Long-term effects of maternal deprivation on the corticosterone response to stress in rats

Abstract

Twenty-four hours of maternal deprivation result in activation of the infant rat’s adrenocortical axis. In the present study we examined the long-term effects of maternal deprivation on the corticosterone (Cort) response to stress. Pups were maternally deprived (Dep) on postnatal day( PND) 11 and tested immediately ( PND 12) or returned to their mothers and tested at later ages. Testing consisted of a time course of the Cort response to a saline injection (5, 15, 30, and 60 min). At PND 12, the response of Dep pups was higher than that of nondeprived (non-Dep) pups. No group differences were observed at PND 16 and 22. On PND 30, Dep rats showed lower Cort levels than non-Dep pups at 0, 5, and 30 min after saline. At PND 60, non-Dep females showed higher Cort levels than males at 5, 15, and 30 min. This gender difference for Dep pups was observed only at 5 min. Male and female Dep animals presented lower Cort levels than non-Dep counterparts at 60 and 30 min after saline, respectively. These findings indicate that maternal deprivation effects on Cort secretion are long lasting. Dep rats showed a smaller adrenal response to stress at PND 30, whereas as adults the stress response was similar but the turnoff was different.

The arcuate NPY, POMC, and CART expressions responding to food deprivation are exaggerated in young female rats that experienced neonatal maternal separation

“…Previous studies have demonstrated that neonatal maternal separation, an animal model of a stressful experience in childhood, can permanently modify the characteristics of the hypothalamicpituitary-adrenal gland (HPA) axis in the offspring (Plotsky and Meaney, 1993;Suchecki and Tufik, 1997;van Oers et al, 1998;Liu et al, 2000). An elevation in the plasma glucocorticoids (corticosterone in rodents) level is known to be a consequence of the HPA axis activation.…”

“…Dysfunction of the hypothalamicpituitary-adrenal gland (HPA) axis is implicated in the pathogenesis of eating disorders (Koo-Loeb et al, 2000;Putignano et al, 2001;Gluck et al, 2004). Neonatal maternal separation, an animal model of stressful experiences in childhood, can permanently modify the characteristics of HPA axis in the offspring (Plotsky and Meaney, 1993;Suchecki and Tufik, 1997;van Oers et al, 1998;Liu et al, 2000). Neuropeptide Y (NPY), the most potent orexic peptide known, stimulates feeding (Stanley and Leibowitz, 1985;Kalra et al, 1999;Schwartz et al, 2000).…”

Sustained hyperphagia in adolescent rats that experienced neonatal maternal separation

“…[2][3][4] Neonatal maternal separation (MS), an animal model of stressful experiences in childhood, can permanently modify the characteristics of HPA axis in the offspring. [5][6][7][8] Glucocorticoids, stress hormones released by activation of the HPA axis, are known to be involved in the regulation of energy balance, 9,10 and some of the central effects of glucocorticoids are believed to be mediated by hypothalamic neuropeptides. 11,12 It has been reported that experiences of repeated MS during pre-weaning period increase the hypothalamic level of neuropeptide Y (NPY) in rats later in life.…”

Adrenocortical response to stress in fasted and unfasted artificially reared 12‐day‐old rat pups

“…Twelve-day-old rats that have been deprived of their mothers for the previous 24 hr exhibit a pronounced ACTH (Suchecki, Mozaffarian, Gross, Rosenfeld, & Levine, 1993) and corticosteroid response to stress (Levine, Huchton, Wiener, & Rosenfeld, 1992;Suchecki & Tufik, 1997), indicating that mother-infant interactions are at least partly responsible for the regulation of the HPA axis in developing pups (Rosenfeld, Suchecki, & Levine, 1992). While the maternal factors that contribute to the SHRP have not been clearly identified, feeding and stroking of the anogenital region is known to play a role: Pups that have been deprived of their mothers for 24 hr, but cannula fed during that time, show an amelioration of the deprivation effect on the HPA response (van Oers, de Kloet, Whalen, & Levine, 1998).…”