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<dc:title xml:lang="fr">Axe cerveau-intestin et contrôle de la prise alimentaire : exemple d'altérations chez un modèle animal de schizophrénie</dc:title>
<dcterms:alternative xml:lang="en">Brain-gut axis and control of foodintake : example of alterations in an animal model of schizophrenia</dcterms:alternative>
<dc:subject xml:lang="fr">Axe cerveau-intestin</dc:subject>
<dc:subject xml:lang="fr">Leptine</dc:subject>
<dc:subject xml:lang="fr">Système nerveux entérique</dc:subject>
<dc:subject xml:lang="fr">Schizophrénie</dc:subject>
<dc:subject xml:lang="fr">Inflammation</dc:subject>
<dc:subject xml:lang="fr">Fonctions gastro-intestinales</dc:subject>
<dc:subject xml:lang="fr">Nerf vague</dc:subject>
<dc:subject xml:lang="en">Brain-gut axis</dc:subject>
<dc:subject xml:lang="en">Leptin</dc:subject>
<dc:subject xml:lang="en">Enteric nervous system</dc:subject>
<dc:subject xml:lang="en">Schizophrenia</dc:subject>
<dc:subject xml:lang="en">Inflammation</dc:subject>
<dc:subject xml:lang="en">Gastrointestinal functions</dc:subject>
<dc:subject xml:lang="en">Vagus nerve</dc:subject>
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<dcterms:abstract xml:lang="fr">L’axe cerveau-intestin désigne l’interaction bidirectionnelle entre le cerveau et le tube digestif. Bien que la leptine, hormone produite par le tissu adipeux, participe à la régulation de cet axe, son mode d’action dans le système nerveux entérique a été peu étudié. A l’heure actuelle, une relation étroite entre une perturbation de l’axe cerveau-intestin et la schizophrénie est supposée. Par conséquent, les objectifs de ce travail étaient d’évaluer 1) les effets ex vivo de la leptine dans la neurotransmission entérique chez le rat et 2) les altérations périphériques dans un modèle neurodéveloppemental de la schizophrénie (NVHL) chez le rat. Nous avons montré que la leptine module l’activité des neurones entériques inhibiteurs et excitateurs dans le jéjunum et le côlon proximal. L’implication des neurones afférents primaires intrinsèques a été discutée. Chez les rats NVHL, nous avons mis en évidence une réduction de la masse corporelle, des variations hormonales, une inflammation du jéjunum et des altérations motrices digestives. La relation entre les troubles périphériques, notamment vagaux, et la physiopathologie de la schizophrénie a été discutée.</dcterms:abstract>
<dcterms:abstract xml:lang="en">The brain-gut axis refers to the bidirectional interaction between the gut and the brain. Although leptin, a hormone released from fat tissue, is involved in the brain-gut axis control, its mechanism of action in the enteric nervous system has not been studied so far. Nowadays, brain-gut axis dysfunctions are supposed to be in close connection with schizophrenia. Therefore, the goals of this work were to determine 1) the effects of leptin on rat enteric nervous system neurotransmission and 2) peripheral alterations in the NVHL neurodevelopmental rat model of schizophrenia. We showed that leptin modulates inhibitory and excitatory enteric motor neurons activity in jejunum and proximal colon. Implication of intrinsic primary afferent neurons was discussed. In NVHL rats, we showed a decrease in body mass, some hormonal variations, jejunal inflammation and gastro-intestinal mechanical activities alterations. The relation peripheral alterations, like vagus nerve dysfunction, and the physiopathology of schizophrenia was discussed.</dcterms:abstract>
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