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Lookup NU author(s): Professor Colin Ingram
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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.
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
URL: http://dx.doi.org/10.1210/en.2005-1079
DOI: 10.1210/en.2005-1079
PubMed id: 16439458
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