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Thèse D. Dufour 200111 UNIVERSITÉ FRANÇOIS - RABELAIS DE TOURS ÉCOLE DOCTORALE Santé, Sciences et Technologie Unité INSERM 930, Équipe 3 « neurotransmission : de l’imagerie moléculaire à la clinique » THÈSE présentée par : Diane DUFOUR-RAINFRAY soutenue le : 1er mars 2011 pour obtenir le grade de : Docteur de l’université François - Rabelais Discipline/ Spécialité : Sciences de la vie et de la santé Implication du système sérotoninergique dans l’autisme : Étude de marqueurs centraux (modèle animal) et périphériques (plaquette sanguine humaine) THÈSE dirigée par : Monsieur GUILLOTEAU Denis Professeur, Université François – Rabelais de Tours RAPPORTEURS : Monsieur CRUSIO Wim Directeur de recherche, CNRS UMR 5287 de Talence Monsieur ZIMMER Luc Professeur, Université Lyon 1 & Hospices Civils de Lyon JURY : Madame CHALON Sylvie Directrice de recherche, Unité INSERM 930 de Tours Monsieur CRUSIO Wim Directeur de recherche, CNRS UMR 5287 de Talence Monsieur GUILLOTEAU Denis Professeur, Université François – Rabelais de Tours Monsieur ZIMMER Luc Professeur, Université Lyon 1 & Hospices Civils de Lyon 1 Remerciements A Monsieur Denis Guilloteau, Je vous remercie d’avoir accepté d’être mon directeur de thèse. Voici 8 ans que vous me soutenez dans mon parcours professionnel et j’espère fermement qu’il aboutira cette année. Respectueusement. A Monsieur Wim Crusio et Monsieur Luc Zimmer Je vous remercie d’avoir accepté de juger ce travail et de m’avoir fait l’honneur d’être rapporteurs de cette thèse. Respectueusement. A Sylvie Chalon, J’apprécie beaucoup travailler avec toi, nos conversations sont toujours fécondes et motivantes. Je te remercie aussi d’avoir relu ce travail, de l’avoir enrichi par ton expérience. Je t’adresse mes sincères remerciements. A Monsieur Christian Andres, Merci de m’avoir un jour demandé « si je connaissais quelqu’un susceptible de vouloir être AHU en Biochimie ! ». Merci de m’avoir permis d’être AHU dans votre service de biochimie, nos deux services sont voués à fonctionner ensemble. Respectueusement. A Patrick Vourc’h, C’est aussi grâce à toi que cette thèse aboutit. Tu es un collègue formidable, j’apprécie tes qualités humaines et professionnelles. Amicalement. A Monsieur Jean-Claude Besnard, Je vous remercie de m’avoir dessiné un avenir dans le service de médecine nucléaire in vitro. Je vous suis très reconnaissante de votre bienveillance à mon égard. Respectueusement. 2 Je remercie : Sylvie Bodard, Zuhal Gulhan et Emilie Jaumain pour leurs larges participations aux expérimentations animales, Lucette Garreau pour son partage d’expérience, son appui pour l’établissement des protocoles d’études, Marie-Paule Vilar et Jackie Vergote pour les radiomarquages. Merci aussi à tous mes collègues du labo de recherche, Sylvie, Sylvie et Sylvie, Francine, Laurent, Johnny, Clovis, Lucette, Jackie, Emilie et Emilie, Zuhal, Nathalie, Marie-Christine, Marie-Paule, Gaëlle, Nicolas, Stéphanie, Serge, Claire, François-Xavier, Brice, Daniel, Cathie, Kate, Mitch et encore beaucoup d’autres ! Les bureaux ne bougent pas, mais il s’y assoit beaucoup de personnes en 5 ans de thèse ! Merci enfin à tous mes collègues du laboratoire de médecine nucléaire, Denis, Chantal, Christine, Martine, Serge, Sylvie, Josette, Evelyne, Marlène, Agnès, Clarisse, Annie, Christine, Marie-Thérèse, Nicole, Stéphanie, Jean-Louis, Evelyne, Meriem, les internes, externes et stagiaires; et tous les collègues de l’« in vivo » ! J’espère de tout cœur continuer ma vie professionnelle auprès de vous. 3 Voici la deuxième occasion qui m’est donnée de remercier toutes les personnes qui m’entourent et qui me soutiennent dans ma vie professionnelle et familiale. Ma belle famille et ma belle-famille : Thomas, mon cher mari Simon, Sidonie, Alice et …, mes enfants chéris Guy et Martine, mes parents Bruno et Elisabeth, mes beaux-parents Virginie ma soeur, Charles, Daphné ma filleule et Antoine Mathieu, Anne-Sophie, Maëlle, Clémentine, Luc et Max ; Marie ; Grand-Mémie Ma grand-mère Nénette, mes oncles et tantes dont Domi ma marraine Tous mes cousins, leurs valeurs ajoutées et leurs marmots chaque année plus nombreux : Aliénor, Christophe, Victor, Arthur, Elliot mon petit filleul et Elvire; Apolline, Guyaume et…; Grégoire et Frédérique ; Martin ; Manou, Fabien, Laura, Ondine et Célimène ; Ismaël, Noémie, Maïlys, Célia et…; Marie, Thomas, Lena et Liam; Nathanaël; Benoît, Mélanie et Louise Tous mes amis (dites-donc vous avez plus de marmots qu’en 2006 !) : Véronique, David, Marius, Félix et Angèle; Benoît, Bénédicte, Raphaël et Clémence ; Joseph, Carole et Julien ; Pierre, Elsa, Juliette et Joséphine ; Boubouille, Fanny, Basile et Valentin ; Charles, Virginie, Elia et Maé ; Elisabeth, Tony, Léna, Antoine et Malo ; Anne, Jean-Michel, Nel et Zoé ; Marco, Marine, Louise et Fantine ; Carline, Dominique, Baptiste, Hippolyte et Félix ; Virginie, Eric, Paul, Hippolyte et Inès ; Anne-Marie, Benoit, Pierre, Jean et Justine ; Nadège, Rémi, Susie et Lisa ; Nathalie, Mathias, Paul, Camille, Thomas et Léo ; Et tous les autres 4 Je dédie ce travail A mes parents qui m’ont permis de faire de longues études (2010-2011, la dernière carte d’étudiant !) A mon mari adoré et sa phrase favorite « Alors, ça avance ? t’as fini ta thèse ? » A mes enfants chéris qui me demandent régulièrement « Pourquoi tu fais encore une thèse ? » « Pourquoi tu fais encore une thèse ? » 5 Résumé L’autisme est une maladie neuro-développementale débutant avant l’âge de trois ans. Il est caractérisé par une altération des relations sociales et de la communication, des attitudes stéréotypées avec un répertoire restreint d’activités et d’intérêts (APA, DSM-IV, 1994). L’autisme est une maladie complexe qui implique des facteurs génétiques, épigénétiques et environnementaux (dont l’exposition à l’acide valproïque) mais l’étiologie n’est pas connue. Actuellement le diagnostic de l’autisme est basé uniquement sur des critères cliniques. Or ce diagnostic est rendu difficile en raison de l’hétérogénéité clinique de la maladie. Disposer de marqueurs de la pathogénèse de l’autisme permettrait d’améliorer la compréhension de la physiopathologie de la maladie, de compléter les arguments cliniques pour établir le diagnostic et de proposer des voies de recherche thérapeutiques ou préventives. Notre hypothèse de travail est que certaines modifications du système sérotoninergique peuvent être des marqueurs potentiels de l’autisme. Pour tester cette hypothèse, nous avons eu recours à deux modèles d'étude : la plaquette sanguine comme modèle du système sérotoninergique périphérique humain et un modèle animal, le rat exposé en prénatal à l'acide valproïque, comme modèle du système sérotoninergique central. Pour cela, nous avons validé des outils d’exploration (radioligand) et les modèles d’étude. Puis, dans chaque modèle, nous avons étudié différents paramètres sérotoninergiques (taux de sérotonine, densité de transporteurs de la sérotonine). Nous avons montré : - que le taux de sérotonine intraplaquettaire et la densité de transporteurs de la sérotonine peuvent être conjointement analysés chez l’homme. Dans notre échantillon, ces paramètres ne diffèrent pas significativement entre les groupes de témoins, patients autistes et apparentés du premier degré, - que le taux de sérotonine est abaissé de 46% dans l’hippocampe des rats exposés à l'acide valproïque, sans modification de la densité de SERT à l’âge adulte. Ces études renforcent l’intérêt de réaliser, chez des sujets avec autisme, des explorations centrales de ces potentiels marqueurs sérotoninergiques, et notamment à l’aide d’outils d’imagerie moléculaire. 6 Résumé en anglais Autism is a neurodevelopmental disorder beginning before the age of 3 years. It is characterized by qualitative impairments in social interaction and communication, and by restricted repetitive and stereotyped patterns of behaviors, interests and activities (APA, DSM-IV, 1994). Autism is a complex disease involving genetic, epigenetic and environmental factors (e.g. valproic acid exposure) but the etiology is not known. Currently the diagnosis of autism is based on clinical criteria. However this diagnosis is difficult because of the clinical heterogeneity. Development of markers of pathogenesis for autism would improve understanding of the pathophysiology, would complete clinical arguments for diagnosis and would propose preventive or therapeutic research pathways. Our working hypothesis is that modifications to the serotonergic system may be potential markers for autism. To test this hypothesis, we used two study models: the blood platelet as a human peripheral serotonergic system model and an animal model, rats prenatally exposed to valproic acid, as a model of the central serotonergic system. To do this, we validated exploration tools (radioligand) and study models. Then, in each model, we studied various serotonergic parameters (serotonin levels, density of serotonin transporters). We have shown that: - platelet serotonin levels and serotonin transporters density may be jointly tested in humans. In our sample, these parameters do not significantly differ between groups of controls, patients with autism and first-degree related, - serotonin levels were decreased by 46% in the hippocampus of rats exposed to valproic acid, and no significant modification was observed in serotonin transporters density at the adult age. These studies reinforce the interest of central exploration of serotonergic potential markers in patients with autism and especially with molecular imaging tools. 7 Table des matières Remerciements....................................................................................................................
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