Mindfulness is increasingly recognized as an important phenomenon both clinically and empirically, with mindfulness-based interventions demonstrated to be efficacious across a wide variety of patient populations and disorders (i.e., Baer, 2003). Though debate regarding the exact definition of mindfulness continues, generally accepted definitions involve the common elements of intentionally directing attention toward the present moment and adopting an accepting, nonjudgmental, and/or nonreactive orientation, intent, or attitude (i.e., Baer et al., 2006; Bishop et al., 2004). Several testable predictions in the cognitive and emotional domains were derived from the operational definition of mindfulness provided by Bishop et al. (2004). Recent empirical work (i.e., Chambers, Lo, & Allen, 2008; Valentine & Sweet, 1999) has supported Bishop et al.’s predictions, providing initial validation of their operationalization of mindfulness. However, most work on the effects of meditation practice and the mindfulness construct has relied on self-report methodology. The current work transcended past research by using behavioral methods to investigate the effects of meditation practice, correlates of trait mindfulness, and validity of current conceptualizations of mindfulness. Additionally, the current work investigated relationships between meditation, mindfulness, and self-regulation using behavioral methods. This investigation was warranted as recent theoretical work suggested that increased self-control abilities may be the primary mechanism by which mindfulness-based interventions work and that higher levels of trait mindfulness may appear to be related to enhanced well-being due to the unmeasured third variable of enhanced self-regulatory abilities (Masicampo & Baumeister, 2007). Ninety-eight individuals (33 meditators, 33 age-matched nonmeditating controls, and 32 students) completed self-report and behavioral measures of attention, learning, memory, cognitive and emotional biases, and self-regulation in individual sessions. Results demonstrated that meditation practice related to few of the measured constructs, with significant group differences detected between the meditators and nonmeditators in short-term memory, long-term memory, and self-regulation only. Self-reported trait mindfulness in the nonmeditators related only to self-reported psychological well-being. These results stand in stark contrast to most of the current literature on meditation and mindfulness. The research raises more questions about the effects of meditation practice and conceptualization of mindfulness than it answers, though multiple interpretations of the data are possible.

Individuals diagnosed with autism spectrum disorder often experience difficulty during speech-in-noise (SIN) processing tasks. However, it remains unclear how behavioral and cortical mechanisms of auditory processing explain variability in SIN performance in adults with ASD and their neurotypical counterparts. The proposed research explored variability in SIN as it relates to behavioral, perceptual, and objective measures of auditory processing. Results showed significant differences between groups in SIN thresholds. In addition, neurotypicals outperformed the ASD group on measures of sustained auditory attention characterized by reduced impulsivity, increased inhibition, and increased selective auditory attention. Individuals with ASD showed decreased acceptance of noise as compared to neurotypical peers. Overall, results highlighted auditory processing deficits in individuals with ASD that contribute to SIN performance.

MeCP2 est une protéine multifonctionnelle agissant à de nombreux niveaux de contrôle des programmes génétiques. Un mauvais dosage de MeCP2 cause un groupe de maladies neurologiques dont le point commun est une déficience intellectuelle sévère. Des mutations ou une délétion de MECP2 causent le syndrome de Rett chez les filles, alors que sa surexpression cause chez les garçons le syndrome de duplication de MECP2. Plusieurs modèles murins de Mecp2-pathies ont été générés qui permettent d’expliciter les mécanismes qui sous-tendent l’apparition des symptômes dans ces différentes maladies. Dans notre laboratoire, deux modèles murins sont utilisés: le modèle Mecp2tm1Bird qui présente une déficience en Mecp2 et le modèle Mecp2Tg1 présentant une surexpression de Mecp2. Ce travail de thèse a permis de caractériser l’évolution postnatale des déficits moteurs et physiologique affectant la souris Mecp2Tg1. Nos résultats montrent que la surexpression de Mecp2 conduit à l’apparition de problèmes moteurs, et des convulsions chez la souris. En parallèle, nous avons étudié les déficits neuronaux affectants la voie GABAergique et glutamatergique chez la souris déficiente en Mecp2. Nous avons montré que la déficience en Mecp2 cause une dérégulation de la transmission synaptique dépendante du ‘territoire’ et de l’âge de la maladie. Ces dérégulations sous-tendent vraisemblablement des différences neurophysiologiques importantes entre les régions du cerveau qu’il nous reste encore à découvrir. Par ailleurs, nous avons constaté que la stimulation pharmacologique du système GABAergique par la Tiagabine, permet d’augmenter la survie des animaux Mecp2-déficients. / MeCP2 is a multifunctional protein acting on many levels of control of genetic programs. Thus, an abnormal dosage of MeCP2 protein causes a group of neurological disorders with a common feature of severe intellectual disability. Mutations or deletions in MECP2 gene cause Rett Syndrome in females, whereas in boys its overexpression causes the MECP2-duplication Syndrome. Several mouse models of MECP2-pathologies were generated. The use of these models is crucial for understanding the mechanisms underlying the onset of symptoms related to the pathology. In our laboratory, two mouse models are under study: The Mecp2tm1Bird model with an Mecp2 deficiency and the transgenic Mecp2Tg1 model with a double expression of Mecp2. My thesis work enabled the characterization of the postnatal physiological and motor deficits affecting Mecp2Tg1 mice. My work led to a better understanding of the gene dosage effect. Our results showed that overexpression of Mecp2 in mice, led to the occurrence of motor problems, and seizures. In parallel, we studied the neural deficits affecting the GABA and the glutamate pathway in several structures of the Mecp2 deficient brain (Mecp2tm1bird). We showed that Mecp2-deficiency causes deregulation of the synaptic transmission, which is dependent on the area, and the age of the study. These deregulations underlie significant neurophysiological differences between the different regions of the brain that we still have to uncover. Furthermore, we found that pharmacological stimulation of the GABA system with Tiagabine, a molecule capable of acting on GABA transporters to prevent its uptake, increases the survival of Mecp2-deficients animals.