title: Maternal exposure to low levels of corticosterone during lactation protects the adult offspring against ischemic brain damage.
abstract: A growing body of evidence underscores the importance of early life events as predictors of health in adulthood. Abnormalities in maternal care or other forms of early postnatal stress induce long-term changes in behavior and influence the vulnerability to illnesses throughout life. Some of these changes may be produced by the activation of the hypothalamic-pituitary-adrenal (HPA) axis, which is invariably associated with stress. We used a model in which neonate rats are fed by mothers drinking water supplemented with 0.2 mg/ml corticosterone, the main glucocorticoid hormone in rodents. Plasma corticosterone levels increased in the dams to an extent similar to that induced by a mild stress. Corticosterone-treated dams also showed an increase in maternal care. Remarkably, adult rats that had been nursed by corticosterone-treated mothers were protected against neuronal damage and cognitive impairment produced by transient global brain ischemia. Neuroprotection was associated with a reduced HPA response to ischemia and was primarily decreased when corticosterone was injected at a dose that eliminated any difference in endogenous corticosterone levels between rats raised by mothers supplemented with corticosterone and their matched controls. These data suggest that an increased maternal care protects the offspring against ischemic neuronal damage and that at least a component of neuroprotection is mediated by a reduced response of the HPA axis to ischemia.
authors.affiliation: Department of Human Physiology and Pharmacology, University of Rome La Sapienza, Faculty of Medicine, 00185 Rome, Italy.
authors.forename: Paola
authors.initials: P
authors.lastname: Casolini
authors.forename: Maria Rosaria
authors.initials: MR
authors.lastname: Domenici
authors.forename: Carlo
authors.initials: C
authors.lastname: Cinque
authors.forename: Giovanni Sebastiano
authors.initials: GS
authors.lastname: Alemà
authors.forename: Valentina
authors.initials: V
authors.lastname: Chiodi
authors.forename: Mariangela
authors.initials: M
authors.lastname: Galluzzo
authors.forename: Marco
authors.initials: M
authors.lastname: Musumeci
authors.forename: Jerome
authors.initials: J
authors.lastname: Mairesse
authors.forename: Anna Rita
authors.initials: AR
authors.lastname: Zuena
authors.forename: Patrizia
authors.initials: P
authors.lastname: Matteucci
authors.forename: Giuseppe
authors.initials: G
authors.lastname: Marano
authors.forename: Stefania
authors.initials: S
authors.lastname: Maccari
authors.forename: Ferdinando
authors.initials: F
authors.lastname: Nicoletti
authors.forename: Assia
authors.initials: A
authors.lastname: Catalani
mesh_terms: D000375:Aging / Q000502:physiology*; D000818:Animals; D000831:Animals, Newborn; D002545:Brain Ischemia / Q000188:drug therapy / Q000378:metabolism* / Q000517:prevention & control; D003345:Corticosterone / Q000378:metabolism* / Q000494:pharmacology; D005260:Female; D007030:Hypothalamo-Hypophyseal System / Q000187:drug effects / Q000378:metabolism; D007774:Lactation / Q000502:physiology*; D008297:Male; D018696:Neuroprotective Agents / Q000378:metabolism* / Q000494:pharmacology; D010913:Pituitary-Adrenal System / Q000187:drug effects / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D013312:Stress, Physiological / Q000378:metabolism / Q000503:physiopathology; D013995:Time
chemical_list: D018696:Neuroprotective Agents; D003345:Corticosterone