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32. Environnement précoce et vulnérabilité neuropsychiatrique

Author

Rincel, Marion, LEPINAY, Amandine, Gabory, Anne, Theodorou, Vassilia, Koehl, Muriel, Dauge, Valerie, Maccari, Stéfania, Darnaudéry, Muriel, Nutrition et Neurobiologie intégrée (NutriNeur0), Université Bordeaux Segalen - Bordeaux 2-Institut National de la Recherche Agronomique (INRA)-Université Sciences et Technologies - Bordeaux 1-Institut Polytechnique de Bordeaux-Ecole nationale supérieure de chimie, biologie et physique, Université Paris-Saclay, ToxAlim (ToxAlim), Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Institut National Polytechnique (Toulouse) (Toulouse INP), Université Fédérale Toulouse Midi-Pyrénées-Ecole Nationale Vétérinaire de Toulouse (ENVT), Institut National Polytechnique (Toulouse) (Toulouse INP), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Ecole d'Ingénieurs de Purpan (INPT - EI Purpan), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Institut National de la Recherche Agronomique (INRA), INSERM, Neurocentre Magendie, U1215, Physiopathologie de la Plasticité Neuronale, F-33000 Bordeaux, France, stress périnatal et maladies neurodégénératives, Université de Lille, and Ecole nationale supérieure de chimie, biologie et physique-Institut Polytechnique de Bordeaux-Université Sciences et Technologies - Bordeaux 1-Institut National de la Recherche Agronomique (INRA)-Université Bordeaux Segalen - Bordeaux 2

Subjects
Adult, MESH: Disease Susceptibility, Epigenesis, Genetic, MESH: Prenatal Exposure Delayed Effects, MESH: Brain, MESH: Pregnancy, Pregnancy, Animals, Humans, MESH: Mental Disorders, MESH: Animals, MESH: Epigenesis, Genetic, MESH: Humans, Mental Disorders, MESH: Infant, Newborn, Infant, Newborn, Brain, MESH: Adult, MESH: Stress, Psychological, Disease Models, Animal, Prenatal Exposure Delayed Effects, Female, [SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC], Disease Susceptibility, MESH: Disease Models, Animal, MESH: Female, Stress, Psychological
Abstract

International audience; The human newborn is highly dependent on parental care for its survival but also for the healthy development of its brain. A large body of literature demonstrates the impact of early life adversity, even during the prenatal period, on the adult's health. The susceptibility to neuropsychiatric diseases is often potentiated by early stress. If there is an agreement that a critical developmental period exists, the mechanisms underlying the long term effects of early life adversity are still poorly understood. Recent studies in animals highlight the involvement of epigenetic processes in the transmission of such vulnerabilities, notably via modifications in germ cells, which can be transmitted in the next generations.

Published
2016
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34. Croissance et puberté : évolutions séculaires, facteurs environnementaux et génétiques

Author

Amselem, Serge, Carel, Jean-Claude, de Roux, Nicolas, Issad, Tarik, Maccari, Stéfania, Prevot, Vincent, Susanne, Charles, CHU Trousseau [APHP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU), Diabète de l'enfant et développement ((U 690)), Université Paris Diderot - Paris 7 (UPD7)-Institut National de la Santé et de la Recherche Médicale (INSERM), Institut Cochin (IC UM3 (UMR 8104 / U1016)), Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), stress périnatal et maladies neurodégénératives, Université de Lille, Centre de Recherche Jean-Pierre AUBERT Neurosciences et Cancer - U837 (JPArc), Université Lille Nord de France (COMUE)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Lille, Université libre de Bruxelles (ULB), Institut national de la santé et de la recherche médicale(INSERM), Service de Génétique et d'Embryologie Médicales [CHU Trousseau], Assistance publique - Hôpitaux de Paris (AP-HP)-CHU Trousseau [APHP], Diabète de l'enfant et développement, Université Paris Diderot - Paris 7 ( UPD7 ) -IFR2-Institut National de la Santé et de la Recherche Médicale ( INSERM ), Institut Cochin ( UM3 (UMR 8104 / U1016) ), Université Paris Descartes - Paris 5 ( UPD5 ) -Institut National de la Santé et de la Recherche Médicale ( INSERM ) -Centre National de la Recherche Scientifique ( CNRS ), U837, Développement et Plasticité du cerveau post-natal, Centre de Recherche Jean-Pierre Aubert, Institut National de la Santé et de la Recherche Médicale, Université Libre de Bruxelles [Bruxelles] ( ULB ), ORANGE, Colette, Service de génétique et embryologie médicales [CHU Trousseau], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris Diderot - Paris 7 (UPD7), Centre National de la Recherche Scientifique (CNRS)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM), and Institut National de la Santé et de la Recherche Médicale (INSERM)

Subjects
Habitudes alimentaires, [SDV.EE.SANT]Life Sciences [q-bio]/Ecology, environment/Health, Anthropométrie, Taille, [SDV.EE.SANT] Life Sciences [q-bio]/Ecology, environment/Health, Courbe de croissance, Poids, Obésité, Stress, Alimentation, [ SDV.EE.SANT ] Life Sciences [q-bio]/Ecology, environment/Health, Nutrition
Abstract

Dans la plupart des pays occidentaux, la taille moyenneatteinte à l’âge adulte a augmenté depuis la deuxièmemoitié du xixe siècle. Néanmoins, cette tendancecommence à s’infléchir dans certains pays sans que l’onen connaisse la cause. Parallèlement à l’augmentationde la taille, on observe une tendance à une pubertéplus précoce en particulier chez les filles. Certainsscientifiques suggèrent une relation avec l’épidémied’obésité. L’exploration des facteurs génétiques etenvironnementaux qui influencent la croissance et lamaturation constitue un vaste champ de recherche.À la demande du Régime social des indépendants (RSIex Canam), l’Inserm a réalisé une expertise collectivesur le thème de la croissance et de la puberté et leursévolutions afin de dégager des recommandations utilespour la santé publique et la recherche. Mieux connaîtrel’évolution de la croissance moyenne de la populationen France, approfondir les liens entre l’initiation de lapuberté, les facteurs d’environnement et la survenue demaladies sont des pistes à explorer.

Published
2007

35. Individual vulnerability to substance abuse and affective disorders: role of early environmental influences

Author

Koehl, Muriel, Lemaire, Valerie, Mayo, Willy, Abrous, Djoher Nora, Maccari, Sefania, Piazza, Pier Vincenzo, Le Moal, Michel, Vallée, Monique, Maccari, Stéfania, Moal, Michel, INSERM, Neurocentre Magendie, U1215, Physiopathologie de la Plasticité Neuronale, F-33000 Bordeaux, France, Physiopathologie du système nerveux central - Institut François Magendie, Université Bordeaux Segalen - Bordeaux 2-IFR8-Institut National de la Santé et de la Recherche Médicale (INSERM), Aquitaine, stress périnatal et maladies neurodégénératives, Université de Lille, Neurocentre Magendie : Physiopathologie de la Plasticité Neuronale (U1215 Inserm - UB), and Université de Bordeaux (UB)-Institut François Magendie-Institut National de la Santé et de la Recherche Médicale (INSERM)

Subjects
0303 health sciences, General Neuroscience, Dentate gyrus, [SCCO.NEUR]Cognitive science/Neuroscience, Brain morphometry, Vulnerability, Cognition, Toxicology, medicine.disease, Developmental psychology, Substance abuse, 03 medical and health sciences, 0302 clinical medicine, Prenatal stress, medicine, Neurochemistry, Psychology, 030217 neurology & neurosurgery, 030304 developmental biology, Psychopathology, Clinical psychology
Abstract

International audience; One of the most important questions raised by modern psychiatry and experimental psychopathology is the origin of mental diseases. More concisely, clinical and experimental neurosciences are increasingly concerned with the factors that render one individual more vulnerable than another to a given pathological outcome. Animal models are now available to understand the sources of individual differences for specific phenotypes prone to behavioral disadaptations. Over the last 10 years we have explored the consequences of environmental perinatal manipulations in the rat. We have shown that prenatal stress is at the origin of a wide range of physiological and behavioral aberrances such as alterations in the activity of the hormonal stress axis, increased vulnerability to drug of abuse, emotional liability, cognitive impairments and predisposition to pathological aging. Taken together, these abnormalities define a bio-behavioral syndrome. Furthermore, the cognitive disabilities observed in prenatally-stressed rats were recently related to an alteration of neurogenesis in the dentate gyrus, thus confirming the impact of early life events on brain morphology. A second model (handling model) has also been developed in which pups are briefly separated from their mothers during early postnatal life. In contrast with prenatally-stressed animals, handled rats exhibited a reduced emotion response when confronted with novel situations and were protected against age-induced impairments of both the hormonal stress axis and cognitive functions. Taken together, the results of these investigations show that the bio-behavioral phenotype that characterizes each individual is strongly linked to the nature and timing of perinatal experience. Furthermore, data collected in prenatally-stressed animals indicate that this model could be used profitably to understand the etiology and pathophysiology of affective disorders.

Published
2003
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37. Long-term effects of prenatal stress and postnatal handling on age-related glucocorticoid secretion and cognitive performance: a longitudinal study in the rat

Author

Vallée, Monique, Maccari, Stéfania, Dellu, Françoise, Simon, Hervé, Le Moal, Michel, Mayo, Willy, Aquitaine, stress périnatal et maladies neurodégénératives, Université de Lille, EURORAD, Physiopathologie du système nerveux central - Institut François Magendie, and Université Bordeaux Segalen - Bordeaux 2-IFR8-Institut National de la Santé et de la Recherche Médicale (INSERM)

Subjects
Male, Aging, Receptors, Steroid, [SCCO.NEUR]Cognitive science/Neuroscience, Handling, Psychological, Hippocampus, Rats, Rats, Sprague-Dawley, Cognition, Fetus, Animals, Newborn, Memory, Stress, Physiological, Animals, Protein Isoforms, Longitudinal Studies, Corticosterone, Maze Learning, Glucocorticoids
Abstract

International audience; There is growing evidence that stress during prenatal and postnatal periods of life can modify adaptive capacities in adulthood. The hypothalamo-pituitary-adrenal axis may mediate an animal's responses to perinatal stressful events and thus serve as a neurobiological substrate of the behavioural consequences of these early events. However, little is known about the long-term effects of prenatal stressors throughout the entire life of the animals. The focus of the present study was to examine the long-term influences of a prenatal and postnatal stress on glucocorticoid secretion and cognitive performance. Prenatal stress of rat dams during the last week of pregnancy and postnatal daily handling of rat pups during the first 3 weeks of life were used as stressors. The long-term effects of these manipulations were analysed using a longitudinal approach throughout the entire life of the animals, and were repeatedly tested in adulthood (4-7 months), middle age (13-16 months) and in later life (20-24 months). The study demonstrated that prenatal stress and postnatal handling induced opposite effects on both glucocorticoid secretion and cognitive performance. Prenatal stress accelerated the age-related hypothalamo-pituitary-adrenal axis dysfunctions; indeed, circulating glucocorticoids levels of prenatally stressed middle-aged animals are similar to old control ones, and also induced cognitive impairments. In contrast, postnatal handling protected from the age-related neuroendocrine and behavioural alterations. These results show that the altered glucocorticoid secretion induced by early environmental manipulations is primary to the cognitive alterations observed only later in life and could be one cause of age-related memory deficits.

Published
1999
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