Toggle Main Menu Toggle Search

Open Access padlockePrints

Gonadal steroid modulation of stress-induced hypothalamo-pituitary-adrenal activity and anxiety behavior: Role of central oxytocin

Lookup NU author(s): Professor Colin Ingram


Full text for this publication is not currently held within this repository. Alternative links are provided below where available.


Intracerebroventricular administration of oxytocin reduces anxiety behavior and hypothalamo-pituitary-adrenal (HPA) responses to stress in female rats. Similar changes are seen in late-pregnant rats, and oxytocin-sensitive pathways may mediate these effects. This study investigated anxiety behavior and stress responses using a gonadal steroid model of late pregnancy, which is known to increase endogenous oxytocin expression. Compared with continuous progesterone treatment, 3-d withdrawal of progesterone after 11-d treatment of ovariectomized rats with estradiol and progesterone resulted in increased binding of the oxytocin receptor ligand [125I]d(CH2)5[Tyr(Me)2,Thr 4,Tyr-NH29]ornithine vasotocin in selective forebrain regions, including the ventrolateral septum and ventromedial hypothalamus. Behavior in the elevated plus-maze indicated that progesterone withdrawal had an anxiolytic effect, and this was associated with lower levels of c-fos mRNA expression in the ventral hippocampus, an area previously shown to be sensitive to oxytocin. In other groups of animals, the plasma corticosterone response to a psychological stress (10 min of 114 dB white noise) was significantly attenuated by this steroid manipulation. Furthermore, simultaneous infusion of the selective oxytocin receptor antagonist desGlyNH2,d(CH2)5[Tyr(Me)2,Thr 4]OVT during the period of progesterone withdrawal reversed this attenuation of noise-induced HPA activation, indicating a role for endogenous oxytocin in this effect. Thus, mimicking the steroid profile of late pregnancy leads to a reduction in anxiety behavior and attenuates HPA activity induced by mild stress. These effects appear to be mediated through the involvement of central oxytocin neurotransmission. Copyright © 2006 by The Endocrine Society.

Publication metadata

Author(s): Windle RJ, Gamble LE, Kershaw YM, Wood SA, Lightman SL, Ingram CD

Publication type: Article

Publication status: Published

Journal: Endocrinology

Year: 2006

Volume: 147

Issue: 5

Pages: 2423-2431

ISSN (print): 0013-7227

ISSN (electronic): 1945-7170

Publisher: The Endocrine Society


DOI: 10.1210/en.2005-1079

PubMed id: 16439458


Altmetrics provided by Altmetric


Funder referenceFunder name
Wellcome Trust
BB/C51297X/1Biotechnology and Biological Sciences Research Council