Adoption reverses the long-term impairment in glucocorticoid feedback induced by prenatal stress

Abstract

The development of the organism is subjected to critical and complex influences during the perinatal period. Prenatal and postnatal stresses can have different long-term behavioral effects, and appropriate postnatal manipulations can counteract the behavioral effects of prenatal stress. In the present study, we investigated the involvement of changes in the activity of the hypothalamo-pituitary-adrenal (HPA) axis in the long-term effects of prenatal and postnatal events and of interactions between them. We investigated stress-induced corticosterone secretion and hippocampal corticosteroid receptors in male adult rats submitted to prenatal and/or postnatal manipulations.Repeated restraint during the last week of pregnancy was used as prenatal stressor, and adoption at birth was used to change the postnatal environment. We found that (1) prenatal stress prolongs stressinduced corticosterone secretion in adult rats, which was attributed to the observed decrease in central corticosteroid receptors; (2) adoption, irrespective of the stress experience of the foster mother, reverses the effects of prenatal stress; and (3) adoption per se increases maternal behavior and decreases the stress-induced corticosterone secretion peak in the adult offspring. In conclusion, certain prenatal and postnatal manipulations appear to have opposite long-term effects on the activity of the HPA axis, and adoption, probably by modifying maternal behavior, can protect against the effects of prenatal stress. Thus, changes in the activity of the HPA axis may be one of the biological substrates of the long-term effects of certain perinatal events.[Key words: corticosterone, corticosteroid receptors, hippocampus, prenatal stress, adoption, postnatal stress, pefinatal environment] Prenatal and postnatal environments exercise complex influences on the development of an organism. In particular, life events occurring during these two early periods of life can have different long-term behavioral effects. For example, in man, prenatal stress can induce mental retardation and sleep distur-

Attenuation by a sigma1 (σ1) receptor agonist of the learning and memory deficits induced by a prenatal restraint stress in juvenile rats

“…PS has also been reported to affect hippocampal corticosteroid receptors. Both glucocorticoid type I and II receptors are reduced in the hippocampus after PS, in relation with the HPA axis hyperactivity (Maccari et al, 1995). This decrease could be reversed by postnatal adoption, suggesting that environmental factors are sufficient to allow attenuation of the developmental deficits (Maccari et al, 1995).…”

“…Both glucocorticoid type I and II receptors are reduced in the hippocampus after PS, in relation with the HPA axis hyperactivity (Maccari et al, 1995). This decrease could be reversed by postnatal adoption, suggesting that environmental factors are sufficient to allow attenuation of the developmental deficits (Maccari et al, 1995). PS thus results in deficits affecting several neurotransmission systems, with the hippocampal formation appearing as a particularly vulnerable brain region.…”

“…A prenatal stress (PS) results in the hyperactivation of the maternal hypothalamo-pituitary-adrenal (HPA) axis, leading to enhanced production of stress hormones. Consequently, PS offspring exhibits elevated neuroendocrine responses to stress, including elevated secretions of corticotropin-releasing factor (CRF), adrenocorticotropin-releasing hormone (ACTH) and corticosterone (Peters, 1982;Maccari et al, 1995;Weinstock et al, 1998), and a reduction in the density of corticosteroid receptors in the hippocampus (Weinstock, 1997;Valle´e et al, 1999). Finally, the hippocampus appears as a brain structure sensitive to PS (Weinstock, 1997;Valle´e et al, 1999) and PS offspring shows from infancy to senescence and throughout adulthood marked memory deficits in numerous, and particularly hippocampal-dependent, behavioral tasks (Szuran et al, 1994;Lordi et al, 1997;Valle´e et al, 1999).…”

The Size and Distribution of Midbrain Dopaminergic Populations are Permanently Altered by Perinatal Glucocorticoid Exposure in a Sex- Region- and Time-Specific Manner

“…Moreover, another study using double our prenatal concentration of dexamethasone in the drinking water made a detailed analysis of maternal behavior in the first week after birth and reported a positive rather than negative effect (Hauser et al, 2006). It would also appear that cross-fostering per se may not be without significant effects on maternal behaviors (Maccari et al, 1995) and has been reported to reduce baseline and nicotine-stimulated DA secretion in the nucleus accumbens (Kane et al, 2004). On the other hand, certain programming effects of prenatal dexamethasone treatment were unaffected by cross-fostering to control dams, suggesting that the GC effects operate directly in the fetus (Nyirenda et al, 2001).…”

Cocaine disrupts pup-induced maternal behavior in juvenile and adult rats

“…The cross-fostering of large groups of animals requires intensive observation and control to optimize the time of foster placement, and there are disagreements as to possible effects of fostering alone [10,27]. The CS and IS control groups were quite similar to each other and generally to UN control groups although the CSCS group had the highest success rates as adults.…”