Thèses sur le sujet « Cortex cérébral – Modèles animaux »
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Ballain, Thierry. « Modélisation de l'activité du cortex primaire olfactif (piriforme) chez le rat ». Université Joseph Fourier (Grenoble), 2000. http://www.theses.fr/2000GRE19001.
Texte intégralMallet, Nicolas. « Fonction des interneurones GABAergiques rapides dans le striatum : étude électrophysiologique invivo chez lz rat normal et hémiparkinsonien ». Bordeaux 2, 2005. http://www.theses.fr/2005BOR21227.
Texte intégralQin, Yi. « The thalamocortcal symphony : how thalamus and cortex play together in schizophrenia and plastcity ». Electronic Thesis or Diss., Strasbourg, 2023. http://www.theses.fr/2023STRAJ102.
Texte intégralThe work presented in this report consisted in studying using rodent models the functional and dysfunctional properties of the cortico-thalamo-cortical (CTC) circuit in order to understand certain aspects of the mechanisms underlying schizophrenia (Strasbourg) as well as the neuronal plasticity that depends on the visual experience (Amsterdam). Their possible links are discussed. In psychotic disorders, such as schizophrenia, sleep disturbances, abnormal behaviors, cognitive deficits, molecular and genetic abnormalities, and aberrant neural oscillations (or oscillopathies) are common. For example, electroencephalographic (EEG) oscillations (spindles and delta waves) during sleep are reduced. Neural oscillations are electro-biomarkers of connectivity state within highly distributed systems, which include corticothalamic (CT) and thalamocortical (TC) pathways. Oscillopathies can be recorded from the prodromal phase. Thanks to its oscillatory-type bioelectric properties, the thalamus plays a central role in the process and transfer of specific (sensory and motor) and contextual information during ascending and descending sensorimotor, cognitive and emotional processing (mutual functional connections between cortical and subcortical structures). Information processing and transfer are affected in the illness. Visual cortical plasticity is also impaired in schizophrenia. Much clinical and experimental evidence has accumulated over the years supporting both the involvement of the thalamus and glutamatergic (NMDA-type glutamate receptors) and GABAergic transmissions in psychiatric disorders and neuronal plasticity. Pharmacological and genetic models of NMDA receptor antagonism reproduce symptoms and oscillopathies recorded in psychiatric patients. A single systemic administration at a subanesthetic dose of ketamine, a noncompetitive NMDA glutamate receptor antagonist, transiently reproduces, in humans and rodents, oscillopathies with a clinical picture reminiscent of psychotic transition. Such an acute pharmacological model could aid the research and development of innovative treatments in patients with a high-risk mental state toward psychotic conversion
Burg, Thibaut. « Détermination du rôle des neurones corticospinaux dans le déclenchement et la progression de la sclérose latérale amyotrophique chez les souris Sod1G86R ». Thesis, Strasbourg, 2019. http://www.theses.fr/2019STRAJ046.
Texte intégralAmyotrophic lateral sclerosis (ALS) is a disease characterized by progressive and combined degeneration of corticospinal neurons (CSN) and bulbar and spinal motoneurons (MN). Studies in patients suggest a cortical origin and a corticofugal spread of the pathology. However, this hypothesis has never been demonstrated in ALS patients nor tested in mouse models. The work of this thesis allowed to test the role of subcerebral projection neurons (SCPN) in the onset and progression of ALS in Sod1G86R mice. To do so, we generated a new mouse model developing ALS in the absence of SCPN. Results show that the absence of SCPN delays the onset of the pathology, prolongs the survival of the animals, while reducing the decline of their motor abilities. These data suggest that the absence of SCPN is beneficial and that, in an ALS context, SCPN would be toxic and have a preponderant role in the onset and establishment of the pathology. This work shows the importance of including the CSN study for the development of future therapeutic strategies
Haushalter, Carole. « Rôle de l'acide rétinoïque dans la neurogenèse corticale chez la souris ». Thesis, Strasbourg, 2016. http://www.theses.fr/2016STRAJ063/document.
Texte intégralRetinoic acid (RA), an active vitamin A (retinol) metabolite, is a small lipophilic molecule controlling numerous events during central nervous system development in vertebrates. RA is involved in early forebrain development by controlling cell proliferation and survival in the prosencephalic neuroepithelium. Neural development is a process progressing through three key steps: a phase of lateral expansion (E9.5-E10.5 in the mouse), a phase of neurogenesis (E11.5-perinatal stages) and a gliogenic phase (perinatal stages-adult). My work has shown that RA produced by the developing meninges from E13 influences neuronal specification and migration during the phase of neurogenesis. Moreover, our data suggest an earlier role of RA during the production and proliferation of progenitor and neuronal populations, before and at the onset of the neurogenic phase. A combination of extrinsic and intrinsic signals is required to orchestrate the various aspects of cortical development. RA is likely to be one of such extrinsic factors modulating cortical neurogenesis
Dupont, Erwan. « Caractérisation de la plasticité corticale induite par une privation sensorielle chez le rat et étude des mécanismes par des approches électrophysiologique et moléculaire ». Lille 1, 2003. https://pepite-depot.univ-lille.fr/LIBRE/Th_Num/2003/50376-2003-143-144.pdf.
Texte intégralDelcour, Maxime. « Développement d'un modèle animal de paralysie cérébrale : basé sur l'ischémie prénatale et l'expérience sensorimotrice anormale ». Thesis, Aix-Marseille, 2012. http://www.theses.fr/2012AIXM4744/document.
Texte intégralCerebral palsy (CP) corresponds to various motor, sensory and cognitive disorders related to white matter damage (i.e. periventricular leucomalacia, PVL) often occurring after perinatal hypoxic-ischemic events. To reproduce PVL in rodents, we used a prenatal ischemia (PI) that induces white and gray matter damage. The ischemic rats exhibit visual-spatial cognitive deficits and hyperactivity, as observed in patients with CP, related to lesions of entorhinal, prefrontal and cingular cortices. Only mild locomotor disorders are induced by PI, associated to signs of spasticity, along with anatomical and functional degradation in the primary somatosensory cortex (S1), while the primary motor cortex (M1) remains unchanged. Thus, PI recapitulates the main symptoms found in children born preterm. Abnormal spontaneous movements (i.e. general movements) observed in infants who develop CP later on suggest that abnormal sensorimotor experience during maturation is key in the development of this catastrophic disease. The combination of a sensorimotor restriction (SMR) and PI in animal induces fewer cognitive deficits but still hyperactivity. Such a combination leads to severe postural and motor disorders, and spasticity, associated with musculoskeletal pathologies, as observed in patients with CP. In addition to motor disorders, drastic topographical disorganization of cortical maps in S1 and M1 suggest a major dysfunction of sensorimotor loops
Cachia, Arnaud. « Modèles statistiques morphométriques et structurels du cortex pour l'étude du développement cérébral ». Phd thesis, Télécom ParisTech, 2003. http://pastel.archives-ouvertes.fr/pastel-00001246.
Texte intégralEl-Hassar, Lynda. « Réorganisation des réseaux glutamatergiques et GABAergiques de la région CA1 de l'hippocampe au cours de l'épileptogenèse dans un modèle animal d'épilepsie du lobe temporal ». Aix-Marseille 2, 2007. http://www.theses.fr/2007AIX22030.
Texte intégralGuigon, Emmanuel. « Modélisation des propriétés du cortex cérébral : comparaison entre aires visuelles, motrices et préfrontales ». Châtenay-Malabry, Ecole centrale de Paris, 1993. http://www.theses.fr/1993ECAP0305.
Texte intégralEthier, Christian. « Propriétés fonctionnelles et organisation du cortex moteur chez le chat ». Thesis, Université Laval, 2007. http://www.theses.ulaval.ca/2007/25023/25023.pdf.
Texte intégralAlexandre, Frédéric. « Une modélisation fonctionnelle du cortex : La colonne corticale : aspects visuels et moteurs ». Nancy 1, 1990. http://docnum.univ-lorraine.fr/public/SCD_T_1990_0054_ALEXANDRE.pdf.
Texte intégralJouve, Bertrand. « La multiplicité des aires visuelles du cortex : approche par la théorie des graphes ». Paris, EHESS, 1999. http://www.theses.fr/1999EHESA007.
Texte intégralLukaszewicz, Agnès. « Rôle des régulateurs du cycle cellulaire dans la différenciation des précurseurs : implications pour la corticogénèse cérébrale ». Lyon 1, 2003. http://www.theses.fr/2003LYO10089.
Texte intégralLelong, Dominique. « Etablissement d'un nouveau modèle murin d'accident vasculaire cérébral : l'amaurose transitoire chez la souris ». Paris 7, 2012. http://www.theses.fr/2012PA077144.
Texte intégralThis study aims to characterize a new murin model of retinal ischemia, reproducing amaurosis fugax physiopathology. Amaurosis is a therapeutic emergency but its acute treatment remains controversial. Its poor prognosis when it is not quickly reversible, the difficulty to conduct decisive randomized prospective clinical trials, and the limitations of the existing animal models, makes the establishment of a new retinal ischemia preclinical model a priority for the field. We established, for the mouse, by observation of flat-mounted retinas after fluorescein systemic injection that the ligature of the pterygopalatin artery, coupled with the section of the homolateral external carotid artery interrupts the ipsilateral retinal blood circulation. Ligature's withdrawal comes along with retina reperfusion. Four weeks after a 30 min ischemic episode, significant functional changes quantitatively measurable by electroretinography contrast with a preserved histology. A preliminary qRT-PCR study of some ischemic key genes expression had for purpose to supply temporal biomarkers useful for the later design of therapeutic protocols. This purely vascular amaurosis fugax model is simple, reversible, reproducible, usable to the rat as to the mouse. It comes to complete the already available murin stroke models and can be also adapted to modelize diverse clinical situations of retinal ischemia
Gakuba, Clément. « Le potentiel thérapeutique des agents anesthésiques dans l'infarctus cérébral : du modèle animal à l'essai clinique ». Caen, 2015. http://www.theses.fr/2015CAEN3001.
Texte intégralStroke is one of the leading causes of death and disability worldwide. Thrombolysis mediated by tissue type plasminogen activator (tPA) remains the only approved treatment in the early hours of acute ischemic stroke but only a minority of patients are eligible to this therapeutic. To date, no other molecule tested in laboratory was found to be effective to improve stroke patients’ outcome. Moreover, tPA is a double-sided molecule, with beneficial intravascular action but with potential deleterious effect due to its ability to interact with NMDA receptor, a neuronal receptor aimed by anesthetics. The aim of the present work was i/ to develop animal stroke models allowing a better translation from experimental findings to clinical trials ii/ to study tPA-anesthetic interactions in order to counteract tPA neurotoxicity iii/ to investigate the impact of stroke on a recently described system of brain metabolites clearance, the glymphatic system influenced by anesthetic status. Herein i/ we developed a non-human primate stroke model with MRI characterization and a murine model allowing the future launch of large multicenter preclinical trials ii/ we demonstrated in vitro and in vivo synergistic effect of tPA-ketamine and initiated the realization of a clinical trial with aiming to confirm the efficacy of this bitherapy iii/ we observed the impairment of the glymphatic in the early hours of stroke and the restauration of this system after recanalization of the occluded artery
Côté, Éric. « Contrôle de la respiration chez la préparation du tronc cérébral isolé du poisson rouge (Carassius auratus ; Linnaeus) ». Thesis, Université Laval, 2013. http://www.theses.ulaval.ca/2013/30021/30021.pdf.
Texte intégralWe conducted a two-part in vitro study on the isolated brainstem preparation of the goldfish (Carassius auratus; Linnaeus). In the first part, we investigated the central chemosensibility of the goldfish. Our results indicate that decreasing the PO2 of the superfusate increases the frequency of the fictive respiratory bursts. However, decreasing the pH of the superfusate by increasing its PCO2 had no effect on the respiratory rhythm. In the second part, we investigated the relative importance of GABA- or glycine-mediated Cl--dependent reciprocal inhibition for respiratory rhythmogenesis by disrupting this mechanism with three different treatments. Here, our results indicate that 1) bathing the brainstem in a Cl--free superfusate abolishes the respiratory rhythm, 2) activating GABA receptors with exogenous GABA decreases the frequency of the fictive respiratory bursts and 3) simultaneously inactivating GABA receptors and glycine receptors with antagonists increases both the frequency and the amplitude of the fictive respiratory bursts.
Laplante-Campbell, Marie-Pier, et Marie-Pier Laplante-Campbell. « Caractérisation de modèles murins de la maladie de Parkinson (MPTP, PITX3) et modification des cellules souches hématopoïétiques pour stimuler la production du " Brain-derived neurotrophic factor " (BDNF) ». Master's thesis, Université Laval, 2008. http://hdl.handle.net/20.500.11794/20555.
Texte intégralLa maladie de Parkinson est une maladie neurodégénérative caractérisée par des dysfonctions locomotrices causées, en grande partie, par la perte de neurones dopaminergiques de la substance noire. Les patients atteints de la maladie de Parkinson présentent un déficit en « brain-derived neurotrophic factors » (BDNF). Cette neurotrophine est nécessaire pour le développement, le maintien et la survie des neurones dopaminergiques. Nous avons utilisé la capacité naturelle des cellules souches hématopoïétiques à infiltrer les régions lésées du cerveau pour libérer ce facteur neurotrophique. Nous avons démontré que la modification des cellules de la moelle osseuse pour favoriser la production du BDNF permet d’améliorer les déficits locomoteurs des souris parkinsoniennes. De plus, la modification des cellules hématopoïétiques permet d’augmenter les niveaux de BDNF dans la substance noire, le cortex et le thalamus. La surproduction de BDNF permet également de stimuler la production de la dopamine au niveau de la substance noire.
Parkinson’s disease is a common neurodegenerative disorder characterized by locomotor dysfunctions. These motor symptoms are due to a severe loss of dopaminergic neurons in the substantia nigra pars compacta. Parkinson’s patients also have a deficit in the expression of the brain-derived neurotrophic factor (BDNF). This neurotrophin plays an important role in the development, survival and neurotransmission of dopaminergic neurons. Considering that hematopoietic stem cells can infiltrate damaged brain regions, we have modified these cells to deliver the neurotrophic factor in Parkinson’s disease mouse models. We have demonstrated that modification of bone marrow cells attenuates the locomotor dysfonctions in Parkinson’s mice. In addition, overproduction of BDNF by hematopoietic cells increases BDNF levels in the substantia nigra, cortex and thalamus. Overproduction of BDNF also stimulates biosynthesis of dopamine in the substantia nigra.
Parkinson’s disease is a common neurodegenerative disorder characterized by locomotor dysfunctions. These motor symptoms are due to a severe loss of dopaminergic neurons in the substantia nigra pars compacta. Parkinson’s patients also have a deficit in the expression of the brain-derived neurotrophic factor (BDNF). This neurotrophin plays an important role in the development, survival and neurotransmission of dopaminergic neurons. Considering that hematopoietic stem cells can infiltrate damaged brain regions, we have modified these cells to deliver the neurotrophic factor in Parkinson’s disease mouse models. We have demonstrated that modification of bone marrow cells attenuates the locomotor dysfonctions in Parkinson’s mice. In addition, overproduction of BDNF by hematopoietic cells increases BDNF levels in the substantia nigra, cortex and thalamus. Overproduction of BDNF also stimulates biosynthesis of dopamine in the substantia nigra.
Hilber, Pascal. « Conséquences d'une neurodégénérescence précoce du cortex cérébelleux sur le vieillissement chez la souris : utilisation d'un mutant neurologique, la souris Lurcher ». Rouen, 1999. http://www.theses.fr/1999ROUES004.
Texte intégralFatma, Mena. « Approches transcriptionelles dans des modèles animaux de stress et de dépression majeure ». Doctoral thesis, Université Laval, 2021. http://hdl.handle.net/20.500.11794/68545.
Texte intégralMajor depressive disorder (MDD) is the leading cause of disability for three decades with over 300 million affected worldwide. Indeed, it is a major contributor to the overall global economic burden of disease. Despite its significant societal impact, the biological mechanisms of depression remain poorly understood. Unfortunately, only around 30% of patients treated for depression show complete improvement in their symptoms. Given, the high failure rate of antidepressant clinical trials, there has been increased scrutiny recently regarding their use for deciphering the neurobiology of depression and to design potential treatment interventions. Given the fact that most of our knowledge of the field comes from animal models, indeed, these models reproduce some aspects of human MDD but to what degree remains unknown. This work elucidates the extent to which they recapitulate the molecular pathology of the human disorder. In this thesis, we leveraged differential expression and co-expression network analyses to catalogue the overlap between human MDD and 3 mouse model of stress, namely chronic variable stress, social isolation and chronic social defeat stress, and evaluated their capacity of reproducing the transcriptional profiles associated with human MDD in two brain regions, mPFC and NAc, widely implicated in depression. Our results show that each model efficiently reproduces common but also unique transcriptional features of the human syndrome.Overall, by identifying strongly co-expressed groups of genes shared between humans and mice, our results suggest that these transcriptional signatures are similarly involved in the control of functional pathways in both species and confer strong support for the use of these mouse models for the study of the molecular alterations seen in MDD while providing important implications for future research and clinical applications.
Desgranges, Bertrand. « Etude des apprentissages olfactifs alimentaires : importance de l'amygdale basolatérale et du cortex insulaire chez le rat ». Thesis, Tours, 2009. http://www.theses.fr/2009TOUR4004/document.
Texte intégralTo better understand the mechanisms involved in food olfactory learning, the neurobiological basis of conditioned odor aversion (COA) and the conditioned odor preference (COP) were investigated. We study the basolateral amygdala (BLA) and the insular cortex (IC), which receive olfactory, gustatory and visceral information. Using a pharmacological approach, we show that the BLA is involved in acquisition, consolidation and both recent and remote memory retrieval of COA. By contrast, the IC is not necessary to any of these memory phases. Using a cellular imaging technique (catFISH), we find that COP leads to an increase of odor-taste convergence onto individual neurons in the BLA, but not the IC, by means of the recruitment of a new population. Whether the approach is systemic or cellular and the learning is aversive or appetitive, our study highlights the importance of the BLA in food olfactory learning
Bezerra, Silvio José. « Un modèle de perception visuelle pour la vision artificielle ». Paris 6, 1993. http://www.theses.fr/1993PA066026.
Texte intégralBrochier, Camille. « Analyse des transcriptomes du cerveau de souris : Mise en évidence de patrons régionaux d’expression conservés chez l’homme et altérés dans des modèles de maladies neurodégénératives ». Paris 11, 2007. http://www.theses.fr/2007PA112123.
Texte intégralIn order to get a better understanding of brain complexity at a molecular level, we explored the mouse brain transcriptome using the Serial Analysis of Gene Expression method. SAGE libraries were generated from 11 mouse brain territories, including six cortical regions, striatum, accumbens nucleus, thalamus, substantia nigra and ventral tegmental area. The entire project delivered 1. 2 million SAGE tags, allowing the detection of rare mRNAs. Comparison of all transcriptomes revealed 308 transcripts differentially expressed, a number of which have no documented function. We further analyzed the expression profiles by real-time RT-PCR or in situ hybridization (ISH). Since the brain is a heterogeneous organ, it was important to determine the cell types that are expressing the novel markers. A combination of in situ hybridization with immunohistochemistry showed the expression of 3 midbrain-enriched mRNAs in dopaminergic neurons. We tested whether mouse markers could be human markers. There was a good overall conservation of expression patterns in both species. To evaluate the assumption that genes predominantly expressed in a given brain structure may indeed be relevant to its function, we chose pathophysiological conditions that target specific neuron populations. Using quantitative RT-PCR, we so far measured the abundance of striatum- or cortex-enriched transcripts in the mouse R6/2 genetic model of Huntington’s disease. Likewise, we showed the regulation of transcripts enriched in the striatum or substantia nigra in pharmacological rodent models of Parkinson’s disease, in which the nigro-striatal dopaminergic pathway has been lesioned
Poittevin, Marine. « Implication des processus inflammatoires et de la microangiopathie diabétique dans la sévérité de l'infarctus cérébral et le retard de réparation dans des modèles d'ischémie cérébrale chez la souris ». Paris 7, 2013. http://www.theses.fr/2013PA077082.
Texte intégralCerebral ischemia is the leading cause of acquired disability in adults and the second cause of death m developed countries. Currently, the only effective treatment is thrombolysis with rt-PA administration restricted to less than 5% of patients. The development of new therapies is therefore a crucial issue. The inflammatory process after cerebral ischemia is essential for clearance of injured brain tissue but also contributes to the worsening of brain damage and neurological deficit. In addition, inflammatory cytokines released after cerebral ischemia contribute to promote or block neurogenesis, a process essential for brain repair. The first part of this research has focused on the modulation of the inflammation to keep the beneficial component and decrease the deleterious one by the mean of an immunomodulatory drug, Glatiramer Acétate or Copaxone®. This drug was injected into two munne modeb of cerebral ischemia, which are permanent and transient Middle Cerebral Artery occlusion (pMCAo and tMCAO). Glatiramer Acetate did not diminish the infarct volume nor improve the neurological deficit despite an increase of neurogenesis in pMCAo model and reduced microglial pro-inflammatory cytokines in tMCAO. In parallel a follow-up in vivo study of microglial inflammation in stroke induced by pMCAo was conducted in MRI, particularly mteresting for the non-invasively validation of new anti-inflammatory therapeutics. As we obtained limited results in our study models, we decided to include diabetes, a strong risk factor for incidence and severity of cerebral ischemia. Diabetes is know in peripheral organs to induce an inflammatory and vascular response. It results in microangiopathy whose role in ischemic brain injury is poorly understood. The second part of this research has therefore focused on the characterization of this microangiopathy in a type I diabetic mouse model by injection of streptozotocin and the consequences of this microangiopathy in the severity of cerebral infarction. Our work has shown that after cerebral ischemia in diabetic mice, the inflammatory response was more intense and angiogenesis, the vascular repair process, was delayed. This allows targeting new therapeutic strategies following cerebral ischemia in the diabetic field
Rougier, Nicolas. « Modèles de mémoires pour la navigation autonome ». Nancy 1, 2000. https://tel.archives-ouvertes.fr/tel-01746477v2.
Texte intégralWe propose a method for autonomous agent navigation problem grounded on a connectionist architecture inspired by neurobiological data concerning cortex and hippocampus. Our approach is grounded on distinction between memories : cerebral cortex is believed to be implied within declarative memory, allowing explicit memorization of facts and events. Our works concerns modeling of these memories in the framework of autonomous behavior. The study of these different memories underlines the importance of this procedural/declarative dichotomy in cognitive tasks while autonomous navigation study underlines the topological cognitive map notion as well as the necessity of having at disposal ad hoc memory systems. Our modeling work is separated in two parts. Available data concerning human cortex allow us to model a procedural memory for the construction of links between places of a simulated environment allowing a goal-guided search as well as the possibility of reaching anytime any known place in the environment. Furthermore, available data concerning hippocampus allow us to model a declarative memory system. The architecture of the model as well as the original mechanisms implied make this system able to handle both simulated and real-world data. This model finally allows to characterize and memorize the different places of a given environment
Dupré, Nicolas. « Etude de la réponse différenciée à l'hypoxie-ischémie au cours du développement cérébral périnatal chez la souris ». Thesis, Normandie, 2019. http://www.theses.fr/2019NORMR013.
Texte intégralHypoxia-ischemia and inflammation are the major triggers of cerebral palsy (CP) in preterm and term new-born. CP is defined as a group of nonprogressive disorders of movement and posture, associated with cognitive and behavioural disorders. CP prevalence is about 1.7‰ living birth and leads to life-long medical care which altogether makes CP a healthcare issue. Preterm and term new-born exhibit specific structural damages and long-term outcomes. In the perinatal period, therapeutic or preventive strategies are limited due to the risk of interference with the ongoing development. To further explore lesion mechanisms, we used the well described “Rice-Vannucci” model of HI adapted in mice aged 5 or 10 days (P5/P10). At these developmental stages, mouse cortical development mimics those of human preterm and term new-born respectively.Methods. To explore the differentiated response to HI between P5 and P10 mice, we first performed a longitudinal MRI study associated with learning and social behaviour testing at adulthood. We also used targeted enzymatic approaches in perinatal period. In a second time, we performed a global, non-targeted assessment of early HI-induced transcriptome modifications during the first 24h after HI.Results I. Our results validated the HI model for the study of age-dependent lesions corresponding to preterm or term new-born lesions. We confirmed the P5-specific white matter lesions mimicking periventricular leukomalacia of preterm infants (30GW). We showed that these white matter lesions originate from age-dependent vascular vulnerability. This vascular vulnerability involved P5 restricted vascular MMP-9 activity which also depends on tPA activity. We showed age-dependent long-term cognitivo-behavioural outcomes, allowing us to associate white matter damages to social behaviour and hyperactivity, whereas learning deficits were more pronounced in P10 mice and associated with hippocampal and retrosplenial cortex damages.Results II. The transcriptome study has generated a useful database for further research. It also showed very important differences in HI-induced transcriptomic responses. Five highlights emerged: i) identical processes (pathways, GO terms) were affected by HI in both P5 and P10 mice: i.e. regulation of transcription, inflammation, cell death/apoptosis and angiogenesis, but the genes induced or repressed associated to these processes were highly different at the two stages, ii) the HI-induced transcription response at P10 mainly counteracted the development-induced transcription changes, iii) the kinetics of induction/repression were different between P5 and P10 mice; P10 mice exhibiting a global delayed response to HI compared to P5 in terms of delay of induction/repression and maximum amplitude, iv) twenty-four hours after HI, the response at P5 was slowing down, apparently returning to basal state, whereas in P10 mice the changes appeared uncontrolled, v) a P5 specific coordinated repression of genes coding proteins involved in synaptic function was observed 12h post-HI, perhaps at the origin of the global slowing-down of transcription alterations observed 24h post-HI.Conclusion. These complementary studies provide a better understanding of the pathogenesis of neonatal brain injury. They also open routes towards new research areas such as: i) the specific vascular vulnerability, depending on brain structures and developmental stage, ii) the consideration of the maturation stage in the further development and experimentation of new neuroprotective strategies
Chénard-Poirier, Marie-Pierre. « Rôle des récepteurs nucléaires Nur77, Nurr1 et Nor-1 dans l'hippocampe en lien avec le BDNF, la mémoire et l'anxiété ». Master's thesis, Université Laval, 2014. http://hdl.handle.net/20.500.11794/25508.
Texte intégralPuy, Laurent. « Mécanismes et Conséquences de l’Oedème Cérébral sur le Pronostic des Hémorragies IntraCérébrales Spontanées ». Thesis, Université de Lille (2018-2021), 2021. http://www.theses.fr/2021LILUS058.
Texte intégralSpontaneous intracerebral haemorrhage (ICH) is associated with a dramatic prognosis and remains devoid of specific treatment. Therefore, understanding the mechanisms of ICH pathology and repair is a matter of high priority. The peri-haemorrhagic zone, commonly called "peri-haematomal oedema" (PHE), might be a promising candidate for therapeutic interventions. However, its underlying mechanisms, natural evolution and prognostic value remain to date unclear. This thesis aimed at studying the mechanisms and consequences of this PHE. To do so, we combined an experimental (animal model of ICH) and a neuropathological (post-mortem study on human tissue) approach.We used the double autologous blood injection model to reproduce ICH in a large cohort of male and female rats. In a first study, we showed how multimodal MRI is a reliable tool to track the dynamic progression of peri-haematomal injuries and we characterized the kinetics of different PHE components (water content, [micro]-vessel injuries, neuro-inflammation and iron deposits). In a second study, we investigated the short and long-term consequences of ICH. We reported that a deep ICH provokes long term cognitive impairments in rats that affects both hippocampal and non hippocampal aspects of cognition contrasting with early spontaneous locomotor recovery. We also showed that focal striatal ICH induces distant brain atrophy and hypometabolism involving limbic system structures and cortical areas. We included 19 cases of patients who died from ICH in a post-mortem study. We provided evidence for Neutrophil extracellular Traps (NETs) infiltration within the haematoma core but also and within the PHE. We also investigated the natural kinetic of natural blood clearance process after ICH in human brain tissue with a focus on the monocyte-macrophage scavenger receptor (CD163)/hemoxygenase-1 (HO-1) pathway. Our findings contribute to refine our perception of PHE, to optimize the translational pipeline and, hopefully, to identify innovative therapeutic strategies for ICH
Alves, de Oliveira Laurent. « Effets de l'acidose chronique et d'un excès de sulfate sur le métabolisme microbien de la thiamine dans le rumen ». Lyon 1, 1997. http://www.theses.fr/1997LYO10226.
Texte intégralPetite, Didier. « Cryopréservation de neurones embryonnaires humains et animaux dans une perspective de transplantation ». Paris, EPHE, 2000. http://www.theses.fr/2000EPHE3016.
Texte intégralEscola, Ludovic. « Propriétés fonctionnelles des neurones de l'aire motrice supplémentaire chez le singe normal et parkinsonien ». Bordeaux 2, 2002. http://www.theses.fr/2002BOR28978.
Texte intégralChemla, Sandrine. « A biophysical cortical column model for optical signal analysis ». Nice, 2010. http://www.theses.fr/2010NICE4004.
Texte intégralVoltage-sensitive dye imaging (VSDI) is a powerful modern neuroimaging technique whose application is expanding worldwide because it offers the possibility to monitor the neuronal activation of a large population with high spatial and temporal resolution. In this thesis, we investigate the biological sources of the voltage-sensitive dye signal (VSD signal), since this question remains unresolved in the literature. What does the voltage-sensitive dye imaging signal measures? This question is difficult to resolve at the physiological level as the signal is multi-component: The dye reflects the dynamics of the membrane potential of all membranes in the neuronal tissue, including all layers of the circuitry, all cell types (excitatory, inhibitory, glial) and all neuronal compartments (somas, axons, dendrites). To answer this question, we propose to use a biophysical cortical column model, at a mesoscopic scale, taking into account biological and electrical neural parameters of the laminar cortical structure. The model is based on a cortical microcircuit, whose synaptic connections are made between six specific populations of neurons, excitatory and inhibitory neurons in three main layers. Each neuron is represented by a reduced compartmental description with conductance-based Hodgkin-Huxley neuron model. The model is fed by a thalamic input with increasing activity, background activity and lateral connections. Isolated neurons and network behavior have been adjusted to fit data published in the literature. The so-calibrated model offers the possibility to compute the VSD signal with a linear formula. We validated the model by comparing the simulated and the measured VSD signal. Thanks to the compartmental construction of this model, we confirm and quantify the fact that the VSD signal is the result of an average from multiple components, with excitatory dendritic activity of superficial layers as the main contribution. It also suggests that inhibitory cells, spiking activity and deep layers are contributing differentially to the signal dependently on time and response strength. We conclude that the VSD signal has a dynamic multi-component origin and propose a new framework for interpreting VSD data
Hellal, Farida. « Récepteur B2 de la bradykinine : une nouvelle cible thérapeutique pour le traitement du traumatisme cérébral diffus ? » Paris 5, 2003. http://www.theses.fr/2003PA05P635.
Texte intégralThe aim of our work was to evaluate the therapeutic potential of the bradykinin B2 receptor (B2R) blockade in diffuse cerebral trauma using a mouse closed head injury model (CHI). Previously, we showed that CHI leads to a neurological deficit, a diffuse degeneration, cerebral hemorrhage and edema concomitantly with blood brain barrier (BBB) disruption. Moreover, CHI induces an oxidative stress (OS) and neutrophil infiltration (NI). In a second part, using a selective non-peptide antagonist, the LF 16-0687 Ms and B2R knock-out mice, we showed that B2R blockade improves the neurological outcome, decreases the BBB disruption, NI, edema and hemorrhage and also the OS and the inducible NO synthase (NOS) expression and activity. Besides these effects, the antagonist treatment sets against decrease of the neuronal NOS activity. These data indicating the B2R contribution to post-traumatic events, emphasize the therapeutic potential of its blockade for the treatment of diffuse cerebral trauma
Delattre, Claire. « Approches physiopathologiques des interactions entre accident vasculaire cérébral et démence vasculaire ». Phd thesis, Université du Droit et de la Santé - Lille II, 2013. http://tel.archives-ouvertes.fr/tel-00982049.
Texte intégralBardoul, Michèle. « Récepteurs AMPA et kai͏̈nate précoces dans le tronc cérébral embryonnaire : effets de leur blocage ou de leur stimulation "in vitro" ». Montpellier 2, 1997. http://www.theses.fr/1997MON20177.
Texte intégralBilbao, Fabienne de. « La voie septo-hippocampique chez le rat : étude neuroanatomique, altérations au cours du vieillissement et réponses aux lésions du cortex entorhinal ». Paris 5, 1993. http://www.theses.fr/1993PA05P615.
Texte intégralBesson, Valérie. « Inhibition de la poly(ADP-Ribose) polymérase : une nouvelle stratégie thérapeutique pour le traitement du trauma cérébral ? » Paris 5, 2004. http://www.theses.fr/2004PA05P604.
Texte intégralThe aim of this work was to evaluate if poly(ADP-ribose)polymerase inhibition could be a therapeutic strategy for traumatic brain injury (TBI), as excessive activation of this enzyme by oxidative stress (OS) induces cell death by energetic depletion. A cerebral OS in vivo leads to nitrosative stress and PARP activation. 3?aminobenzamide (3AB), a PARP inhibitor, reduces the lesion and PARP activation, showing the deleterious role of this enzyme in cell death induced by cerebral OS. TBI caused by fluid percussion leads to nitrosative stress and PARP activation. 3AB reduces the neurological deficit, the lesion and PARP activation. Two PARP inhibitors more potent than 3AB, PJ34 and INO-1001 reduce the deficit, the PARP activation without affecting the brain lesion. In conclusion, our work shows that PARP is involved in the pathogenesis of TBI and may be a promising therapeutic target for brain trauma. However, complementary studies are needed to evaluate which PARP isoforms to inhibit
Blot, Kévin. « Plasticité neuronale dans le cortex préfontal du rat induite par un antagoniste non compétitif des récepteurs NMDA : vers un modèle des symptômes cognitifs de la schizophrénie ». Thesis, Paris 5, 2013. http://www.theses.fr/2013PA05P604.
Texte intégralSchizophrenia affects about 1% of the world population and is a major socioeconomical problem in ours societies. Cognitive symptoms are particularly resistant to current treatments. These cognitive symptoms are believed to be closely related to an altered function of prefrontal cortex (PFC) in patients. Animal pharmacological models of cognitive symptoms, with non-competitive NMDA receptors antagonists such as MK801, are commonly used to investigate the underlying mechanism. In this thesis, we decided to study neural plasticity of the CPF by stimulation of the ventral hippocampus (HPC-CPF pathway) in a rodent MK801 model (acute systemic MK801 injection, 0.1 mg/kg), since an abnormal neural plasticity may be involved in the genesis of a number of psychiatric illnesses (including schizophrenia). First, we analyzed the in vivo effect of acute systemic MK801 injection on the HPCmPFC pathway in anesthetized rats. In this objective, a stimulation electrode and a recording electrode were implanted respectively in ventral hippocampus and the prelimbic area of PFC. A single MK801 injection induced a long-term potentiation (LTP) of synaptic responses in the HPC-PFC pathway. This LTP seems to have common expression mechanisms with the LTP usually induced by high frequency stimulation (HFS). Indeed, the induction of one preventedthat of the other, and the local infusion in PFC of a competitive NMDA receptors antagonist, AP5, blocked the induction of both forms of LTP. Furthermore, this MK801-induced LTP requires ERK1/2 signaling activation, frequently involved in cortical neural plasticity, since inhibition of this signaling by SL327 (10 mg/kg) did not allow a consecutive MK801 injection to induce LTP. However, unlike HFS-induced LTP, MK801-induced LTP did not need synchronized inputs conferring an aberrant characteristic. Second, we confirmed whether our rodent pharmacological model exhibits cognitive deficits. For this purpose, we conducted attentional set-shifting task to evaluate PFCdependent cognitive flexibility. We also studied HPC-PFC pathway-dependent spatial working memory with delayed spatial alternation task in Y-maze. We observed that MK801- treated rats had impairments in cognitive flexibility and spatial working memory. Moreover, these behavioral effects were no longer observed 24 hours after injection, like MK801 effects on neural plasticity of the HPC-PFC, suggesting a potential correlation between cognitive deficits and MK801-induced LTP. Finally, we tested whether an mGluR2/3 receptors agonist, LY379268, could prevent MK801 effects. LY329268 pretreatment (3 mg/kg) blocked MK801-induced deficits in cognitive flexibility and ameliorated spatial working memory in MK801-treated rats. Interestingly, LY379268 pretreatment had no effects on HFS-induced LTP, suggesting that it does not disturb “normal” LTP induction. Taken together, these results revealed an aberrant plasticity in PFC of MK801 pharmacological model in rats, which is probably related to the cognitive deficits observed. They also suggest that mGluR2/3 receptors could be a therapeutic target to treat cognitive symptoms of schizophrenia
Cui, Yi. « Neurogenesis regulation and homeostasis : role of Pax6 signalling and mathematical modelling Lhx2 regulates the timing of β-catenin-dependent cortical neurogenesis Enhanced Abventricular Proliferation Compensates Cell Death in the Embryonic Cerebral Cortex ». Thesis, Sorbonne université, 2018. http://www.theses.fr/2018SORUS309.
Texte intégralA tight control of the organization of the cerebral cortex is vital for most species. Understanding the regulatory mechanisms supporting these processes is an important endeavor in developmental biology. We focused on the processes taking place during neurogenesis of the cerebral cortex, and took a multi-disciplinary approach combining biological experiments and mathematical models. We start with a model describing the probability of progenitor divisions sequence as a function of time during the neurogenesis. It is parsimonious, but sufficient to explain and draw predictions on the phenotype observed in Lhx2 conditional knock-out mutant that precocious neurogenesis affected cortical surface and thickness. The second topic we studied is how the brain compensates cell death to maintain homeostasis during development. In two mutant mouse models with neuronal death between embryonic days 11 to 14, different compensation phenotypes are observed. Here, we develop a unified mathematical model that reconciles those two opposite observations. This model is based on two fundamental compensation mechanisms: 1) an increase in the probability and maximal number of intermediate progenitor proliferative divisions; 2) a delay in the switching time between upper- and deep-layer neurons generation by a maximum of 24h. The third topic we studied is the role of extracellular Pax6 on neurogenesis. Pax6 is one of the master regulators of neuronal progenitor proliferative division and differentiation. With its homeodomain, it can transfer between cells and exert non-cell autonomous activities. We showed that blocking extracellular Pax6 induces Cajal-Retzius neurons generation ectopically
Acerra, Francesca (1970. « Modélisation d'un aspect du développement cognitif : la reconnaissance des visages dans la première année de vie ». Aix-Marseille 1, 1999. http://www.theses.fr/1999AIX11071.
Texte intégralXia, Lin. « Analyse de profils d'expression génique dans des modèles murins d'anxiété/dépression ». Phd thesis, Université Paris Sud - Paris XI, 2012. http://tel.archives-ouvertes.fr/tel-00923149.
Texte intégralVinet, Jonathan. « Implication des calcium/calmoduline-dépendente kinase kinases et du facteur neurotrophique BDNF dans le mécanisme d'action des antidépresseurs ». Thesis, Université Laval, 2005. http://www.theses.ulaval.ca/2005/22416/22416.pdf.
Texte intégralMajor depression is a mood disorder that affect 15% of the population and that can be caused by various factors, including stress. Hypothalamo-pituiary-adrenal axis hyperactivity is present in a majority of depressive patients. Antidepressant drugs are the best therapy that exists to treat depression. They exert their therapeutic action by activating the AMPc signaling pathway and the transcription factor CREB, which leads to an increase in the transcription of genes implicated in cell protection and surviving, like BDNF. CREB can also be activated by the calcium-signaling pathway. This thesis reports the possible implication of the CaMKKα and CaMKKβ in the mechanism of action of antidepressants. We first cloned the mRNA of the mouse CaMKKβ and described the distribution of both CaMKKs in the mouse central nervous system. They were strongly expressed in brain regions that are implicated in major depression. Next, we used in situ hybridization to study the effect of chronic antidepressant treatment on the gene expression of the CaMKKs. Moreover, we used a transgenic mouse characterized by a dysfunction of the glucocorticoid receptors (GR) as a neuroendocrine model of depression. The analysis of the different levels of expression of the CaMKKs and BDNF shows that different brain areas react to antidepressants or to GR dysfunction. For instance, prefrontal cortex and hippocampus are of particular importance due to their implication in depression. Our results suggest that the calcium siganling pathway might be a target of antidepressant drugs.
Rocha, Felix Tiago Manuel. « Inhibition périsomatique dans les oscillations gamma et dans l'apprentissage auditif ». Thesis, Strasbourg, 2016. http://www.theses.fr/2016STRAJ098/document.
Texte intégralConvergent evidence has attributed to perisoma-inhibiting interneurons (PIIs) a key role in the generation of gamma oscillations (GO). I optogenetically probed the effect of reduced perisomatic inhibition on GO and associative learning in the auditory cortex of freely behaving mice. Contrary to expectations, I did not observe a reduction in GO during inhibition of PIIs, but rather a strong increase in the amplitude of GO. The amplification of the auditory-evoked potential (AEP) N15, together with the absence of an increase in synchrony between the cortex and the thalamus, suggest that decreased perisomatic inhibition disinhibits the auditory cortex and promotes the intracortical generation of GO. In a different experiment, I showed that inhibition of PIIs impaired learning and produced an experience-related reduction in the AEP N15. Lastly, I found that lowering the optogenetic inhibition delivered to PIIs and retraining mice enhanced auditory-induced GO
Perrot, Matthieu. « Reconnaissance automatique des sillons corticaux ». Phd thesis, Cachan, Ecole normale supérieure, 2009. https://theses.hal.science/tel-00457072/fr/.
Texte intégralThe determination of specific biomarkers of brain pathologies at population scale is extremely difficult because of the huge inter-individual variability of the sulco-gyral topography. This thesis addresses this issue by automatically identifying 125 sulcal structures and pairing them through individuals, thanks to a manually labeled database of 62 subjects. Relying on the sulcal roots theory, cortical folds are split into elementary segments to be labeled. In a first time, the structural approach proposed earlier by Jean-François Mangin and Denis Rivière has been revisited to manage the increasing amount of morphometric features involved in the identification process. In a second time, this model has been fully reviewed in favor of a Bayesian framework based on localized information (positions or directions) previously neglected, thus allowing effective optimization schemes. In this context, data normalization is essential ; this issue has been considered through global or sulciwise local a ne registration techniques, jointly to the sulcal identification. In order to introduce more structural informations, a Markovian model has been successfully introduced to reflect the local neighbored cortical folds organization. Finally, the overall recognition rate has reached 86 % for each hemisphere. From now on, only atypical patterns or the most variable anatomical structures remain a real issue
Perrot, Matthieu. « Reconnaissance automatique des sillons corticaux ». Phd thesis, École normale supérieure de Cachan - ENS Cachan, 2009. http://tel.archives-ouvertes.fr/tel-00457072.
Texte intégralGentric, Jean-Christophe. « La diversion de flux dans le traitement des anévrismes cérébraux : des études pré-cliniques aux études cliniques ». Thesis, Brest, 2016. http://www.theses.fr/2016BRES0027/document.
Texte intégralFlow Diversion is one of the relevant technical improvements of the past decade in the endovascular treatment of cerebral aneurysms. When the efficacy and safety of a new tool allow treating challenging aneurysms, this adoption in daily practice can be fast even if the benefit of use is not clearly, scientifically show. We performed a systematic review of studies of these stents called “Flow Diverters” (FD) in animal models. Then we performed 4 animal studies in models we create in order to isolate the propriety of the FD we wanted to study. By using this methodology, we have been able to show that Flow Diversion is more likely to occlude small neck aneurysms, aneurysms in which the jailed branch has been occluded, or when the operator compact the FD in order to decrease the porosity of the device. In a 6th study, we test the result of the use of a clip to occlude a FD. Regarding the results of the test, we recommand to avoid clipping FDs.Then by using a questionaire; we showed the poor agreement of using FD in daily practice by using clinical vignettes. Then we presented the design and the result of the first randomized clinical study on flow diverters FIAT (Flow diversion In Aneurysm Treatment)
Gorgievski, Victor. « Étude des déficits de la fonction exécutive dans un modèle animal hyperdopaminergique de la schizophrénie ». Thesis, Paris 5, 2013. http://www.theses.fr/2013PA05P636.
Texte intégralSchizophrenia is a severe mental illness with a large spectrum of clinical manifestations. Since the introduction of antipsychotic medications in the 40’s, only modest progress has been made in the treatment of the disease. Currently used antipsychotics have only partial efficacy, controlling positive symptoms but usually failing to stop the mental decline of the patient. This lack of full-blown efficacy is particularly evident in the treatment of executive function deficits, which are now considered as core symptoms of schizophrenia. Increased dopamine (DA) neurotransmission is considered as a core neurochemical alteration in schizophrenia and all prescribed antipsychotics are dopamine-D2 receptor antagonists. In addition, major cognitive functions that are disarrayed in schizophrenia depend on proper DA regulation. However, there are no studies investigating the link between increased DA-ergic tone and executive function. The present thesis focuses on executive function deficits in a hyperdopaminergic mouse model, the genetically engineered mouse that lacks the dopamine transporter (DAT; DATKO mouse). First, we characterized our animal model in the Attentional Set-Shifting Test (ASST), which is a rodent adaptation of the Wisconsin Card Sorting Test, a test used to evaluate executive function in humans. DATKO mice had impaired performances in the ASST, confirming our working hypothesis. Systemic administration of the selective D1 antagonist SCH23390 ameliorated the performance of the DATKO in the ASST. In contrast, the D2 antagonist sulpiride had no effect, suggesting that the overactivation of D1 (but not D2) receptors might be involved in hyperdopaminergia-induced ASST deficits. To further investigate a possible causal link between elevated DA and ASST deficits we have induced a hyperdopaminergic state selectively in the prefrontal cortex (PFC), the region involved in executive function. This was done (i) pharmacologically, with local microinfusions of the DAT inhibitor GBR12935; (ii) optogenetically, by generating and utilising a novel transgenic tool the DATcre/ChR2 mice which express Channel-Rhodopsin selectively in DA-ergic neurons. In both constructs, PFC hyperdopaminergia resulted in ASST deficits. These, were reversed with SCH23390 but not with sulpiride, clearly establishing a role for D1 receptors in the deleterious effects of PFC hyperdopaminergia on executive function. It has been postulated that dopamine modulates PFC synaptic plasticity and associated cognitive functions through two distinct but interconnected neuronal populations: glutamatergic (Glu-) pyramidal neurons and GABA- interneurons. Immunocytochemistry experiments combining neuronal activation markers (p-ERK; c-fos) and selective labelling of Glu- versus GABA- neurons allowed to parse the role of these two populations in the ASST. A balaced Glu- versus GABA- activation was necessary for a succesful ASST performance. A dysregulated pattern of Glu- versus GABA- activation correlated with ASST deficits, leading us to speculate a putative link between cortical hyperdopaminergia and cortical Gluhypoactivation. Interestingly, glutamatergic ligands such as the mGluR2/3 agonist LY3979268 and the mGluR5 potentiator CDPPB (which are under current investigation in schizophrenia) corrected both the behavioral deficits and the altered neuronal activation pattern of hyperdopaminergic mice in the ASST. Overall, this work: (i) demonstrates for the first time a causal link between PFC hyperdopaminergia and executive deficits; (ii) proposes and validates a new model to study the cellular, molecular and synaptic mechanisms underlying executive dysfunction; (iii) suggests D1 receptor antagonism, in adjunct with current antipsychotic medications, as a novel therapeutic strategy to treat cognitive dysfunction in schizophrenia
Fall, Anna. « Rôles différentiels du cortex cingulaire antérieur sous-génual et de l'insula antérieure dans la régulation des conséquences socio-affectives de l'exclusion sociale chez le rat ». Thesis, Sorbonne université, 2019. http://www.theses.fr/2019SORUS097.
Texte intégralHumans are motivated by a fundamental need to create and maintain strong and stable relationships. Numerous behavioral studies showed that social exclusion negatively affect this fundamental need. At the neuronal level, imaging studies highlighted the involvement of the subgenual anterior cingulate cortex (sgACC) and anterior insula (AI). Interestingly, these regions are also involved in the physiopathology of major depressive disorder, where social rejection constitutes a risk factor. To this day, the role of the sgACC and AI in the integration and regulation of social exclusion signals remains relatively unknown. To investigate the behavioral consequences of social exclusion, and the differential roles of the sgACC and AI, we first developed a new behavioral task of social exclusion in rats. This tasks allowed us to investigate i) the socio-affective consequences of being exposed to a social stress, ii) the consequences of excitotoxic lesion in the rodent homologous of the sgACC (infralimbic cortex or A25) and the AI (agranular insula) on affective behavior, iii) the impact of oxytocin (OT) administration, a neuropeptide involved in affiliative behaviors, on social interactions. Our results showed that exposure to social exclusion affected social interactions and increased depressive-like behaviors. The administration of OT and lesions of the infralimbic cortex reduced this negative impact and modulated neuronal activation. In conclusion, our work highlighted a differential role of the sgACC and the AI, and allowed us to propose a framework for the mechanisms of detection and processing of social exclusion signals
Hamoui, Samar. « Etude d'un modèle lésionnel du noyau basal magnocellulaire chez le rat et développement d'une méthode de quantification de l'ARN m par PCR ». Bordeaux 2, 1993. http://www.theses.fr/1993BOR28253.
Texte intégralJoly, Fanny. « Impacts d’une perturbation de la voie TSC2/mTOR dans l’amygdale dès l’adolescence sur le comportement de peur et la fonctionnalité du cortex préfrontal chez le rat adulte Disruption of Amygdala Tsc2 in Adolescence Leads to Changed Prelimbic Cellular Activity and Generalized Fear Responses at Adulthood in Rats ». Thesis, université Paris-Saclay, 2021. http://www.theses.fr/2021UPASL016.
Texte intégralAdolescence is a highly sensitive developmental period characterized by massive structural and functional changes in networks regulating emotional and cognitive behaviors, with maturational processes influenced by environmental and genetical factors. Post-traumatic stress disorder (PTSD) is a psychiatric disorder characterized by an exaggerated fear, overgeneralization, and deficits in fear extinction. Nowadays, genetical and/or environmental predisposal factors for PTSD are not fully understood, but we know that an intense stress or a trauma endured during adolescence promotes the appearance of PTSD at adulthood following a novel trauma exposure.In this thesis, we particularly studied two structures that belong to the fear-network, the amygdala and prefrontal cortex, which follow an asynchronous maturation. While the amygdala is functionally mature at a juvenile age, its activity could impact the late maturation of the medial prefrontal cortex (mPFC). We aimed to study the impact of a disruption of Tsc2/mTOR pathway in the excitatory cells of the basolateral nucleus of the amygdala (BLA) in rats at young adolescence (post-natal day 25, PN25) or at the end of adolescence (PN50). When animals had reached adulthood, we assessed emotional behavior through a Pavlovian fear conditioning protocol, and the basal mPFC activity through the measure of expression of immediate early gene c-FOS. We show that only animals altered during young adolescence presented at the adult age typical symptoms of PTSD (fear extinction deficits, overgeneralization of fear), associated with an increase of mPFC basal activity, especially in cortical layers known to be involved in the maintenance of fear memory and expression. Thus, we suggest that a developmental dysfunction of the amygdala early in adolescence could be a predisposal factor to PTSD appearance at adulthood