-dopa therapy were concomitant factors involved in striatal remodeling underlying the ppx-induced place preference. Molecular and pharmacological data suggested a key involvement ofthe glutamatergic pathway in this behavioral outcome. These data were consistent with literature describing major striatal glutamate imbalance as a common feature of drug addiction and Parkinson’s disease physiopathological contexts. Hence, we designed a second study aiming to further investigate the therapeutic potential of glutamatergic receptors inhibition. A bilateral lesion of the SNc was performed in the rat using AAV-mediated overexpression of the alpha-synuclein. This lesion was followed by chronic L-dopa administrations. Then, the effect of the metabotropic glutamate receptor 5 (mGluR5) antagonist MPEP on ppx reinforcing properties was assessed in a place conditioning paradigm. Finally, analysis at the protein level was conducted to associate drug and lesion induced behavioral changes to molecular endpoints. Acquisition and expression of the ppx-induced place preference was abolished by the MPEP. Furthermore, we identified neural networks and protein changes underlying the striatal remodeling associated with the behavioral outcome. All this work provides new insights into the physiopathological context associated to the PD/DRT related reward bias. Convergent molecular and pharmacological data strongly suggest mGluR5 as a promising therapeutic target
Reisiger, Anne-Ruth. "Pathologie du système de récompense : effets à long terme d’une exposition chronique à la nicotine et au sucrose." Thesis, Bordeaux 1, 2013. http://www.theses.fr/2013BOR14870/document.
Learning mechanisms associated with active responding for nicotine enhanced the excitability of the ILCx-BNST pathway. The objective of this project was to better understand the involvement of the ILCx-BNST pathway in nicotine self-administration. Since the endocannabinoid system controls nicotine reinforcement and nicotine-induced synaptic modifications, we examined the role of CB1 receptors in the BNST. We showed that acquisition of nicotine IVSA was associated with a persistent facilitation of LTP induction at ILCx-BNST synapses. Behaviorally, electrical stimulation temporarily increased excessive responding to nicotine when nicotine was not available. Moreover, using intra-BNST pharmacology, we revealed that stimulation of BNST CB1 receptors enhanced sensitivity to nicotine-paired cue. In contrast, after a prolonged history of nicotine intake, it blocked drug-seeking in a reinstatement model of relapse. Drug addiction is partly due to the inability to stop using despite negative consequences. The hypothesis that palatable food induces similar uncontrolled consumption is becoming more widespread. As drug addiction is known to increases activity of VTA DA neurons, we aimed to examine whether exposure to sucrose would induce similar neuronal modifications and impair the capacity to respond to an aversive stimulus. We found that sucrose enhanced spontaneous activity of DA VTA neurons. In addition, while a footshock caused a nearly complete inhibition of activity of VTA DA neurons in control rats, sucrose disrupted signaling of an aversive stimulus. These modifications were independent from the caloric state of the rats
Gobeil, Simard Alexis. "Étude de l'implication des enképhalines et des récepteurs mu opioïdes dans la sensibilisation au sel au sein du système de récompense." Thesis, Université Laval, 2012. http://www.theses.ulaval.ca/2012/28927/28927.pdf.
Parnaudeau, Sébastien. "Rôle du récepteur des glucocorticoïdes dans la vulnérabilité aux drogues d'abus : mutagénèse conditionnelle chez la souris." Paris 6, 2008. http://www.theses.fr/2008PA066350.
Saint-Périer, Amaury de. "Valéry Giscard d'Estaing, la France et l'Europe monétaire de 1974 à 1981 : la persévérance récompensée." Paris 4, 2008. http://www.theses.fr/2008PA040058.
From 1974 to 1978, Valéry Giscard d'Estaing strives to achieve monetary stability for the European community (EC). His aim is to put an end to the monetary anarchy caused by oil shock and the inflation which is devastating Europe. He fails however to secure the support of his German partner. His project clashes witch the position of chancellor Helmut Schmidt who will only agree to a monetary project if inflation is controlled in the long term. Germany's attitude changes in 1978. It now wishes to stabilize the deutschmark in order to improve trade and diminish the influence of the dollar in the EC. Their common purpose leads the two countries to the creation of the European monetary systems (EMS), which should permit the convergence of the economies and the stabilisation of the currencies, as well as improve trading and growth in the EC member states. The EMS also entails the creation of the European Currency Unit designed to become the Common Market single currency. The nine member states adhere to the EMS, with the United Kingdom participating in the ECU, but not in the Exchange Rate Mechanism (ERM) since it seek to menage its own currency freely. In their endeavour, Giscard and Schmidt risked unpopularity by confronting their countries' conservatism. Giscard face the supporters of monetary
Rakotobé, Malalaniaina. "Bases neuro-développementales de la susceptibilité à l’anxiété : apports de l’étude du système habénulo-interpédonculaire." Electronic Thesis or Diss., Université Côte d'Azur, 2021. http://www.theses.fr/2021COAZ6002.
Reward circuits of the brain are neuronal networks that modulate positively or negatively the motivation to act according to the situation. They are essential for the survival of the subject and of species by selecting the appropriate behaviors, such as fleeing the danger or searching for food. Dysfunctions of these circuits can lead to mood disorders and addictions. Although these psychiatric disorders can emerge in adulthood, according to the neurodevelopmental hypothesis they can find their origins at a much earlier stage. Indeed, there are periods of development, called critical periods of development, during which genetic and environmental factors influence the maturation of neuronal circuits. A stressful environment and/or defaults in the expression of developmental genes during these critical periods can lead to the malformation of neuronal circuits, including the reward circuits, creating a predisposition to psychiatric disorders. The habenulo-interpeduncular system (HIPS), composed of the medial habenula (MHb) and its main target, the interpeduncular nucleus (IPN), emerges as a key component of the reward circuits. It is notably involved in disorders such as addiction, anxiety and depression. Our team has recently identified the Otx2 transcription factor as an essential genetic factor for the formation of the MHb and IPN. Otx2 expression is maintained in the HIPS throughout life, strongly in the last neurons generated in the MHb (Otx2High neurons) and in neurons of the lateral and central subnucleus of the caudal IPN, suggesting that it might also play a role in the maturation and functioning of the HIPS. We already know that in the ventral tegmental area (VTA), another actor of the reward circuits, a chronic stress, endured during a specific period of childhood decreases the expression level of Otx2 and predisposes to depression and anxiety. It is thus possible that Otx2 might play a similar function in the HIPS response to stress during periods of development. This thesis work aimed to better understand how genetic and environmental factors affecting the development of the HIPS could lead to the development of psychiatric disorders.The first part of this thesis shows that Otx2High neurons of the MHb project on the Otx2+ neurons of the IPN, revealing an Otx2-dependant sub-circuit in the HIPS. The MHb was then chemogenetically activated with the use of DREADD to verify that Otx2High neurons of the MHb are indeed able to modulate the activity of the Otx2+ neurons of the IPN and confirmed the idea that these neurons constitute a sub-circuit of the HIPS, labelled with the expression of Otx2, that we will call the HIPOPS (Habenulo-InterPeduncular-Otx2-Positive-System).In the second part of this project, a critical period of development during which the HIPS is more sensitive to stress has been searched. By using Fos and Egr1, two neuronal markers of activity, we identified a preadolescent period during which the HIPS is more responsive to chronic stress. Interestingly, that chronic stress involves more particularly the activity of the HIPOPS, emphasizing the implication of that sub-circuit in the stress response.In the third part, a “2-hit” stress protocol of chronic stress has been developed and revealed that a chronic stress endured during preadolescence predisposes to anxiety but not to depression in the long-term. In the last part, the effects of Otx2 conditional deletion in the HIPS has been assessed. This study shows that Otx2 deletion in the MHb protects from the deleterious effects of preadolescent chronic stress on anxiety symptoms. This work, therefore, demonstrates that the interaction between environment (stress) and genes (Otx2) during preadolescence determines the susceptibility to develop chronic anxiety in the long term and that one of the cellular support of that susceptibility is the HIPOPS, a circuit lodged inside the HIPS, recognizable by Otx2 expression
Tolu, Stefania. "Rôle du récepteur nicotinique des sous-populations neuronales de l'aire tegmentale ventrale dans le renforcement induit par la nicotine." Paris 11, 2010. http://www.theses.fr/2010PA114847.
The ventral tegmental area (VTA) is the principal brain area responsible for the reinforcing properties of nicotine. Within the VTA, nicotine activates both dopaminergic and GABAergic neurons by acting on β2 nicotinic acetylcholine receptors (β2*-nAChR) expressed on both neuronal populations. Here we used a novel system for gene expression, in combination with electrophysiology and self-administration approaches, to dissociate the contributions of dopaminergic and GABAergic neurons in nicotine reinforcement. This work demonstrates a major role played by β2*-nAChRs situated on dopaminergic neurons in the initial action of nicotine and the correlation between the burst activity, due to the interaction between the two neuronal populations of the VTA, and the long term maintenance of nicotine-taking behavior
Ducrocq, Fabien. "Vulnérabilité du réseau neuronal du noyau accumbens à la déficience développementale en acides gras polyinsaturés n-3 : conséquences sur le système de récompense et de motivation." Thesis, Bordeaux, 2018. http://www.theses.fr/2018BORD0415/document.
Various, though distinct psychiatric disorders, such as Schizophrenia, bipolar disorder or major depression are associated with a dysfunction of the reward system linked to an alteration of dopamine transmission. Furthermore, these pathologies are also accompanied by changes in lipid metabolism and in particular a decrease in the brain content of docosahexaenoic acid (DHA), the main n-3 polyunsaturated fatty acid (PUFA) in the nervous system. However, despite that n-3 PUFA supplementation seems to improve or prevent some psychiatric symptoms, these results are still controversial and the implication of brain lipid composition in the etiology of psychiatric endophenotypes has been overlooked. The aim of this study was to investigate a potential causal link between n-3 PUFA deficiency and common neurobiological and behavioral endophenotypes of psychiatric disorders. In particular, the hypothesis was that n-3 PUFA deficiency could lead to dysfunctions of mesolimbic dopamine transmission and associated behaviors. Using operant conditioning tasks in mice, we showed that developmental n-3 PUFA deficiency leads to a motivational deficit at adulthood, that is partially reversed by n-3 PUFA supplementation starting at birth, but not at weaning. This motivational deficit was associated with an alteration of dopaminergic transmission as revealed by the reduced sensitivity to the psychostimulant amphetamine. More precisely, we showed that n-3 PUFA deficiency leads to alterations in electrophysiological properties of medium spiny neurons (MSNs) in the nucleus accumbens (NAc), main actors in motivational processes. Indeed, MSNs from the direct pathway (dMSNs), that express dopaminergic D1 receptors, displayed a decrease in neuronal excitability in parallel with an increase of inhibitory input onto these neurons. These alterations were reversed by the dopaminergic D2 receptor (D2R) agonist quinpirole. These data led us to hypothesize that the decreased dMSN excitability induced by n-3 PUFA deficiency could result from an increase of the inhibitory input of MSNs from the indirect pathway (iMSNs that expresses D2R), called lateral inhibition. Accordingly, using a transgenic approach that allows the expression of the fatty acid desaturase FAT1 in a credependent manner, we showed that rescuing appropriate PUFA levels in D2R-expressing neurons selectively (including iMSNs), was sufficient to reverse alterations in electrophysiological properties of MSNs induced by n-3 PUFA deficiency. Moreover, the selective expression of FAT1 in D2-expressing neurons – but not in D1-expressing neurons – reversed the motivational deficit observed in n-3 PUFA deficient mice. We demonstrated the existence of a causal link between modifications in PUFA levels in a discrete neuronal population and behavioral alterations. Overall, this study suggests that altered PUFA levels, observed in some psychiatric disorders, could directly participate in the development of symptoms such as avolition or apathy
Skvortsova, Vasilisa. "Neural mechanisms of instrumental learning : neuroimaging, pharmacological and stimulation studies in humans." Thesis, Paris 6, 2015. http://www.theses.fr/2015PA066297.
Learning from actions is a key ability for survival. But do we learn differently depending on whether the action outcome is positive or negative? Did the brain integrate different choice dimensions such as rewards, punishments or physical efforts in the same way? Do they all rely on the same neural circuit? Does dopamine influence both learning from rewards and efforts? Reinforcement learning theory postulates that learning follows stepwise minimization of the difference between prediction (e.g. internal representation of expected outcome) and actual outcome. We investigated how brain activity relates to these internal variables in different types of learning and how these representations are altered by pharmacological manipulation and deep brain stimulation.In study 1, we found an increase in power in beta band (10-20Hz) in response to reward in the peduncolopontine nucleus (PPN) of patients with Parkinson’s disease. Stimulation of the PPN specifically improved learning from rewards but not from punishments. This brainstem structure might contribute to the reward-related representations in the midbrain dopamine neurons that are known for their computations of reward prediction errors.In the studies 2 and 3, we compared learning to maximize reward with learning to minimize effort. FMRI results suggest that reward and effort related computations are carried by partially dissociable neural networks. Moreover, dopamine, a neuromodulator known to enhance reward maximization did not influence learning to minimize efforts.Overall, this PhD helps generalizing learning algorithms across different choice dimensions and specifying their implementation in different neural networks
Montalban, Enrica. "Long-lasting effects of operant conditioning and cocaine on D1 pyramidal neurons in prefrontal cortex and on the D1 and D2 striatal neurons mRNAs." Thesis, Paris 6, 2016. http://www.theses.fr/2016PA066723/document.
Dopamine (DA) controls movement execution, action selection, and incentive learning by regulating the activity and plasticity of corticostriatal transmission. Long-term modifications require changes in gene transcription. The aim of this work is to study the changes in transcriptions following an operant learning protocol or mimicking stimulation of the reward system with cocaine in the dorsal striatum and the nucleus accumbens in the striatum, and in the prefrontal cortex. The medium-size spiny striatal projection neurons (SPNs) can be divided into 2 different populations based on the expression of the D1 or D2 DA receptor that participate in distinct pathways, which have opposite functional effects on their target regions. We used transgenic mice that express a tagged ribosomal protein (L10a-EGFP) under control of the D1 or D2 receptor promoter to isolate currently translated mRNA and nuclei from each population of SPNs, as well as from D1 neurons of the prefrontal cortex following passive stimulation of the reward system (chronic treatment with cocaine) and active recruitment of the reward system (operant learning for food). Firstly we compared the basal gene expression in the different neuronal populations characterized by the expression of D1 or D2 receptors and their regional localization. We identified hundreds of differentially expressed mRNA providing a precise characterization of the cellular and regional differences. In the second part, we characterized the changes induced in each neuronal population by a 1-week exposure to cocaine or after operant training for food
Besson, Morgane. "Rôle des récepteurs nicotiniques neuronaux de l'acétylcholine dans la dépendance à la nicotine." Paris 6, 2006. http://www.theses.fr/2006PA066445.
Roeckel, Laurie-Anne. "Le récepteur opioïde Mu et les interactions entre systèmes opioïde et cannabinoïde dans les effets nociceptifs et addictogènes de la morphine." Thesis, Strasbourg, 2018. http://www.theses.fr/2018STRAJ012.
The opioid system controls pain and reward, and the Mu opioid receptor plays a central role in these effects. In the first part of the thesis, we showed that Mu receptor is also involved in the development of hyperalgesia induced by chronic opiate exposure. In the second part of the thesis, we studied the impact of opioid and cannabinoid interactions on effects associated to chronic morphine administration. We explored the effects of a pretreatment with a CB1 cannabinoid receptor selective agonist, arachidonyl-2-chloroethylamide (ACEA), on morphine-associated nociceptive, withdrawal, reward and naturalistic behaviors. To complete this behavioral study, we performed transcriptional and functional analyses to identify the neuroadaptative processes involved. Our study demonstrates that dual activation of CB1 and Mu receptors has a beneficial effect on behavioral parameters related to addiction, pointing to potential usefulness of combining both medications for therapeutic interventions
Asri, Layla El. "Learning the Parameters of Reinforcement Learning from Data for Adaptive Spoken Dialogue Systems." Thesis, Université de Lorraine, 2016. http://www.theses.fr/2016LORR0350/document.
This document proposes to learn the behaviour of the dialogue manager of a spoken dialogue system from a set of rated dialogues. This learning is performed through reinforcement learning. Our method does not require the definition of a representation of the state space nor a reward function. These two high-level parameters are learnt from the corpus of rated dialogues. It is shown that the spoken dialogue designer can optimise dialogue management by simply defining the dialogue logic and a criterion to maximise (e.g user satisfaction). The methodology suggested in this thesis first considers the dialogue parameters that are necessary to compute a representation of the state space relevant for the criterion to be maximized. For instance, if the chosen criterion is user satisfaction then it is important to account for parameters such as dialogue duration and the average speech recognition confidence score. The state space is represented as a sparse distributed memory. The Genetic Sparse Distributed Memory for Reinforcement Learning (GSDMRL) accommodates many dialogue parameters and selects the parameters which are the most important for learning through genetic evolution. The resulting state space and the policy learnt on it are easily interpretable by the system designer. Secondly, the rated dialogues are used to learn a reward function which teaches the system to optimise the criterion. Two algorithms, reward shaping and distance minimisation are proposed to learn the reward function. These two algorithms consider the criterion to be the return for the entire dialogue. These functions are discussed and compared on simulated dialogues and it is shown that the resulting functions enable faster learning than using the criterion directly as the final reward. A spoken dialogue system for appointment scheduling was designed during this thesis, based on previous systems, and a corpus of rated dialogues with this system were collected. This corpus illustrates the scaling capability of the state space representation and is a good example of an industrial spoken dialogue system upon which the methodology could be applied
Gueye, Aliou. "Alimentation durant l'adolescence : facteurs de troubles comportementaux et neurobiologiques à l'âge adulte : modèle animal chez le rat." Thesis, Bordeaux 2, 2010. http://www.theses.fr/2010BOR21805/document.
Adolescent diet often contains an excessive amount of palatable food with high caloric and sugar contents. Clinical and epidemiological data show that overconsumption of these large foods and sugar beverage consumption may have consequences in adolescence during which the brain is still maturing.Several studies have shown that sugar overconsumption during adolescence have long lasting effect of disease incidence such as obesity, diabetes … However, little is known in the long lasting effect of behavior disorder related to sugar overconsumption early in life. Therefore we set up an animal model to investigate the long lasting effect of sugar overconsumption during adolescence (PND 30 - 46) in neurobiological and behavioral alterations at adulthood. Our results reveal that chronic free access to sugar during adolescence decreases motivation and induce a vertical downshift of dose response curve for natural sweet and no sweet solution at adulthood with no behaviour consequences for pharmacological reward such as cocaine. These behavioral alterations are specific: 1) to the 5% sucrose concentration which is the more rewarding dose in our rats; 2) to a long access to 5% sucrose because only these alterations of behavior are observed after 12h et 24h/day access but not after 2h/day access; 3) to the sweet taste of the solution exposure during adolescence but not to its caloric effect since saccharine (a no caloric and sweet solution) induces these behavioral alterations; 4) to the adolescent period because we show no effect when adult rats have access to a sucrose solution; 5) is not dependent on the rearing conditions during adolescence since singly housed or group housed rats show the same behavioural disorder. We also show that these long lasting behavioral alterations to palatable foods are associated to anxiogenic-like behaviors and a depressive-like state evaluated in the Novelty suppressed feeding test and the forced swimming test respectively. Chronic imipramine treatment from the end of adolescence onwards (PND 47) prevents this behavioral disorder. Immunohistochemical studies show that sucrose exposure during adolescence decreases neurogenesis in the dentate gyrus of the hippocampus and imipramine treatment restores this deficit. These results suggest the importance of diet during adolescence in the development of neuropsychiatric disorders at adulthood. Given our high sweet environment, all these data suggest that considerable effort must be conducted to control early life initiation of sugar
Asri, Layla El. "Learning the Parameters of Reinforcement Learning from Data for Adaptive Spoken Dialogue Systems." Electronic Thesis or Diss., Université de Lorraine, 2016. http://www.theses.fr/2016LORR0350.
This document proposes to learn the behaviour of the dialogue manager of a spoken dialogue system from a set of rated dialogues. This learning is performed through reinforcement learning. Our method does not require the definition of a representation of the state space nor a reward function. These two high-level parameters are learnt from the corpus of rated dialogues. It is shown that the spoken dialogue designer can optimise dialogue management by simply defining the dialogue logic and a criterion to maximise (e.g user satisfaction). The methodology suggested in this thesis first considers the dialogue parameters that are necessary to compute a representation of the state space relevant for the criterion to be maximized. For instance, if the chosen criterion is user satisfaction then it is important to account for parameters such as dialogue duration and the average speech recognition confidence score. The state space is represented as a sparse distributed memory. The Genetic Sparse Distributed Memory for Reinforcement Learning (GSDMRL) accommodates many dialogue parameters and selects the parameters which are the most important for learning through genetic evolution. The resulting state space and the policy learnt on it are easily interpretable by the system designer. Secondly, the rated dialogues are used to learn a reward function which teaches the system to optimise the criterion. Two algorithms, reward shaping and distance minimisation are proposed to learn the reward function. These two algorithms consider the criterion to be the return for the entire dialogue. These functions are discussed and compared on simulated dialogues and it is shown that the resulting functions enable faster learning than using the criterion directly as the final reward. A spoken dialogue system for appointment scheduling was designed during this thesis, based on previous systems, and a corpus of rated dialogues with this system were collected. This corpus illustrates the scaling capability of the state space representation and is a good example of an industrial spoken dialogue system upon which the methodology could be applied
Leonetti, Maud. "Régulation in vivo de l'efflux de dopamine dans le système mésocorticolimbique par la neurotensine et les neuroleptiques : étude par des approches neurochimiques chez le rat." Lyon 1, 2002. http://www.theses.fr/2002LYO1T095.
Miguet, Maud. "Adaptations nutritionnelles à l'activité physique chez l'adolescent en situation d'obésité : implication du système cognitif." Thesis, Université Clermont Auvergne (2017-2020), 2019. http://www.theses.fr/2019CLFAC064.
A large body of evidence supports the beneficial effects of exercise, favoring physiological, psychological and social improvements. Recent studies also suggest that exercise may be implicated in the control of appetite and energy intake, which remains to be further explored. These compensatory mechanisms, occurring after exercise, could be responsible for a limited weight loss achievement. Understanding the relation between exercises and eating behavior is a main priority. In this context, the purpose of this work was to explore the nutritional responses to physical activity in adolescents with obesity. In particular, we questioned the mechanisms that can explain the interactions between exercise and food intake. Different exercise modalities have been questioned and the physiological and neurocognitive pathways involved in the post-exercise regulation of energy intake were explored during and in response to multidisciplinary weight loss programs. During the first months of weight loss achievement, results indicate increase in compensatory mechanisms leading to higher appetite sensations, food reward and ad libitum energy intake. This phase of "weight loss resistance" was higher in adolescents with high level of cognitive restriction. Finally, the extension of the weight loss program results in a phase of stabilization and improvement of the control of energy intake. During this second phase, sensations of appetite, food reward, emotional and external eating as well as ad libitum energy intake decreased. In conclusion, physical activity appears to favor the reconnection between the hedonic system and the homeostatic system control of food intake
Nicolas, Céline. "Étude des modifications à long terme induites par la prise chronique de cocaïne : approches anatomique, métabolique et comportementale." Thesis, Poitiers, 2014. http://www.theses.fr/2014POIT2334/document.
Drugs addiction is a chronic brain disorder representing a major public health problem. Although important advances allowed a better understanding of the cerebral modifications induced by chronic exposure to drugs, the therapies still nowadays limited. Therefore the investigation of cerebral processes that underlie the persistent risks of relapse, seem to be crucial to offer new therapeutic strategies. A part of this thesis aims at investigating the cerebral modifications induced in a long term during the withdrawal, due to a chronic voluntary intake of cocaine. In our first study we found a reduction of the density of cerebral vessels during the early withdrawal selectively localized in the cingular cortex. In our second study we found that cocaine intake leads to modifications of cerebral metabolism that evolve during the withdrawal. After one month of withdrawal, at a time when the phenomenon of incubation of craving is found, we found a decrease in cortical and striatal metabolism and a hyperactivation of the amygdala which demonstrates a persistent disregulation of brain functioning. Finally, in our third study, we tried to dissect the mechanism underlying the anti-craving effect of the enriched environment (EE). We hypothesized that the EE acts as an alternative reward to decrease the cocaine seeking behavior. Thus we tested the effects of exposure to sucrose or the physical exercise on relapse to cocaine. We demonstrated that the access to an alternative reward during the withdrawal does not allow reducing cocaine seeking which suggests that the EE does not act exclusively as an alternative reward
Berland, Chloé. "Triglyceride-sensing in the mesocorticolimbic system and reward-driven behaviour control." Thesis, Sorbonne Paris Cité, 2018. https://theses.md.univ-paris-diderot.fr/Berland_Chloe_2_va_20180911.pdf.
Obesity spreading is due to an imbalance of energy homeostasis, with excessive consumption of sweet and fat food, and sedentary lifestyles. Food intake partly depends on dopamine release in the mesocorticolimbic system, and calorie-rich hedonic food, among other objects of desire, stimulate this reward circuit. Dopaminergic release in the mesocorticolimbic system is a main factor for compulsive feeding, and calorie-rich food could be responsible for abnormal feeding behaviours, where excessive food intake is assimilated to MCL malfunctions similar to drugs addiction. More particularly, postprandial triglycerides represent a major source of dietary lipids, and obesity is often associated with hypertriglyceridemia, but also with dopaminergic signalling impairments. Mesocorticolimbic system neurons express several enzymes involved in triglycerides hydrolysis, such as the lipoprotein lipase, suggesting an ability to sense triglycerides and modulate their activity accordingly. The aim of this thesis is to identify cellular and molecular mechanisms by which dietary triglycerides act onto dopaminergic structures and control food intake
Piccin, Alessandro. "Role of the CRF system in the rewarding and motivational effects of morphine." Thesis, Bordeaux, 2018. http://www.theses.fr/2018BORD0414.
The neurobiology underlying poor social behavior of opiate users and dependent individuals remains largely unknown, hampering the development of noveleffective therapies for opiate use disorders. However, recent pre-clinical evidence suggests that the corticotropin-releasing factor (CRF) system might be involved.In this light, we employed the three-chamber (3-CH) task and genetic/pharmacological approaches to assess the impact of morphine administrationand withdrawal upon social behavior in mice with regard to the CRF system. In a first set of experiments, we found that male subjects displayed increasedhostility-driven pseudo-social interest during opiate withdrawal, indicative of longlasting effects of chronic drug administration upon normal social functioning. On theother hand, female subjects displayed lower social interest during opiate withdrawal, a phenotype that more straightforwardly replicates what observed in humans.Notably, CRF1 receptor-deficiency completely rescued the latter social deficit, adding to the growing evidence linking the CRF system to substance-induced behavioraldysfunctions. In a second set of experiments, we investigated the initial effects of morphine more widely on naturally” rewarding activities. We found that a single, acuteadministration of a relatively low dose of the drug was sufficient to produce brain reward and at the same time to induce profound deficits in social interest and fooddriven motivation, providing initial experimental evidence of “hijacking” of brain reward systems by substances of abuse. Interestingly, systemic administration of the CRF receptor antagonist antalarmin completely reversed the latter social deficit, indicating a critical role of the CRF system in mediating substance-induced decreased interest for “naturally” rewarding activities and strengthening the notion of a therapeutic potential for CRF-targeting pharmacological agents
Faton, Sina. "Le récepteur 5-HT2c : lien entre activité locomotrice et prise alimentaire." Thesis, Montpellier, 2016. http://www.theses.fr/2016MONT3508/document.
Central serotonin systems have long been associated with the control of ingestive behavior, and the modulation of behavioral effects of psychostimulants.The 5-HT2C receptor is present in hypothalamic centers particularly the arcuate nucleus (ARC) controlling homeostatic regulation of food intake as well as in the ventral tegmental area (VTA), a region important for motivational aspects of multiple behaviors, including feeding.In the present study, the hypothesis was tested that the 5-HT2CR in the VTA may control amphetamine-evoked locomotor activity and 5-HT2CR in the ARC may regulate food consumption. Localized microinjections into the VTA or into the ARC were used to assess the effects of a highly selective 5-HT2C agonist, AR231630, on the locomotor stimulant effect of amphetamine as well as food intake. In the tests for locomotor activity, AR231630 into the VTA, but not into the ARC, dose-dependently reduced locomotor activity elicited by amphetamine. Unexpectedly, in tests for food intake, intra-ARC injection of AR231630 did not reduce food intake even at doses of 10ug, whereas intra-VTA injection of 10ug AR231630 did. A subsequent experiment determined that the suppressant effect of peripheral administration of AR231630 (5 mg/kg) on feeding was partially reversed by pretreatment with the selective 5-HT2CR antagonist SB242084 into the VTA (5ug). These findings suggest that 5-HT2CR in the VTA participates in both food intake and brain reward function, and possibly through the same pathway
Varazzani, Chiara. "Motivation and behavioural energization : exploring the motivational brain in the reward/effort tradeoff." Thesis, Sorbonne Paris Cité, 2015. http://www.theses.fr/2015USPCB116.
There is perhaps no more critical factor for the behaviour of an animal than the way it chooses between action and inaction. A simple way to formalise such choices is to evaluate the predicted benefit (e.g. food, money) and costs (e.g. punishments, losses, delays) associated with each action and optimise the rates at which rewards are received and costs avoided. Our motivation to perform a given action depends upon such value ratio. In the current behavioural economics literature, the optimisation of the benefits/costs ratio stands as the fundamental principle that regulates and explains agents’ behaviour. In my Ph.D. studies, I implement a realistic model of such concepts from behavioural economics by using an empirical type of cost: physical effort. In our everyday life, if we are asked to choose between two options that imply the same reward but different efforts (e.g., working 3 or 7 days per week for the same salary), we usually opt for the alternative that requires the slightest energy expenditure, thus the least effort. However, physical effort has been far less studied compared to other decision costs such as delay or uncertainty. The present Ph.D. work aims at highlighting the neuronal bases of such reward/effort tradeoff. Understanding how effort cost affects the discounting of potential rewards has a clear significance for economic decisions and clinics, since the reduced willingness to exert effort is a key signature of several clinical disorders such as apathy and depression We suggest that disorders such as apathy could result from two different behavioural processes: (a) a decreased responsiveness to future benefits and/or (b) an excessive sensitivity to potential costs. For instance, when asked why they would not go see a movie they like, patients may say that (a) the movie is not good enough (i.e. low responsiveness to expected value) or that (b) the theatre is too far away (i.e. high sensitivity to anticipated effort). To test our hypothesis, we combined behavioural tasks and pharmacological approach with neuron recordings in monkeys, targeting specifically two majors actors of the rewarding and effort system, dopamine and noradrenaline. We found that dopamine and noradrenaline have distinct but complementary roles. On the one hand, dopamine tracks the reward value of future outcomes and orient the behaviour towards the least effortful options. On the other hand, noradrenaline enables subjects to face the effort at hand, reducing the sensitivity to anticipated effort. Using a pharmacological approach, we found that, when we increase noradrenaline, monkeys exerted significantly more effort. Moreover, we have found that local field potentials in the ventromedial prefrontal cortex recorded in the same task encode the expected value and predict action selection. In summary, this Ph.D. work allows to disentangle some of the neuronal circuits implicated in the computation of the reward/effort tradeoff, mainly encoded by dopaminergic neurons and in the local field potential of the ventromedial prefrontal cortex. On the other hand, this work highlights the role of noradrenaline in the energization of behaviour to face the challenge represented by the physical effort
Fillon, Alicia. "Optimisation des stratégies interdisciplinaires de prise en charge de l'obésité pédiatrique : de l'évaluation clinique aux effets du Timing exercice-repas sur le comportement alimentaire de l'adolescent en situation d'obésité." Thesis, Université Clermont Auvergne (2017-2020), 2020. http://www.theses.fr/2020CLFAC063.
The rise of pediatric overweight, obesity and of their metabolic complications calls for the development of innovative, effective and integrative weight management strategies. Physical exercise is an essential component of multidisciplinary weight loss interventions that is no longer considered as a simple source of additional energy expenditure but is now recognized for its potential effects on energy intake (EI) and appetite control. The aim of the present work was to assess the effect of the exercise-meal timing (TIMEX program, for Timing Meal - Exercise) on energy intake, appetite sensations and food reward in adolescents with obesity. Based on our results, it would seem beneficial to encourage exercise close to the meal, which will also depend on the time between the exercise and the preceeding meal. Furthermore, our results suggest that these nutritional adaptations to exercise can be further optimized through a timing - intensity interaction, with a potentiated effect through high intensity exercise. As our experimental studies are the first in adolescents with obesity, they call for further works to confirm the present results. However, it seems essential today to consider the timing of exercise as an essential element of our physical activity prescriptions in order to empower our interventions among adolescents with obesity
Marion, Candice. "Novel insights on ghrelin receptor signaling in energy homeostasis and feeding behavior using the GhsrQ343X mutant rat model." Thesis, Sorbonne Paris Cité, 2017. http://www.theses.fr/2017USPCB109.
The stomach-derived hormone acyl ghrelin promotes body weight gain, mostly in the form of fat mass, by means of several central and peripheral mechanisms mediated by the growth hormone secretagogue receptor (GHSR). The GHSR is a G protein-coupled receptor that, in addition to respond to acyl ghrelin, displays agonist-independent signaling through high constitutive activity and possibly heteromerization with dopamine receptors. Despite the potent biological properties of exogenous acyl ghrelin, the lack of animal models able to apprehend the complexity of the acyl ghrelin-GHSR system in vivo has been hampering the elucidation of its physiological roles. Indeed, genetic mouse models generated so far lack specificity either at the level of the hormone (not able to discriminate between acyl ghrelin versus desacyl ghrelin) and/or at the level of the GHSR (not able to discriminate between GHSR signaling modes). In this context, new models differentially affecting GHSR signaling pathways would represent valuable tools to decipher the acyl ghrelin-GHSR system in vivo. We therefore aimed at characterizing a new rat model carrying a point mutation in Ghsr that predicts truncation of a regulatory domain in the C-terminus, the GhsrQ343X mutation. In cellular models, this mutation was found to uncouple the GHSR from agonist-dependent receptor internalization and β-arrestin recruitment, while enhancing GHSR responsiveness in the G protein pathway. Accordingly, homozygous mutant GhsrM/M rats show enhanced responsiveness to exogenous GHSR agonists in terms of growth hormone release, food intake and locomotor activity. Physiological and behavioral exploration of GhsrM/M rats supports that the GhsrQ343X mutation is associated with increased body weight gain and adiposity independently of calorie intake, reduced whole-body fat oxidation, metabolic flexibility and glucose tolerance, without any critical impact on homeostatic feeding behavior. Moreover, given that circulating ghrelin levels are not increased by the GhsrQ343X mutation, the overall metabolic phenotype of GhsrM/M rats is consistent with enhanced GHSR sensitivity to the endogenous tone of acyl ghrelin. Furthermore, preliminary results suggest that the GhsrQ343X mutation could be associated with behavioral alterations related to reward and memory functions, through mechanisms that remain to be elucidated. Altogether, we propose the GhsrQ343X mutant rat model as a novel tool, more specific than knockout mouse models in its mechanism-of-action, to explore GHSR signaling across biological functions in vivo, and ultimately help in the design of efficient GHSR-targeting drugs
Fakhoury, Marc. "Diencephalic and Mesencephalic Substrate for Brain Stimulation Reward." Thèse, 2018. http://hdl.handle.net/1866/21593.