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This Article Accepted manuscript (PDF) All Versions of this Article: JOE-09-0175v1 202/2/279    most recent Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Evuarherhe, O. Articles by Lightman, S. Search for Related Content PubMed PubMed Citation Articles by Evuarherhe, O. Articles by Lightman, S.

O Evuarherhe, HW LINE, University of Bristol, Bristol, BS1 3NY, United Kingdom
J Leggett, HW LINE, University of Bristol, Bristol, United Kingdom
E Waite, HW LINE, University of Bristol, Bristol, United Kingdom
Y Kershaw, HW LINE, University of Bristol, Bristol, United Kingdom
S Lightman, HW LINE, University of Bristol, Bristol, United Kingdom

Correspondence: Obaro Evuarherhe, Email: obaro.evuarherhe{at}bristol.ac.uk

The neuroendocrine gender-dimorphism which begins during perinatal development is completed during puberty. We have previously described how perinatal gonadal steroids programme HPA activity in adulthood and we now assess the role of peripubertal ovarian hormones. Prepubertal females were treated subcutaneously with either cholesterol or 17β-oestradiol and their pituitary-adrenal activity was assessed 5 days later. Oestradiol suppressed the ACTH and corticosterone responses to restraint stress in the prepubertal female. Further groups of female rats were ovariectomized either before or after puberty and adult animals were subsequently treated with subcutaneous implants containing either 17β-oestradiol or cholesterol. Corticosterone pulsatility was assessed using an automated blood sampling system to collect blood from freely moving animals at 10-min intervals over 24 hours. Oestradiol administered to adults that had been ovariectomized either pre- or post-pubertally displayed a significantly higher mean corticosterone level as well as increased pulse frequency and pulse amplitude compared to cholesterol treated controls. These data demonstrate a reversal in the effect of oestrogens on HPA axis activity over the time of puberty with inhibitory effects prepubertally and stimulatory actions after puberty and imply an ovarian steroid independent mechanism of pubertal maturation of HPA sensitivity to oestrogens.