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Auswahl der wissenschaftlichen Literatur zum Thema „Stress par défaite sociale“
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Zeitschriftenartikel zum Thema "Stress par défaite sociale"
Hotta, Miho. „The development of social psychology in japan and its political context/[le développement de la psychologie sociale au japon et son contexte politique]“. Sociétés contemporaines 13, Nr. 1 (01.01.1993): 113–19. http://dx.doi.org/10.3917/soco.p1993.13n1.0113.
Der volle Inhalt der QuelleThibouville, Grégoire, und André Sirota. „De l’absence de répondant à la défaite du récit des origines à l’adolescence“. Connexions 119, Nr. 1 (30.11.2023): 137–48. http://dx.doi.org/10.3917/cnx.119.0137.
Der volle Inhalt der QuelleHenderson, F., V. Vialou, S. El Mestikawy und V. Fabre. „Modifications des états de vigilance suite à un stress psychosocial : la défaite sociale“. Médecine du Sommeil 15, Nr. 1 (März 2018): 41. http://dx.doi.org/10.1016/j.msom.2018.01.108.
Der volle Inhalt der QuelleBordat, Élodie M. „« Les héros ne sont le patrimoine unique de personne ». Les enjeux des célébrations du Bicentenaire de l’Indépendance et du Centenaire de la Révolution mexicaine de 2010“. Revista Trace, Nr. 63 (05.10.2016): 60. http://dx.doi.org/10.22134/trace.63.2013.77.
Der volle Inhalt der QuelleUbéda-Saillard, Muriel. „La prévention de la guerre civile par le droit et les institutions“. Pouvoirs N° 188, Nr. 1 (22.01.2024): 61–71. http://dx.doi.org/10.3917/pouv.188.0061.
Der volle Inhalt der QuelleTaleb, M. „Adversité sociale et troubles psychotiques“. European Psychiatry 29, S3 (November 2014): 630–31. http://dx.doi.org/10.1016/j.eurpsy.2014.09.134.
Der volle Inhalt der QuelleVEISSIER, I., und M. MIELE. „Petite histoire de l’étude du bien-être animal : comment cet objet sociétal est devenu un objet scientifique transdisciplinaire“. INRA Productions Animales 28, Nr. 5 (14.01.2020): 399–410. http://dx.doi.org/10.20870/productions-animales.2015.28.5.3042.
Der volle Inhalt der QuelleTERLOUW, E. M. C. „Stress des animaux et qualités de leurs viandes. Rôles du patrimoine génétique et de l’expérience antérieure“. INRAE Productions Animales 15, Nr. 2 (12.04.2002): 125–33. http://dx.doi.org/10.20870/productions-animales.2002.15.2.3693.
Der volle Inhalt der QuelleKato, Satoshi. „Troubles mentaux liés au Covid-19, au Japon, en 2020“. Perspectives Psy 60, Nr. 3 (Juli 2021): 281–90. http://dx.doi.org/10.1051/ppsy/2021603281.
Der volle Inhalt der QuelleΦραγκίσκος, Εμμ Ν. „Ιχνηλατήσεις στις σελίδες της αλληλογραφίας Κοραή“. Gleaner 28 (30.12.2011): 211. http://dx.doi.org/10.12681/er.134.
Der volle Inhalt der QuelleDissertationen zum Thema "Stress par défaite sociale"
Chouvaeff, Mathilde. „Régulation du sommeil paradoxal en condition de stress : implication des projections corticales au noyau préoptique ventrolatéral“. Electronic Thesis or Diss., Université Paris sciences et lettres, 2024. http://www.theses.fr/2024UPSLS023.
Der volle Inhalt der QuelleAlthough much attention has been dedicated to dissect the complex circuits underlying basic sleep architecture, how sleep centers dynamically adapt to environmental challenges remains to be fully understood. The objective of this thesis was to determine, in mice, how and by which mechanisms sleep is influenced by stress.The first part of my thesis demonstrates that the social defeat stress (SDS) induces an initial state of insomnia before sleep quantities return to normal. Beside this apparent recovery, mice showed a REM sleep fragmentation that persisted many hours after SDS. Using chemogenetic inhibition, we demonstrated that prefrontal cortex (PFC) projections to the VLPO are selectively recruited under stressful situations and necessary for the SDS-induced REM sleep fragmentation. We further demonstrate that the optogenetic activation of the PFC- VLPO pathway is sufficient to mimic the REM sleep fragmentation in the absence of an actual stressor. Finally, using ex vivo optogenetics, we precise the cellular mechanism underlying this pathway by showing that the PFC directly modulates VLPO sleep-promoting neurons. Consistent with that, we show that in vivo activation of the PFC-VLPO pathway interrupts REM sleep in favor of NREM sleep, which is in line with the well established role of the VLPO. Altogether these results provide a mechanism to shorten the time spent in REM sleep, a state of great vulnerability, allowing the individual to be more responsive and ready to face a danger, without suppressing the total amount of sleep, essential for survival.In the second part of my work, we showed that the CRH-expressing neurons (VLPOCRH) were a predilection target from the PFC excitatory projections. We then investigated the role of the VLPOCRH neurons in basal sleep regulation. Our results highlight that activation of the VLPOCRH neurons strongly suppress REM sleep, favoring a more consolidated NREM sleep. However, chemogenetic inhibition of the VLPOCRH neurons had no effect on the sleep architecture.The third, and last part, of my work sought to establish a novel method to accurately and automatically classify REM sleep. Indeed, previous parts of my thesis highlighted that stress can cause REM sleep bouts to be particularly short. These brief periods can be overlooked by classical scoring methods. We developed an approach capable of capturing these fine sleep modifications and tracking parameters that can be usually subjective with manual scoring, thus ensuring maximal reproducibility
Martin, Vincent. „Rôle du récepteur 5-HT3 dans la physiopathologie de la dépression et son traitement“. Thesis, Sorbonne Paris Cité, 2016. http://www.theses.fr/2016USPCB022.
Der volle Inhalt der QuelleSSRI (selective serotonin reuptake inhibitor) antidepressants are among the most prescribed drugs to treat major depression. However, their efficacy is not optimal yet. Indeed, they possess a long delay of action, various side effects and show not efficacy in some patients. As depression is currently a global burden, there is a great need for new molecules with a better therapeutic efficacy. Recently, an increased attention has been taking to 5-HT3 receptors, notably since the development of vortioxetine, a new generation SSRI that antagonizes this receptor. The aim of the study was to assess the role of 5-HT3 receptor in the antidepressant response and the physiopathology of depression. In this context, we used a genetic approach, by characterizing a knockout (KO) mice model lacking the 3A subunit of the 5-HT3 receptor. Their phenotype and the one of wild-type (WT) control mice was first evaluated in behavioral tests widely used for antidepressant and anxiolytic drugs screening, then following acute SSRI treatments. Effect of chronic SSRI administration was assessed by in vitro electrophysiology. Finally, mice were submitted to the chronic social defeat stress (CSDS) model, to determine the role of 5-HT3 receptor in stress response. In basal conditions, 5-HT turnover was decreased in 5-HT3 KO mice compared with WT mice. This effect was accompanied by an increase in the 5-HT1A receptor gene expression and their coupling to G proteins at the dorsal raphe nucleus (DRN) level. 5-HT3 KO mice displayed anxiolytic-like and antidepressive-like phenotype. When injected with citalopram, a very selective SSRI, 5-HT3 KO mice behaved similarly as WT mice in antidepressant screening tests. However, in the same tests, the effect of fluoxetine, a SSRI that possesses 5-HT3 receptor antagonist properties, was blunted in 5-HT3 KO mice. Chronic treatment with citalopram (20 mg/kg/d) induced in WT and KO mice a similar desensitization of 5-HT1A autoreceptors located on DRN 5-HT neurons. In the same conditions, but using a lower citalopram dose (5 mg/kg/d), 5-HT1A autoreceptor desensitization was higher in 5-HT3 KO mice than in WT mice, thus reinforcing the potentiating effect of the 5-HT3 receptor in the SSRI efficacy. In order to assess the role of 5-HT3 receptor in chronic stress response, CSDS paradigm was validated using agomelatine, a new generation antidepressant drug. This stress model provoked long term memory alterations, linked with modifications in hippocampal mRNA levels of BDNF exon IV and epigenetic modifying enzymes. These deleterious stress effects were prevented by chronic agomelatine treatment (50 mg/kg/d), but this molecule did not modify the stress-induced anxious- and depressive-like phenotypes. We showed that subunit 3A gene expression was increased in various WT mice brain structures subjected to CSDS. Moreover, stress-induced modifications of CamkIIa and SOD1 gene expression in the prefrontal cortex of WT mice were not present in KO mice. Genetic invalidation of 5-HT3 receptor blocked the effects of social stress in some behavioral tests (splash test, saccharine preference test) and on body weight gain. Taken altogether, these data show that 5-HT3 receptor plays an important role in anxiety- and depression-related behaviors. Moreover, invalidation of this receptor increased the effect of a low dose chronic SSRI treatment, and blunted the effect of a SSRI targeting 5-HT3 receptor. These results highlight the interest of this receptor in the development of innovating therapies to treat anxio-depressive disorders. Finally, the reduced sensitivity of 5-HT3 KO mice to chronic stress suggests an involvement of this receptor in stress-related behaviors and depression physiopathology
Larrieu, Thomas. „Impact d’une déficience en acides gras polyinsaturés (AGPI) de la série n-3 sur les comportements émotionnels et la plasticité cérébrale chez la souris“. Thesis, Bordeaux 2, 2012. http://www.theses.fr/2012BOR22000/document.
Der volle Inhalt der QuelleLow dietary intake of n-3 polyunsaturated fatty acids (PUFAs) has been associated with the prevalence of mood disorders in humans. In rodents, nutritional approaches aiming at modeling poor dietary n-3 PUFAs intake have been extensively developed in the last century. As a result, one- or multi-generation dietary n-3 deficiency induces depressive and anxiety-like behaviors. We have shown in the Nutrineuro lab that mice fed with a diet deficient in n-3 PUFAs exhibit decreased n-3 PUFAs levels, especially docosahexaenoic acid (DHA, a n-3 PUFA) levels in the prefrontal cortex (PFC) and in the nucleus accumbens (NAc). We showed that dietary n-3 PUFA is able to modulate endocannabinoid (eCB) dependent plasticity since DHA reduction in PFC and NAc is accompanied with eCB dependent long term depression (eCB-LTD) and eCB signaling impairment in the PFC (Lafourcade et al., 2011; Larrieu et al., 2012). Our data indicate that LTD alteration results from region-specific uncoupling of CB1 receptor from its effector Gi/o protein. In addition, n-3 deficient mice display behavioral deficits in several tests measuring emotional behavior. To further understand the mechanisms underlying DHA decrease in the PFC and emotional behavior alteration, we thoroughly investigated neuronal morphology and hypothalamic-pituitary-adrenal (HPA) axis in n-3 deficient mice. We showed that n-3 deficient diet induced dendritic atrophy in pyramidal neurons within the PFC. The dendritic atrophy was comparable to the one measured in control diet mice submitted to chronic social defeat stress (CSDS). No additional effect of CSDS on both neuronal morphology and emotional behavior was measured in n-3 deficient mice. We therefore investigated the role of the HPA axis deregulation in the development of behavioral and neurobiological alterations of n-3 deficient mice. We found a decreased expression of glucocorticoid receptor (GR) in the PFC of n-3 deficient mice together with increased circulating levels of corticosterone. Collectively, we unraveled one crucial mechanism underlying n-3 deficiency-induced alterations. Our results show that low dietary n-3 PUFAs can alter eCB-dependent plasticity and neuronal dendritic atrophy within the PFC leading to emotional behavior impairment. Importantly, we further demonstrated that corticosterone elevation in n-3 deficient mice was involved in the n-3 deficiency-induced emotional behavior and dendritic arborization alterations
Sader, Myra. „Soutien social des collègues et stress au travail : une approche par l'analyse des réseaux sociaux“. Thesis, Toulon, 2018. http://www.theses.fr/2018TOUL2005.
Der volle Inhalt der QuelleThe literature on workplace stress often considers that people who lack social support tend to have higher levels of perceived stress. This is empirically confirmed, but it is not always taken into account and offers limited scope. Indeed, why do some employees have more access to social support? What renders support more available and more varied from one person to the other? These questions allow us to situate perceived social support, and more accurately the perceived support of colleagues, in a larger theoretical model, enhanced by social network theory. Through an explanatory model, the objective of this research is to explore the role of the positioning of the individual in the social network on perceived workplace stress. Based on a “complete network” data in a medium-sized IT services company, we used partial least squares to test our hypothesis (N = 343). The strength of ties affects stress through social support, such that people with stronger ties perceive more support and ultimately exhibit less stress. However, the direct link between strength and stress is not established. Bridging ties (supportive ties to other departments) negatively influence social support (a situation which increases stress) but also have a direct negative effect on stress. By stressing the role of social relationships as an antecedent of social support and stress, our results offer new potential managerial actions within organizations
Sader, Myra. „Soutien social des collègues et stress au travail : une approche par l'analyse des réseaux sociaux“. Electronic Thesis or Diss., Toulon, 2018. http://www.theses.fr/2018TOUL2005.
Der volle Inhalt der QuelleThe literature on workplace stress often considers that people who lack social support tend to have higher levels of perceived stress. This is empirically confirmed, but it is not always taken into account and offers limited scope. Indeed, why do some employees have more access to social support? What renders support more available and more varied from one person to the other? These questions allow us to situate perceived social support, and more accurately the perceived support of colleagues, in a larger theoretical model, enhanced by social network theory. Through an explanatory model, the objective of this research is to explore the role of the positioning of the individual in the social network on perceived workplace stress. Based on a “complete network” data in a medium-sized IT services company, we used partial least squares to test our hypothesis (N = 343). The strength of ties affects stress through social support, such that people with stronger ties perceive more support and ultimately exhibit less stress. However, the direct link between strength and stress is not established. Bridging ties (supportive ties to other departments) negatively influence social support (a situation which increases stress) but also have a direct negative effect on stress. By stressing the role of social relationships as an antecedent of social support and stress, our results offer new potential managerial actions within organizations
Bücher zum Thema "Stress par défaite sociale"
Derrière l'écran de la révolution sociale: Quand le monde de l'informatique et des SSII sert de laboratoire social et induit une précarisation par le haut. [Gémenos]: Res publica, 2010.
Den vollen Inhalt der Quelle findenBuchteile zum Thema "Stress par défaite sociale"
Legendre, Alain, und Virginie Grygielski. „Stress des enfants en crèche et perception de l'insertion sociale par les éducatrices“. In L'enfant dans le lien social, 87–92. Érès, 2003. http://dx.doi.org/10.3917/eres.zaouc.2003.01.0087.
Der volle Inhalt der QuelleCLAIRAY, Philippe. „Epidémies et pandémies : quelles leçons de l’histoire?“ In Les épidémies au prisme des SHS, 115–26. Editions des archives contemporaines, 2022. http://dx.doi.org/10.17184/eac.5997.
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