help button home button Endocrine Society Endocrinology
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS

This Article
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow Request Copyright Permission
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Hoffman, G. E.
Right arrow Articles by Nathanielsz, P. W.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Hoffman, G. E.
Right arrow Articles by Nathanielsz, P. W.

Endocrinology, Vol 129, 3227-3233, Copyright © 1991 by Endocrine Society


ARTICLES

Activation of cFos in ovine fetal corticotropin-releasing hormone neurons at the time of parturition

GE Hoffman, T McDonald, R Shedwick and PW Nathanielsz
Department of Physiology, University of Pittsburgh, Pennsylvania 15261.

The ovine fetal pituitary adrenal axis plays an important role in parturition. While lesions of the paraventricular nucleus (PVN) in the fetal sheep delay parturition, suggesting that the PVN is necessary for the processes that lead up to parturition, evidence for stimulation of PVN neurons at time of delivery/labor is lacking. The present study tested the hypothesis that activation (evidenced by expression of the oncogene product cFos) of a specific population of PVN neurons containing CRH accompanies labor in sheep. Monitoring of uterine electromyogram activity determined the onset of labor. The brains of nine fetuses (removed by ceasarian section under anesthesia at gestational ages of 125-145 days) and four newborn sheep were perfused and stained for cFos and CRH. Before labor, less than 5% of fetal paraventricular CRH neurons expressed cFos. Verification that the CRH neurons could express cFos when adequately stimulated was made by exposing an additional group of four preterm animals (125 days gestational age) to hypoxemia; the six untreated fetuses served as controls. Activation of the CRH neurons by hypoxemia produced a rapid induction of cFos in CRH neurons, with approximately 50% of the cells strongly expressing cFos protein 1 h after exposure to hypoxia. At the time uterine contractions were first detected, 70% of CRH neurons expressed cFos, and cFos immunoreactivity persisted until just after birth. cFos staining declined rapidly, reaching prelabor levels in some animals by 2-3 h after birth. These data are consistent with the hypothesis that in addition to their potential role in the processes that initiate parturition over several days before birth, fetal CRH neurons are stimulated during labor, and termination of stimulation probably occurs rapidly after delivery.





HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Endocrinology Endocrine Reviews J. Clin. End. & Metab.
Molecular Endocrinology Recent Prog. Horm. Res. All Endocrine Journals
Copyright © 1991 by The Endocrine Society