title: Maternal deprivation effect on the infant's neural stress markers is reversed by tactile stimulation and feeding but not by suppressing corticosterone.
abstract: After 24 hr of maternal deprivation, significant elevations in ACTH and the naturally occurring glucocorticoid corticosterone (CORT) are observed during the stress-hyporesponsive period. The deprived pups also showed in the paraventricular nucleus (PVN) a marked increase of stress-induced c-fos mRNA and a reduction of corticotropin-releasing hormone (CRH) and glucocorticoid receptor (GR) mRNA; in hippocampal CA1, a reduction of the mineralocorticoid receptor (MR) and GR was observed. Here, we examined whether these changes are reversed by (1) preventing the elevations of CORT characteristic for the 11-d-old deprived pups by administering the synthetic glucocorticoid dexamethasone (DEX); or (2) reinstating some aspects of maternal behavior. The pups were either (1) left undisturbed, (2) stroked, or (3) stroked and episodically fed by cheek cannulation. At postnatal day 12, peripheral and neural stress markers were measured. Nondeprived animals served as controls. Experiment 1 demonstrates that although CORT was kept low by DEX, the central effects on CORT receptors, CRH, and c-fos mRNA were still present, except for MR in hippocampal CA1. Experiment 2 shows that stroking alone prevented the stress-induced rise in ACTH and c-fos mRNA and in the reduction in CRH and MR mRNA. In pups that were fed and stroked, CORT and GR mRNA resembled nondeprived controls. In conclusion, the changes in peripheral endocrine responses and in the brain cannot be attributed to the effect of elevated CORT concentrations, which are characteristic of the maternally deprived neonate. However, reinstating some components of the dams' nurturing behavior can reverse the effects evoked by maternal deprivation.
authors.affiliation: Department of Psychology, University of Delaware, Newark, Delaware 19716-2577, USA.
authors.forename: H J
authors.initials: HJ
authors.lastname: van Oers
authors.forename: E R
authors.initials: ER
authors.lastname: de Kloet
authors.forename: T
authors.initials: T
authors.lastname: Whelan
authors.forename: S
authors.initials: S
authors.lastname: Levine
mesh_terms: D000324:Adrenocorticotropic Hormone / Q000097:blood; D000818:Animals; D000833:Animals, Suckling; D000893:Anti-Inflammatory Agents / Q000494:pharmacology; D001923:Brain Chemistry / Q000187:drug effects / Q000502:physiology; D003345:Corticosterone / Q000097:blood*; D003346:Corticotropin-Releasing Hormone / Q000235:genetics; D003907:Dexamethasone / Q000494:pharmacology; D005247:Feeding Behavior / Q000502:physiology*; D005260:Female; D015870:Gene Expression / Q000502:physiology; D007030:Hypothalamo-Hypophyseal System / Q000502:physiology; D008297:Male; D008426:Maternal Deprivation; D010913:Pituitary-Adrenal System / Q000502:physiology; D016760:Proto-Oncogene Proteins c-fos / Q000235:genetics; D012333:RNA, Messenger / Q000032:analysis; D051381:Rats; D020318:Rats, Long-Evans; D017207:Rats, Sprague-Dawley; D011987:Receptors, Steroid / Q000235:genetics; D013312:Stress, Physiological / Q000503:physiopathology*; D014110:Touch / Q000502:physiology*
chemical_list: D000893:Anti-Inflammatory Agents; D016760:Proto-Oncogene Proteins c-fos; D012333:RNA, Messenger; D011987:Receptors, Steroid; D003907:Dexamethasone; D000324:Adrenocorticotropic Hormone; D003346:Corticotropin-Releasing Hormone; D003345:Corticosterone