title: Postnatal maternal deprivation produces long-lasting modifications of the stress response, feeding and stress-related behaviour in the rat.
abstract: The hypothalamo-pituitary-adrenal (HPA) axis plays a central role both in the regulation of the stress response, and in the control of feeding behaviour. Sensitivity of the HPA axis to respond to stress varies both during ontogeny and between individuals, and can be altered by neonatal events. The aim of our experiments was to determine whether early events that affect the HPA axis could also induce persistent modifications in food intake (quantitatively and qualitatively), as well as alterations of anxiety-related behaviour. Twenty-four-hour maternal deprivation was introduced at two different periods of HPA maturation, on day 5 (DEP5) or day 14 (DEP14) after birth. Sequential measurements of plasma levels of adrenocorticotropin hormone (ACTH) and corticosterone showed that this deprivation altered the HPA axis of adults; the response to restraint stress was prolonged in DEP5 and a higher ACTH peak appeared in DEP14. The neonatal stress also produced long-lasting modifications of rat behaviour, as DEP14 adults became more anxious. Standard food intake decreased in both groups of deprived rats. Diet preferences also changed, as carbohydrate intake decreased in DEP5 rats. Corticosteroid receptor binding did not vary in the hippocampus of the deprived rats. The modifications of the stress response and the behaviour parameters could be due to the alteration of corticosteroid receptors in the hypothalamic paraventricular nucleus and/or corticotropin-releasing hormone or vasopressin function, but these parameters have yet to be determined. This early stress paradigm altering feeding behaviour could become an interesting model for research into human eating disorders.
authors.affiliation: Laboratoire de Biologie Cellulaire, Université Henri Poincaré, 38 rue Lionnois, 54000 Nancy, France.
authors.forename: Z
authors.initials: Z
authors.lastname: Penke
authors.forename: K
authors.initials: K
authors.lastname: Felszeghy
authors.forename: B
authors.initials: B
authors.lastname: Fernette
authors.forename: D
authors.initials: D
authors.lastname: Sage
authors.forename: C
authors.initials: C
authors.lastname: Nyakas
authors.forename: A
authors.initials: A
authors.lastname: Burlet
mesh_terms: D000324:Adrenocorticotropic Hormone / Q000097:blood; D000818:Animals; D000831:Animals, Newborn; D001522:Behavior, Animal / Q000502:physiology*; D001835:Body Weight / Q000502:physiology; D003345:Corticosterone / Q000097:blood; D004195:Disease Models, Animal; D004435:Eating / Q000502:physiology; D005247:Feeding Behavior / Q000502:physiology*; D005260:Female; D006624:Hippocampus / Q000378:metabolism; D007030:Hypothalamo-Hypophyseal System / Q000254:growth & development* / Q000378:metabolism; D008297:Male; D008426:Maternal Deprivation; D009043:Motor Activity / Q000502:physiology; D009747:Nutritional Physiological Phenomena / Q000502:physiology; D010913:Pituitary-Adrenal System / Q000254:growth & development* / Q000378:metabolism; D051381:Rats; D020318:Rats, Long-Evans / Q000502:physiology*; D011965:Receptors, Glucocorticoid / Q000187:drug effects / Q000378:metabolism; D018161:Receptors, Mineralocorticoid / Q000187:drug effects / Q000378:metabolism; D011987:Receptors, Steroid / Q000378:metabolism; D012149:Restraint, Physical / Q000009:adverse effects; D013312:Stress, Physiological / Q000503:physiopathology*
chemical_list: D011965:Receptors, Glucocorticoid; D018161:Receptors, Mineralocorticoid; D011987:Receptors, Steroid; D000324:Adrenocorticotropic Hormone; D003345:Corticosterone