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Статті в журналах з теми "Cortex cérébral – Modèles animaux":
Represa, Alfonso. "Modèles animaux des troubles du développement cérébral." Epilepsies 21, no. 1 (January 2009): 71–77. http://dx.doi.org/10.1684/epi.2009.0209.
Remaud, Sylvie, and Barbara Demeneix. "Les hormones thyroïdiennes régulent le destin des cellules souches neurales." Biologie Aujourd'hui 213, no. 1-2 (2019): 7–16. http://dx.doi.org/10.1051/jbio/2019007.
Gueye, Arona, Frans Jongejan, Mb Mbengue, A. Diouf, and Gerrit Uilenberg. "Essai sur le terrain d'un vaccin atténué contre la cowdriose." Revue d’élevage et de médecine vétérinaire des pays tropicaux 47, no. 4 (April 1, 1994): 401–4. http://dx.doi.org/10.19182/remvt.9079.
Gierski, F., J. André, O. Pierrefiche, T. Duka, and M. Naassila. "Impact cérébral du binge drinking et vulnérabilité à l’alcoolodépendance." European Psychiatry 30, S2 (November 2015): S43. http://dx.doi.org/10.1016/j.eurpsy.2015.09.121.
MENANT, O., A. DESTREZ, V. DEISS, A. BOISSY, P. DELAGRANGE, L. CALANDREAU, and Elodie CHAILLOU. "Régulation des émotions chez l’animal d’élevage : focus sur les acteurs neurobiologiques." INRA Productions Animales 29, no. 4 (December 13, 2019): 241–54. http://dx.doi.org/10.20870/productions-animales.2016.29.4.2966.
Cancel, A. "Traumatismes infantiles, morphologie cérébrale et schizophrénie : quels liens ?" European Psychiatry 30, S2 (November 2015): S15. http://dx.doi.org/10.1016/j.eurpsy.2015.09.049.
Domenech, Joseph, M. Wyers, J. P. Braun, and Pierre Formenty. "Le syndrome nerveux des ovins en Côte-d'Ivoire. I. Etude épidémiologique et clinique, méthodes de diagnostic et traitement." Revue d’élevage et de médecine vétérinaire des pays tropicaux 46, no. 3 (March 1, 1993): 423–29. http://dx.doi.org/10.19182/remvt.9431.
Дисертації з теми "Cortex cérébral – Modèles animaux":
Ballain, Thierry. "Modélisation de l'activité du cortex primaire olfactif (piriforme) chez le rat." Université Joseph Fourier (Grenoble), 2000. http://www.theses.fr/2000GRE19001.
Mallet, 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.
Qin, 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.
The 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.
Amyotrophic 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.
Retinoic 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.
Delcour, 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.
Cerebral 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.
El-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.
Guigon, 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.