Faculty Collaboration Database

Augmented hypothalamic corticotrophin-releasing hormone mRNA and corticosterone responses to stress in adult rats exposed to perinatal hypoxia. J Neuroendocrinol 2007 Nov;19(11):907-12

Date

10/12/2007

Pubmed ID

17927669

Pubmed Central ID

PMC2030994

DOI

10.1111/j.1365-2826.2007.01595.x

Scopus ID

2-s2.0-35048852641 (requires institutional sign-in at Scopus site)   33 Citations

Abstract

Stressful events before or just after parturition alter the subsequent phenotypical response to stress in a general process termed programming. Hypoxia during the period before and during parturition, and in the postnatal period, is one of the most common causes of perinatal distress, morbidity, and mortality. We have found that perinatal hypoxia (prenatal day 19 to postnatal day 14) augmented the corticosterone response to stress and increased basal corticotrophin-releasing hormone (CRH) mRNA levels in the parvocellular portion of the paraventricular nucleus (PVN) in 6-month-old rats. There was no effect on the levels of hypothalamic parvocellular PVN vasopressin mRNA, anterior pituitary pro-opiomelanocortin or CRH receptor-1 mRNA, or hippocampus glucocorticoid receptor mRNA. We conclude that hypoxia spanning the period just before and for several weeks after parturition programmes the hypothalamic-pituitary-adrenal axis to hyper-respond to acute stress in adulthood, probably as a result of drive from the parvocellular CRH neurones.

Author List

Raff H, Jacobson L, Cullinan WE

Authors

William E. Cullinan PhD Adjunct Associate Professor in the Neurosurgery department at Medical College of Wisconsin
Hershel Raff PhD Professor in the Academic Affairs department at Medical College of Wisconsin

MESH terms used to index this publication - Major topics in bold

Animals
Animals, Newborn
Body Weight
Corticosterone
Corticotropin-Releasing Hormone
Female
Fetus
Hypothalamus
Hypoxia
Male
Pregnancy
Prenatal Exposure Delayed Effects
RNA, Messenger
Rats
Stress, Psychological