Research has indicated that individuals with ASD have deficits in the ability to correctly identify and interpret the emotions and feelings of others. The ability to recognize the emotions of others has shown to be extremely beneficial in a number of ways. On the other hand, the inability to recognize the emotions of others has been linked to a number of negative outcomes, including inappropriate behaviors, as well as mental health, personal, social, and academic difficulties. The purpose of the current study was to extend the previous literature on effective strategies for teaching individuals with ASD to correctly label the situation-based emotions of others. Overall, the current study’s results suggest that an intervention package combining animated videos with prompt delay, error correction, and reinforcement procedures was effective in teaching participants the ability to label situation-specific emotions. Additionally, the current study’s results also supported the idea that individuals with ASD have stronger deficits in recognizing negative emotions, such as sad, mad, and afraid, as compared to positive emotions, such as happy. Future research should continue to focus on exploring the generalization and maintenance of these results.

Autism Spectrum Disorder (ASD) refers to a heterogeneous neurological condition characterized by repetitive and restrictive behaviors and social communication deficits. ASD diagnoses are at a record high, at approximately 1 in 59 children according to the US Center for Disease Control. Currently, there are no available interventions that effectively treat the core symptoms of ASD. All pharmaceutical options address comorbid side effects of ASD but not core deficits and are particularly associated with negative side effects. Additionally, there are economic and geographic barriers that can prevent families of individuals with ASD from seeking or receiving effective interventions. Many of the available interventions are extremely costly, time-consuming, and age dependent. These factors, as well as others, have led to an increase in families independently utilizing complementary and alternative interventions. Due to the large amount of misinformation available on the Internet, families have become more susceptible to trying alternative forms of interventions that have not been scientifically proven as effective, and in some cases, are significantly detrimental. Thus, the need for accessible and inexpensive evidence-based nonpharmaceutical interventions is critical and must be addressed. Fortunately, recent groundbreaking research has discovered two strains of probiotics, Bacteroides fragilis and Lactobacillus reuteri, that have been shown to ameliorate behavioral and social deficits respectively, in validated ASD mouse models in a non-age-dependent manner. Probiotic intervention with a combination of these specific strains would effectively target both repetitive behaviors and social deficits, core ASD symptoms, and provide families with an accessible and inexpensive form of intervention. The mechanisms underlying the efficacy of these probiotics are thought to be associated with the gastrointestinal (GI) system and the oxytocin pathway. This study seeks to examine the necessity of accessible nonpharmaceutical interventions and to provide an effective intervention that is neither expensive or age dependent. This study also aims to provide greater insight into the pathways and systems in which these probiotics operate.

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This research study consisted of an examination of the role played by the educational psychologist in the emotional and social rehabilitation of the TBI adolescent. A survey of the literature reveals that traumatic brain injury during adolescence negatively impacts on their adaptation, development and functioning after the acute phase of the rehabilitation process. In order to study this phenomenon, a psycho-educational perspective was utilised. An in-depth qualitative study was undertaken by means of a case study design. The two cases being presented offers the reader insight into the cases pre-morbid functioning, the accident and its aftermath, the specific traumatic brain injuries, the emotional and social problems encountered by these adolescents as well as the psychotherapeutic interventions applied by the educational psychologist in the rehabilitation process of the cases under investigation. The conclusions reached from this investigation were that traumatic brain injury during the developmental phase of adolescence, negatively impacts on the emotional and social well being of these adolescents, and that the educational psychologist plays a valuable role in the emotional and social rehabilitation of these adolescents. / Educational Studies / M. Ed. (Guidance and Counselling)

This research study consisted of an examination of the role played by the educational psychologist in the emotional and social rehabilitation of the TBI adolescent. A survey of the literature reveals that traumatic brain injury during adolescence negatively impacts on their adaptation, development and functioning after the acute phase of the rehabilitation process. In order to study this phenomenon, a psycho-educational perspective was utilised. An in-depth qualitative study was undertaken by means of a case study design. The two cases being presented offers the reader insight into the cases pre-morbid functioning, the accident and its aftermath, the specific traumatic brain injuries, the emotional and social problems encountered by these adolescents as well as the psychotherapeutic interventions applied by the educational psychologist in the rehabilitation process of the cases under investigation. The conclusions reached from this investigation were that traumatic brain injury during the developmental phase of adolescence, negatively impacts on the emotional and social well being of these adolescents, and that the educational psychologist plays a valuable role in the emotional and social rehabilitation of these adolescents. / Educational Studies / M. Ed. (Guidance and Counselling)

La voie de signalisation mTORC1 (mechanistic target of rapamycin complex 1) est cruciale pour la croissance de l’organisme. Dans les neurones matures, mTORC1 régule la synthèse des protéines ainsi que la plasticité synaptique à la base de l’apprentissage et de la formation de la mémoire. Des dérégulations de mTOR constituent la cause de plusieurs maladies monogéniques (mTORpathies) et sont impliquées aussi bien dans des troubles neurodéveloppementaux que neuropsychiatriques. L’une des mTORpathies, la sclérose tubéreuse, est causée par des mutations des gènes codant pour les inhibiteurs de mTORC1, les complexes 1 et 2 de la sclérose tubéreuse (Tsc1 et Tsc2). Elle est associée à l’épilepsie, l’autisme et aux déficiences intellectuelles. Le rôle de mTORC1 dans les neurones excitateurs est largement connu, pourtant, son implication dans la modulation des circuits inhibiteurs corticaux a été très peu investiguée. Dans le cerveau, les interneurones inhibiteurs GABAergiques (cellules produisant l’acide gamma-aminobutyrique) sont caractérisés par leur grande diversité de morphologies, connectivités et propriétés électrophysiologiques. Les Basket Cells qui expriment la parvalbumine (PV) ciblent spécifiquement le soma et les dendrites proximales de centaines de neurones excitateurs. Cela étant, les cellules PV sont positionnées de façon stratégique pour contrôler la génération des potentiels d’actions. En particulier, l’arborisation axonale ainsi que la densité synaptique des cellules PV subissent des changements drastiques dans le jeune cerveau en développement. Par ailleurs, des altérations dans le fonctionnement des cellules PV ont été associées aux maladies du spectre de l’autisme. Les mécanismes moléculaires et cellulaires sous-jacents le développement de la connectivité des cellules PV sont très peu investigués. En particulier, dans quelle mesure et comment une dérégulation de la voie de signalisation mTORC1 affecterait le développement des cellules PV est inconnue. D’un autre côté, il a été rapporté qu’en plus de dysfonctionnements cognitifs, les maladies du spectre de iv l’autisme sont également caractérisées par des déficits dans le traitement sensoriel. Environ 90% des patients de cette pathologie subissent des expériences sensorielles atypiques telles qu’une hyper et hypo-réactivité et des réponses anormales aux stimuli tactiles. À cet égard, les anomalies sensorielles font désormais partie intégrante des critères de diagnostic de l’autisme. Pourtant, les mécanismes neurobiologiques à l’origine des déficits sensoriels demeurent encore mal connus. Vu l’importance de la voie mTORC1-TSC1 dans la physiologie neuronale et du fait que les mutations de TSC1 génèrent des traits autistiques, nous proposons l’hypothèse selon laquelle la dérégulation Tsc1-dépendante de la voie mTOR dans les cellules PV engendre une perturbation de la connectivité de ces dernières, provoquant une altération des comportements relatifs à la sclérose tubéreuse. Les résultats présentés dans cette thèse démontrent qu’une haploinsuffisance ou une absence totale de TSC1 soit dans des cellules PV isolées, en cultures organotypiques, ou dans toute la population de cellules PV in vivo entraîne une croissance précoce des branchements axonaux et de la densité des boutons synaptiques formés par les cellules mutantes, ce qui est suivie par une perte exagérée de leur innervation chez les souris adultes. Par ailleurs, les souris hétérozygotes PV-Cre;Tsc1flox/+ et knock-out PV-Cre;Tsc1flox/flox comparativement aux souris saines présentaient des déficits dans les comportements sociaux. Aussi, nous avons identifié les dysfonctionnements dans l’autophagie comme mécanismes moléculaires sous-jacents la perte des synapses PV chez les souris mutantes. Enfin, nous avons démontré l’existence d’une période critique se situant entre les 2e et 3e semaines postnatales durant laquelle un traitement à la Rapamycine qui inhibe l’hyperactivation de mTORC1 découlant de l’haploinsuffisance de TSC1 est suffisante pour renverser de façon permanente les déficits synaptiques et comportementaux des animaux mutants. Aussi, l’haploinsuffisance de TSC1 dans les cellules PV entraîne une augmentation de la discrimination tactile chez les animaux mutants. Par ailleurs, nous avons trouvé que les v connectivités glutamatergiques aussi bien intra-corticales que thalamocorticales sur les cellules PV sont réduites chez les adultes mutants comparativement aux contrôles alors que chez les souris pré-adolescentes, elles ne sont pas affectées. Finalement, une restriction sensorielle par l’intermédiaire de la coupe de moustaches pendant la fenêtre critique identifiée est suffisante pour renverser le phénotype d’hypersensibilité de ces animaux. Dans son ensemble, cette thèse apporte les preuves du rôle particulier de la signalisation mTORC1 dans la régulation du développement et du maintien de la connectivité des cellules PV et établit le ciblage de ces dernières comme bases mécanistiques d’un renversement des déficits dans les comportements sociaux et la discrimination sensorielle relatifs à l’autisme dans la sclérose tubéreuse. / Mechanistic target of rapamcyin (mTORC1) is a central player in cell growth throughout the organism. However, mTORC1 takes on additional, more specialized roles in the brain, for example, regulating neuron differentiation and glutamatergic synapse formation. In addition, in mature neuron, mTORC1 regulates protein synthesis-dependent and synaptic plastic changes underlying learning and memory. mTOR dysfunctions are the root cause of several monogenetic disorders (mTORpathies) and are implicated in both neurodevelopmental and neuropsychiatric disorders. One of the most studied mTORpathy is Tuberous Sclerosis, which is caused by mutations in the mTORC1-negative regulators Tuberous Sclerosis Complex 1 or 2 (TSC1 or TSC2). Tuberous Sclerosis is associated with neurological problems, including epilepsy, autism and intellectual disabilities. The role of mTORC1 in excitatory neurons has been extensively investigated, on the other hand whether and how it modulates cortical inhibitory circuit formation is not known. Within the forebrain, inhibitory GABAergic (γ-aminobutyric acid producing) interneurons possess the largest diversity in morphology, connectivity, and physiological properties. Cortical parvalbumin (PV)-positive basket cells (BC) specifically target the soma and proximal dendrites of excitatory neurons. PV cells are strategically positioned to control the generation of action potentials and are also strongly interconnected, which promotes their synchronous activity. The correct development of inhibitory interneurons is crucial for functional circuits. In particular, the axonal arborisation and synapse density of PV interneurons change in the postnatal brain. Interestingly, altered PV cells function has been associated to neurodevelopmental disorders, such as autism spectrum disorders (ASDs), both in human and animal models. How and whether mTORC1 signaling affects PV cell development is unknown. In addition to cognitive impairments, ASDs often result in sensory processing deficits. About 90% of ASD individuals have atypical sensory experiences, described as both hyper- and hypo-reactivity, with abnormal responses to tactile stimulation representing a very frequent finding. In fact, sensory abnormalities are now commonly recognized as diagnostic criteria in ASDs. However, the neurobiological mechanisms that underlie impaired sensory processing associated with ASDs are poorly understood. Mindful of the importance of TSC1-mTOR pathway for neuronal physiology and since mutations in Tsc1 give rise to autistic traits, we questioned whether and how Tsc1 deletion selectively in PV cells affects their connectivity, and whether and to what extent these alterations in cortical PV cell circuits might be contributing to changes in behaviours downstream of altered mTOR signaling. The results presented in this thesis show that Tsc1 haploinsufficiency causes a premature increase in terminal axonal branching and bouton density formed by mutant PV cells, followed by a loss of perisomatic innervation in adult mice. Further PV cell-restricted Tsc1 haploinsufficient and knockout mice, respectively PV-Cre;Tsc1flox/+ and PV-Cre;Tsc1flox/flox mice show deficits in social behaviour. Moreover, we identify autophagy dysfunctions as molecular mechanisms underlying PV synapses loss in PV-Cre;Tsc1flox/+ and PV-Cre;Tsc1flox/flox mice. Finally, we identify a sensitive period during the third postnatal week during which treatment with the mTOR inhibitor Rapamycin rescues deficits in both PV cell innervation and behavioral deficits in adult conditional haploinsufficient mice. We further find that PV-Cre;Tsc1flox/+ mice show increased texture discrimination. Our data also demonstrate that mutant PV cells show reduced cortical and thalamocortical glutamatergic inputs in adult mice, whereas they do not exhibit any alterations of these inputs in pre-adolescent mice. Finally sensory modulation by whisker trimming during the third postnatal week rescues texture discrimination hypersensitivity in adult conditional haploinsufficient mice. Altogether, this thesis demonstrates the crucial role of mTORC1 signaling in the regulation of the developmental time course and maintenance of cortical PV cell connectivity and support a mechanistic basis for the targeted rescue of social behaviors and sensory processing in disorders associated with deregulated mTORC1 signaling.