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La prise de décision est un processus adaptatif essentiel dont l’efficacité dépend de processus exécutifs, motivationnels, émotionnels et donc de l’intégrité de différents circuits cérébraux. Au sein d’une population saine, il existe des variabilités individuelles décisionnelles influencées par des facteurs génétiques, épigénétiques et environnementaux. De plus, de nombreuses pathologies mentales, neurobiologiques et neurodégénératives provoquent des altérations des processus décisionnels. Ainsi, déterminer des traits comportementaux et des substrats neurobiochimiques impliqués dans ce dysfonctionnement représente un intérêt majeur.Nous avons développé, chez la souris, un test de prise de décision, basé sur le test classiquement utilisé chez l’homme (l’Iowa Gambling Task), qui reproduit une situation incertaine, complexe et conflictuelle de choix : le Mouse Gambling Task (MGT). Grâce à une approche différentielle du comportement, nous avons observé des différences spontanées de capacités décisionnelles : certaines souris ont un comportement rigide et évitent toute pénalité (souris safe), d’autres ont un comportement exploratoire quitte à prendre des risques (souris risky), et une majorité des souris a un comportement intermédiaire (souris average). Nous avons ensuite révélé que les souris safe ont un comportement plus anxieux, une activation préfrontale plus faible que les autres groupes à l’issu du MGT, et un taux de sérotonine à l’état basal plus faible au niveau du cortex préfrontal. Les souris risky ont un comportement plus risqué dans plusieurs tests comportementaux et sont moins sensibles à la récompense. De plus, elles présentent un faible taux de sérotonine au niveau du cortex orbitofrontal ainsi qu’un taux de dopamine, noradrénaline et sérotonine plus important au niveau hippocampique.Afin de tester l’effet d’une modification de l’environnement sur les profils décisionnels caractérisés précédemment, nous avons réalisé le MGT sur un groupe de souris soumises soit à une dette aiguë de sommeil (DAS) soit à une dette chronique de sommeil (DCS). Nous avons alors montré qu’une DCS n’a pas d’effet sur les profils décisionnels mais qu’une DAS accentue ces profils décisionnels: les animaux safe deviennent d’autant plus rigides et évitent encore d’avantage les pénalités alors que les animaux risky choisissent systématiquement les options plus risquées, en adoptant un comportement rigide. Ces observations comportementales peuvent s’expliquer par un métabolisme sérotoninergique diminué au niveau du cortex orbitofrontal et augmenté au niveau hippocampique, ainsi que par un taux élevé de dopamine au niveau du striatum dorsal, structure cérébrale clé des processus d’automatisation.Par conséquent, le MGT permet de révéler, chez des souris consanguines saines, les caractéristiques comportementales et neurobiologiques individuelles de stratégies décisionnelles inadaptées pouvant être amplifiées par un stress environnemental. Ce modèle permettra, notamment, de déterminer les facteurs de vulnérabilité au développement de certaines psychopathologies (l’addiction et la dépression, par exemple) dont le manque de sommeil pourrait être un déclencheur ou un amplificateur. / Affective abilities that rely on the integrity of several neural circuits. In healthy subjects, inter-individual variability during decision-making exists due to genetic, epigenetic and environmental factors. Moreover, many psychiatric and neurobiological disorders are characterized by poor decision-making processes. Therefore, determining behavioral traits and neurobiological substrates involved in these processes is of major interest to unravel markers that could predict the emergence of neuropathologies.Based on the Iowa Gambling Task in humans, we developed a decision-making task in mice that assesses their ability to choose between several conflicting options under uncertainty. Thanks to a differential approach of mice’s behavior, we show that decision-making skills differed between mice: some mice exhibit a rigid behavior and avoid penalty (safe mice); others maintained exploratory behavior even if they took risks (risky mice); a majority of mice exhibit an intermediate behavior (average mice). We found that a combination of behavioral characteristics related to different psychopathologies in humans were specifically associated with extreme behavior in mice: safe mice exhibited a more anxious behavior, a lower prefrontal activation after the MGT than others subgroups of performance together with a lower basal rate of serotonin in the prefrontal cortex. Risky mice displayed a riskier behavior in various behavioral tasks, were less sensitive to reward, and had a lower basal rate of serotonin in the orbitofrontal cortex as well as a higher basal rate of serotonin, dopamine and noradrenaline in the hippocampus.To investigate the consequences of environmental changes on decision-making individual profiles, we performed the MGT on groups of mice either under Acute Sleep Dept (ASD) or under chronic sleep debt (CSD). We show that CSD didn't play any apparent effect but that ASD emphasized decision-making profiles: safe mice became drastically more rigid and avoided penalty; and risky mice chose systematically riskier options and developed rigid and unefficient decisions. These behavioral data could be explained by a decreased serotonin metabolism in the orbitofrontal cortex, an increase in the hippocampus and a high level of dopamine in the caudate putamen, the key brain area of habits.Therefore, in healthy inbred mice the MGT reveals individual inadapted decision-making strategies which are characterized by behavioral and neurobiological substrates exacerbated by an environmental stress. This paradigm also allows the determination of mice vulnerability to develop psychopathologies (e.g. depression, addiction) for which sleep debt could a trigger or a magnifier.

Após um trauma, características de resiliência protegem o indivíduo de desenvolver o transtorno de estresse pós-traumático (TEPT) ou outro transtorno mental. O TEPT é um transtorno mental e comportamental, caracterizado por alta morbidade e grandes prejuízos sociais. Resiliência é o processo de negociação, de manejo e de adaptação frente a uma situação de estresse significativo ou trauma. Acredita-se que fatores ambientais e neurobiológicos estejam envolvidos na capacidade de resiliência e no desenvolvimento de TEPT. Método: estudo transversal de casos e controles pareados por sexo e idade. Foram estudados 33 pacientes com TEPT e 33 controles saudáveis que sofreram trauma. Os instrumentos usados foram a Escala de Resiliência, o Questionário de Estilo Defensivo (DSQ), o Questionário de Trauma na Infância (CTQ) e o instrumento Parental Bonding (PBI). As variáveis biológicas estudadas foram cortisol sérico, Interleucina-6 (IL-6) e Interleucina-10 (IL-10) séricas. Resultado: Houve diferença significativa entre os grupos no fator I da escala de resiliência (p=0,019); nos mecanismos de defesas maduras, maiores em resilientes (p<0,001); no abuso emocional (p=0,001) e físico (p=0,003) durante a infância maior em pacientes com TEPT; e em níveis de IL-10 menores em TEPT (p=0,029). Os níveis de IL-6 e cortisol sérico não mostraram diferença significativa. Conclui-se que a resiliência e o trauma na infância parecem ter influência no desfecho de TEPT e que níveis reduzidos de IL-10 em pacientes com TEPT demonstram a alteração do sistema imune nesta patologia. / After a traumatic event, characteristics of resilience protect individuals from developing posttraumatic stress disorder (PTSD) or other mental conditions. PTSD is a mental and behavioral disorder characterized by high morbidity and significant social impairment. Resilience is the process of negotiating, handling and adapting to a highly stressful situation or trauma. Environmental and neurobiological factors are believed to be involved in the capacity for resilience and the development of PTSD. Method: Cross-sectional study of cases and controls matched for age and sex, consisting of 33 patients with PTSD and 33 healthy controls who experienced trauma. Instruments used were the Resilience Scale, Defense Style Questionnaire (DSQ), Childhood Trauma Questionnaire (CTQ) and the Parental Bonding Instrument (PBI). The biological variables studied were serum cortisol, Interleukin-6 (IL-6) and Interleukin-10 (IL-10) levels. Result: There was a significant intergroup difference in factor I of the resilience scale (p=0.019), with higher results in resilient subjects for mature defense mechanisms (p<0.001) and among patients with PTSD for emotional (p=0.001) and physical abuse (p=0.003) during childhood, as well as lower IL-10 levels for PTSD (p=0.029). No significant difference was recorded in serum cortisol and IL-6 levels. It was concluded that resilience and childhood trauma influence the outcome of PTSD and that lower IL-10 levels in patients with PTSD indicate immune system alterations in this pathology.

Após um trauma, características de resiliência protegem o indivíduo de desenvolver o transtorno de estresse pós-traumático (TEPT) ou outro transtorno mental. O TEPT é um transtorno mental e comportamental, caracterizado por alta morbidade e grandes prejuízos sociais. Resiliência é o processo de negociação, de manejo e de adaptação frente a uma situação de estresse significativo ou trauma. Acredita-se que fatores ambientais e neurobiológicos estejam envolvidos na capacidade de resiliência e no desenvolvimento de TEPT. Método: estudo transversal de casos e controles pareados por sexo e idade. Foram estudados 33 pacientes com TEPT e 33 controles saudáveis que sofreram trauma. Os instrumentos usados foram a Escala de Resiliência, o Questionário de Estilo Defensivo (DSQ), o Questionário de Trauma na Infância (CTQ) e o instrumento Parental Bonding (PBI). As variáveis biológicas estudadas foram cortisol sérico, Interleucina-6 (IL-6) e Interleucina-10 (IL-10) séricas. Resultado: Houve diferença significativa entre os grupos no fator I da escala de resiliência (p=0,019); nos mecanismos de defesas maduras, maiores em resilientes (p<0,001); no abuso emocional (p=0,001) e físico (p=0,003) durante a infância maior em pacientes com TEPT; e em níveis de IL-10 menores em TEPT (p=0,029). Os níveis de IL-6 e cortisol sérico não mostraram diferença significativa. Conclui-se que a resiliência e o trauma na infância parecem ter influência no desfecho de TEPT e que níveis reduzidos de IL-10 em pacientes com TEPT demonstram a alteração do sistema imune nesta patologia. / After a traumatic event, characteristics of resilience protect individuals from developing posttraumatic stress disorder (PTSD) or other mental conditions. PTSD is a mental and behavioral disorder characterized by high morbidity and significant social impairment. Resilience is the process of negotiating, handling and adapting to a highly stressful situation or trauma. Environmental and neurobiological factors are believed to be involved in the capacity for resilience and the development of PTSD. Method: Cross-sectional study of cases and controls matched for age and sex, consisting of 33 patients with PTSD and 33 healthy controls who experienced trauma. Instruments used were the Resilience Scale, Defense Style Questionnaire (DSQ), Childhood Trauma Questionnaire (CTQ) and the Parental Bonding Instrument (PBI). The biological variables studied were serum cortisol, Interleukin-6 (IL-6) and Interleukin-10 (IL-10) levels. Result: There was a significant intergroup difference in factor I of the resilience scale (p=0.019), with higher results in resilient subjects for mature defense mechanisms (p<0.001) and among patients with PTSD for emotional (p=0.001) and physical abuse (p=0.003) during childhood, as well as lower IL-10 levels for PTSD (p=0.029). No significant difference was recorded in serum cortisol and IL-6 levels. It was concluded that resilience and childhood trauma influence the outcome of PTSD and that lower IL-10 levels in patients with PTSD indicate immune system alterations in this pathology.

Após um trauma, características de resiliência protegem o indivíduo de desenvolver o transtorno de estresse pós-traumático (TEPT) ou outro transtorno mental. O TEPT é um transtorno mental e comportamental, caracterizado por alta morbidade e grandes prejuízos sociais. Resiliência é o processo de negociação, de manejo e de adaptação frente a uma situação de estresse significativo ou trauma. Acredita-se que fatores ambientais e neurobiológicos estejam envolvidos na capacidade de resiliência e no desenvolvimento de TEPT. Método: estudo transversal de casos e controles pareados por sexo e idade. Foram estudados 33 pacientes com TEPT e 33 controles saudáveis que sofreram trauma. Os instrumentos usados foram a Escala de Resiliência, o Questionário de Estilo Defensivo (DSQ), o Questionário de Trauma na Infância (CTQ) e o instrumento Parental Bonding (PBI). As variáveis biológicas estudadas foram cortisol sérico, Interleucina-6 (IL-6) e Interleucina-10 (IL-10) séricas. Resultado: Houve diferença significativa entre os grupos no fator I da escala de resiliência (p=0,019); nos mecanismos de defesas maduras, maiores em resilientes (p<0,001); no abuso emocional (p=0,001) e físico (p=0,003) durante a infância maior em pacientes com TEPT; e em níveis de IL-10 menores em TEPT (p=0,029). Os níveis de IL-6 e cortisol sérico não mostraram diferença significativa. Conclui-se que a resiliência e o trauma na infância parecem ter influência no desfecho de TEPT e que níveis reduzidos de IL-10 em pacientes com TEPT demonstram a alteração do sistema imune nesta patologia. / After a traumatic event, characteristics of resilience protect individuals from developing posttraumatic stress disorder (PTSD) or other mental conditions. PTSD is a mental and behavioral disorder characterized by high morbidity and significant social impairment. Resilience is the process of negotiating, handling and adapting to a highly stressful situation or trauma. Environmental and neurobiological factors are believed to be involved in the capacity for resilience and the development of PTSD. Method: Cross-sectional study of cases and controls matched for age and sex, consisting of 33 patients with PTSD and 33 healthy controls who experienced trauma. Instruments used were the Resilience Scale, Defense Style Questionnaire (DSQ), Childhood Trauma Questionnaire (CTQ) and the Parental Bonding Instrument (PBI). The biological variables studied were serum cortisol, Interleukin-6 (IL-6) and Interleukin-10 (IL-10) levels. Result: There was a significant intergroup difference in factor I of the resilience scale (p=0.019), with higher results in resilient subjects for mature defense mechanisms (p<0.001) and among patients with PTSD for emotional (p=0.001) and physical abuse (p=0.003) during childhood, as well as lower IL-10 levels for PTSD (p=0.029). No significant difference was recorded in serum cortisol and IL-6 levels. It was concluded that resilience and childhood trauma influence the outcome of PTSD and that lower IL-10 levels in patients with PTSD indicate immune system alterations in this pathology.

The master thesis deals with theories of temperament from the perspective of their linkages with biological essence of man. In theoretical chapters, it is examined how research of temperament has evolved over time, and there are presented the most important biology- oriented theories, ranging from classical antique temperaments, to Pavlov's differentiation of personalities according the reactivity of nervous system, and finally to Eysenck's, Gray's and Cloninger's modern theories of temperament. Empirical research is dedicated to the testing of interdependencies between temperamental questionnaires. 4Elements Inventory test based on an element approach theory and Cloninger's TCI-R test representing biological approach in temperament observation were analyzed on a research sample, and correlation and regression analysis was performed. If we have to assign the most similar dimensions of both tests to each other according to content analysis, we would expect relationships between the Harm Avoidance and Fire (negative), Novelty Seeking and Air, Reward Dependency and Water and Persistence and Earth. The relationship of Novelty seeking and Air (r = 0.73) and negative relationship of Harm Avoidance and Fire (r = -0.74) were confirmed as the strongest relationships. The correlation between Reward...

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This research project explores the contribution of prenatal stress to the pathogenesis of autism as a neurobiological developmental disorder. The neurobiological impact of stress prior to the 28th week of gestation might produce structural neural changes, specifically regarding the cerebellum, the brain stem and limbic pathways, including the hippocampal area, which concept relates closely to the pathogenesis of autism. In this research project a significant focus is placed on prenatal hipothalamic-pituary-adrenal (HPA) activity due to the HPA axis’ interactivity with cortisol, digoxin and serotonin, as these biochemicals are significantly implicated in programmed foetal development, postnatal cortical behaviour, postnatal learning, as well as in functional impairment of socialization, communication and imagery associated with autism. Based upon the rationale of this research project and the conceptualisation of the topic of interest, the research problem was formulated as follows: In what unique ways does prenatal stress contribute to the pathogenesis of autism as a neurobiological developmental disorder? Sub questions included: Did the mother of the dizygotic twins experience significant stress during the period of gestation? What structural brain differences can be observed among the dizygotic twins at hand of MR-imaging? To which periods of prenatal development can these structural differences be related? How do these differences account for sensory, motor, cognitive, and affective behavioural differences among the dizygotic twins? What plasma differences can be observed among the dizygotic twins at hand of blood sampling? How does elevation of pre- and postnatal glucocorticoids relate to plasma difference among the dizygotic twins? How do these plasma differences account for sensory, motor, cognitive, and affective behavioural differences among the dizygotic twins? This research project represents quantitative research. The mode of inquiry is non-experimental at hand of a single dizygotic twin study. The following data generating strategies were employed: clinical intake interviews, administration of a diagnostic stress inventory and the 16-PF Questionnaire, MR-imaging, and the collection of blood plasma pathology results. / Dissertation (M.Ed)--University of Pretoria, 2006. / Educational Psychology / unrestricted

Le comportement humain est à la fois singulier et universel. La singularité serait principalement due aux trajectoires de vie propre à chaque individu (variant entre autres selon leur culture) alors que l’universalité émanerait d’une nature universelle ancrée dans un génome universel. Démêler les influences de la nature et de la culture sur le comportement humain est le Saint Graal de l’anthropologie biologique. J’aborde cette question en explorant les effets génétiques et environnementaux sur les bases psychiques du comportement. Plus particulièrement, je teste l’hypothèse que la singularité et l’universalité comportementales humaines s’observent au plan psychique par l’exploration de leur substrat neurobiologique, et que ce substrat possède à la fois un ancrage génétique et environnemental. À l’aide de données d’imagerie par résonance magnétique fonctionnelle (IRMf) recueillies auprès de 862 participants du Human Connectome Project (HCP), j’analyse les activations cérébrales liées à sept tâches socio-cognitives qui recoupent diverses facultés, dont le langage, la mémoire, la prise de risque, la logique, les émotions, la motricité et le raisonnement social. Après avoir groupé les sujets selon la similarité de leurs patrons d’activation cérébrale (c.-à-d. leurs sous-types neurobiologiques), j’estime l’influence génétique et environnementale sur la variabilité interindividuelle de ces divers sous-types. Les résultats démontrent bel et bien l’existence d’un regroupement des sujets selon la similarité de leurs cartes d’activation cérébrale lors d’une même tâche socio-cognitive, ce qui reflète à la fois le caractère singulier et universel des corrélats neuronaux d’un comportement observable. La variabilité interindividuelle constatée dans ces regroupements cérébraux témoigne quant à elle d’effets génétiques (héritabilité) ainsi qu’environnementaux (environnementalité), dont les ampleurs respectives varient selon la nature de la tâche effectuée. De plus, les sous-types cérébraux mis à jour révèlent une association avec les mesures comportementales et de performance effectuées lors des diverses tâches à l’étude. Enfin, les sous-types neurobiologiques résultant des diverses tâches partagent certaines bases génétiques. Dans leur ensemble, ces résultats appuient la notion que le comportement humain, ainsi que les processus neurobiologiques le sous-tendant, sont des phénotypes au même titre qu’un caractère morphologique ou physiologique, c’est-à-dire qu’ils sont le résultat de l’expression conjointe de bases génétiques (nature) et environnementales (culture). / Human behaviour is both singular and universal. Singularity is believed to be mainly due to life trajectories unique to each individual (influenced among others by culture), whereas universality would stem from a universal nature resulting from a panhuman genome. Unravelling the influences of nature and nurture on human behaviour is the Holy Grail of biological anthropology. I approach this issue by exploring genetic and environmental influences on the neuropsychological underpinnings of behaviour. In particular, I test the hypothesis that the singularity and universality of human behaviour are also observed at the psychological level through the exploration of the neurobiological basis of behaviour, and that these bases have both genetic and environmental sources. Using Functional Magnetic Resonance Imaging (fMRI) data of 862 participants from the Human Connectome Project (HCP), I analyze brain activation related to 7 socio-cognitive tasks covering language, memory, risk taking, logic, emotions, motor skills, and social reasoning. After grouping subjects according to the similarity of their brain activation patterns (neurobiological subtypes), I estimate the genetic and environmental influences on the variation between participants on these subtypes. The inter-individual variability in cerebral groupings appears to have both genetic (heritability) and environmental (environmentality) sources that vary according to the particular psychological task involved. Moreover, these neurobiological subtypes show an association with behavioural and performance measures assessed by the socio-cognitive tasks. Finally, the neurobiological subtypes across the 7 tasks share common genetic links. Overall, the results support the notion that human behaviour, as well as its underlying neurobiological processes, are phenotypes in the same way as morphology or physiology, i.e., are the results of the integrated expression of a genetic basis (nature) and environmental influences (nurture).

Evidence suggests that adolescence and young adulthood is a transitional stage whereby unique contextual factors may increase the likelihood for certain individuals to engage in risk-taking compared to their peers. In addition to influential environmental aspects (i.e. parenting, societal affiliations, peer influence) an adolescent’s and young adult’s underdeveloped cognitive control system is unable to successfully inhibit early maturing tendencies such as sensation seeking and reward sensitivity. However, previous research indicates that certain parental mechanisms may serve as protective/promotive agents for stabilizing this neurobiological imbalance. Therefore, the focus of the current research was to examine how parenting behaviors and styles moderate the relations between neurobiological variables and risk-taking during young adulthood. It was expected that authoritarian parenting methods would have adverse effects on young adult behavior by inhibiting maturing cognitive control abilities and exacerbating early developing socioemotional tendencies. Conversely, it was suspected that authoritative parenting would serve as a protective agent against young adult risk-taking by increasing cognitive control abilities and suppressing socioemotional tendencies. Additionally, parental monitoring is a behavior that, depending on context, may serve to either inhibit or exacerbate young adult risk-taking. An online survey was conducted to assess young adults from MTurk. Participants completed a variety of questionnaires regarding parent-child interactions, levels of sensation seeking and self-regulatory abilities, and engagement in risky behavior such as alcohol abuse. In sum, this research may be used to inform parents and caregivers of the influence of parent-child interactions on adolescent and young adult risk-taking.