{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,30]],"date-time":"2026-10-30T04:04:14Z","timestamp":1793333054515,"version":"4.5.0"},"reference-count":35,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2013,2,24]],"date-time":"2013-02-24T00:00:00Z","timestamp":1361664000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J Neuroendocrinology"],"published-print":{"date-parts":[[2013,3]]},"abstract":"<jats:p>Female rats show a gonadotrophin\u2010releasing hormone (Gn<jats:styled-content style=\"fixed-case\">RH<\/jats:styled-content>)\/luteinising hormone (<jats:styled-content style=\"fixed-case\">LH<\/jats:styled-content>) surge in the presence of a preovulatory level of oestrogen, whereas males do not because of brain defeminisation during the developmental period by perinatal oestrogen converted from androgen. The present study aimed to identify the site(s) of oestrogen action and the critical period for defeminising the mechanism regulating the Gn<jats:styled-content style=\"fixed-case\">RH<\/jats:styled-content>\/<jats:styled-content style=\"fixed-case\">LH<\/jats:styled-content> surge. Animals given perinatal treatments, such as steroidal manipulations, brain local implantation of oestradiol (<jats:styled-content style=\"fixed-case\">E<\/jats:styled-content><jats:sub>2<\/jats:sub>) or administration of an <jats:styled-content style=\"fixed-case\">NMDA<\/jats:styled-content> antagonist, were examined for their ability to show an <jats:styled-content style=\"fixed-case\">E<\/jats:styled-content><jats:sub>2<\/jats:sub>\u2010induced <jats:styled-content style=\"fixed-case\">LH<\/jats:styled-content> surge at adulthood. Lordosis behaviour was examined to compare the mechanisms defeminising the <jats:styled-content style=\"fixed-case\">G<\/jats:styled-content>n<jats:styled-content style=\"fixed-case\">RH<\/jats:styled-content>\/<jats:styled-content style=\"fixed-case\">LH<\/jats:styled-content> surge and sexual behaviour. A single s.c. oestradiol\u2010benzoate administration on either the day before birth (<jats:styled-content style=\"fixed-case\">E<\/jats:styled-content>21), the day of birth (<jats:styled-content style=\"fixed-case\">D<\/jats:styled-content>0) or day 5 (<jats:styled-content style=\"fixed-case\">D<\/jats:styled-content>5) postpartum completely abolished the <jats:styled-content style=\"fixed-case\">E<\/jats:styled-content><jats:sub>2<\/jats:sub>\u2010induced <jats:styled-content style=\"fixed-case\">LH<\/jats:styled-content> surge at adulthood in female rats, although the same treatment did not inhibit lordosis. Perinatal castration on <jats:styled-content style=\"fixed-case\">E<\/jats:styled-content>21 or <jats:styled-content style=\"fixed-case\">D<\/jats:styled-content>0 partially rescued the <jats:styled-content style=\"fixed-case\">E<\/jats:styled-content>2\u2010induced <jats:styled-content style=\"fixed-case\">LH<\/jats:styled-content> surge in genetically male rats, whereas castration from <jats:styled-content style=\"fixed-case\">E<\/jats:styled-content>21 to <jats:styled-content style=\"fixed-case\">D<\/jats:styled-content>5 totally rescued lordosis. Neonatal <jats:styled-content style=\"fixed-case\">E<\/jats:styled-content><jats:sub>2<\/jats:sub> implantation in the anterior hypothalamus including the anteroventral periventricular nucleus (<jats:styled-content style=\"fixed-case\">AVPV<\/jats:styled-content>)\/preoptic area (<jats:styled-content style=\"fixed-case\">POA<\/jats:styled-content>) abolished the <jats:styled-content style=\"fixed-case\">E<\/jats:styled-content><jats:sub>2<\/jats:sub>\u2010induced <jats:styled-content style=\"fixed-case\">LH<\/jats:styled-content> surge in female rats, whereas <jats:styled-content style=\"fixed-case\">E<\/jats:styled-content><jats:sub>2<\/jats:sub> implantation in the mid and posterior hypothalamic regions had no inhibitory effect on the <jats:styled-content style=\"fixed-case\">LH<\/jats:styled-content> surge. Lordosis was not affected by neonatal <jats:styled-content style=\"fixed-case\">E<\/jats:styled-content><jats:sub>2<\/jats:sub> implantation in any hypothalamic regions. In male rats, neonatal <jats:styled-content style=\"fixed-case\">NMDA<\/jats:styled-content> antagonist treatment rescued lordosis but not the <jats:styled-content style=\"fixed-case\">LH<\/jats:styled-content> surge. Taken together, these results suggest that an anterior hypothalamic region such as the <jats:styled-content style=\"fixed-case\">AVPV<\/jats:styled-content>\/<jats:styled-content style=\"fixed-case\">POA<\/jats:styled-content> region is a perinatal site of oestrogen action where the <jats:styled-content style=\"fixed-case\">G<\/jats:styled-content>n<jats:styled-content style=\"fixed-case\">RH<\/jats:styled-content>\/<jats:styled-content style=\"fixed-case\">LH<\/jats:styled-content> regulating system is defeminised to abolish the oestrogen\u2010induced surge. The mechanism for defeminisation of the <jats:styled-content style=\"fixed-case\">G<\/jats:styled-content>n<jats:styled-content style=\"fixed-case\">RH<\/jats:styled-content>\/<jats:styled-content style=\"fixed-case\">LH<\/jats:styled-content> surge system might be different from that of sexual behaviour, in terms of the site(s) of oestrogen action and critical period, as well as the neurotransmitter system involved.<\/jats:p>","DOI":"10.1111\/j.1365-2826.2012.02389.x","type":"journal-article","created":{"date-parts":[[2012,9,21]],"date-time":"2012-09-21T04:06:46Z","timestamp":1348200406000},"page":"251-259","source":"Crossref","is-referenced-by-count":13,"title":["Different Critical Perinatal Periods and Hypothalamic Sites of Oestradiol Action in the Defeminisation of Luteinising Hormone Surge and Lordosis Capacity in the Rat"],"prefix":"10.1111","volume":"25","author":[{"given":"M.","family":"Sakakibara","sequence":"first","affiliation":[{"name":"Graduate School of Bioagricultural 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