Pythons are a well-studied model of postprandial physiological plasticity. Consuming a meal has been shown by past work to evoke a suite of physiological changes in pythons and elicit one of the largest documented increases in post-feeding metabolic rates relative to resting values. However, little is known about how this plasticity manifests in the brains of ball pythons, Python regius. Previous work using the cell-birth marker 5-bromo-12’-deoxyuridine (BrdU) has shown that cell proliferation in the python brain increases six days following meal consumption. This study aimed to confirm these findings and build on them in the long term by tracking the survival and maturation of these newly created cells across a two-month period. We investigated whether these cells differentiated into neurons using double-immunofluorescence for BrdU and a reptile-specific neuronal marker (Fox3). We did not find significantly greater rates of cell proliferation in snakes six days after feeding, but we did observe more newly created cells in neurogenic regions in fed snakes two months after the meal. Feeding did not influence neurogenesis, but feeding does appear to have a neuroprotective effect. More newly created cells survived in fed snakes two months later, particularly in the olfactory bulbs and lateral cortex. These findings shed light on the extent of postprandial plasticity and regional differences in the creation of new neural cells in the brains of ball pythons.

Worldwide, millions of young and elderly patients receive procedures that could not be performed without the use of anesthetics. Unfortunately, emerging animal and human data suggest an association between exposure to general anesthesia and impairment of cognitive function in pediatric and geriatric patients. Recent laboratory data have shown that general anesthetics are potentially damaging to the developing and aging brain. However, the mechanism by which this happens is still unknown. General anesthetics affect learning and memory, a brain function involving neural plasticity. An important form of neural plasticity receiving attention is postnatal neurogenesis. This process is highly regulated and involved in hippocampal functions under physiological conditions. This dissertation hypothesizes that anesthetic induced alteration of postnatal neurogenesis may explain the cognitive impairment observed in some pediatric and geriatric patients after anesthesia. In order to accurately address this hypothesis, in the first portion of this dissertation, an animal model is used to examine the effects of two different anesthetics on cognition and new cell proliferation in young and aged rats. Furthermore, the second and third portion of this dissertation emphasizes on the effects of these two widely used anesthetics on each of the various stage of postnatal neurogenesis in young and aged rats.

Le cerveau des mammifères abrite deux régions spécifiques où la neurogenèse adulte ne cesse pas après l'embryogenèse, mais persiste dans le cerveau postnatal et adulte. Ces deux régions sont la zone sous-granulaire du gyrus denté de l’hippocampe et la zone sous-ventriculaire (SVZ) des ventricules latéraux.Dans la SVZ, des cellules souches neurales génèrent des neuroblastes qui migrent jusqu’au bulbe olfactif (OB) pour coloniser les couches granulaires et glomérulaires et se différencier en différent types d’interneurones dont une petite fraction sont des interneurones dopaminergiques. La découverte de la neurogenèse postnatale et adultes a changé le point de vue de la plasticité du cerveau remarquable et ouvre de nouvelles perspectives pour la thérapie des maladies neurodégénératives. Etant donné que dans la maladie de Parkinson les symptômes moteurs principaux sont causés par la dénervation dopaminergique du striatum, la compréhension de la génération et de la différenciation des neurones dopaminergiques bulbaires a reçu une attention particulière au vu de leur intérêt potentiel pour la thérapie cellulaire. Dans ce contexte, le neuromédiateur dopamine lui-même a été suggéré d'influencer la neurogenèse olfactive et la spécification des interneurones dopaminergique.Dans ma thèse, j'ai analysé l’influence de l’innervation dopaminergique issue du mésencéphale sur la neurogenèse et le destin cellulaire des précurseurs de la SVZ. J'ai combiné un modèle 6-OHDA de dénervation dopaminergique chez la souris postnatale avec l’électroporation in vivo du ventricule latéral pour marquer spécifiquement les progéniteurs latéraux et dorsaux et suivre leur destin dans le OB. / In the postnatal and adult mammalian brain neurogenesis persists in the subgranular zone of the hippocampal dentate gyrus and the subventricular zone (SVZ). In the SVZ slowly dividing stem cells give rise to neuroblasts that migrate to the olfactory bulb (OB) where they reach the granule and glomerular cell layer of the OB and differentiate into different interneuron subtypes including a small fraction of dopaminergic interneurons. The discovery of postnatal and adult neurogenesis has changed the view of the plasticity of the brain remarkably and raised the hope for new therapeutical approaches in the field of neurodegenerative diseases. Since in Parkinson’s disease the main motor symptoms are caused by the dopaminergic denervation of the striatum adjacent to SVZ, the understanding of the generation and differentiation of OB dopaminergic neurons has received special attention. Interestingly, the neurotransmitter dopamine itself has been suggested to influence olfactory bulb neurogenesis via direct innervation of SVZ by midbrain dopaminergic neurons. However, data on this topic have been contradictory. In this study, I investigated how dopaminergic innervation influences SVZ neurogenesis and the fate of SVZ progenitors. I combined a 6-OHDA model of dopaminergic denervation in postnatal mice with in vivo forebrain electroporation to specifically label lateral and dorsal SVZ progenitors and to follow their fate in the olfactory bulb.