title: Different critical perinatal periods and hypothalamic sites of oestradiol action in the defeminisation of luteinising hormone surge and lordosis capacity in the rat.
abstract: Female rats show a gonadotrophin-releasing hormone (GnRH)/luteinising hormone (LH) 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 GnRH/LH surge. Animals given perinatal treatments, such as steroidal manipulations, brain local implantation of oestradiol (E(2) ) or administration of an NMDA antagonist, were examined for their ability to show an E(2) -induced LH surge at adulthood. Lordosis behaviour was examined to compare the mechanisms defeminising the GnRH/LH surge and sexual behaviour. A single s.c. oestradiol-benzoate administration on either the day before birth (E21), the day of birth (D0) or day 5 (D5) postpartum completely abolished the E(2) -induced LH surge at adulthood in female rats, although the same treatment did not inhibit lordosis. Perinatal castration on E21 or D0 partially rescued the E2-induced LH surge in genetically male rats, whereas castration from E21 to D5 totally rescued lordosis. Neonatal E(2)  implantation in the anterior hypothalamus including the anteroventral periventricular nucleus (AVPV)/preoptic area (POA) abolished the E(2) -induced LH surge in female rats, whereas E(2)  implantation in the mid and posterior hypothalamic regions had no inhibitory effect on the LH surge. Lordosis was not affected by neonatal E(2)  implantation in any hypothalamic regions. In male rats, neonatal NMDA antagonist treatment rescued lordosis but not the LH surge. Taken together, these results suggest that an anterior hypothalamic region such as the AVPV/POA region is a perinatal site of oestrogen action where the GnRH/LH regulating system is defeminised to abolish the oestrogen-induced surge. The mechanism for defeminisation of the GnRH/LH 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.
authors.affiliation: Graduate School of Bioagricultural Sciences, Nagoya University, Nagoya, Japan.
authors.forename: M
authors.initials: M
authors.lastname: Sakakibara
authors.forename: C
authors.initials: C
authors.lastname: Deura
authors.forename: S
authors.initials: S
authors.lastname: Minabe
authors.forename: Y
authors.initials: Y
authors.lastname: Iwata
authors.forename: Y
authors.initials: Y
authors.lastname: Uenoyama
authors.forename: K-I
authors.initials: KI
authors.lastname: Maeda
authors.forename: H
authors.initials: H
authors.lastname: Tsukamura
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D004958:Estradiol / Q000502:physiology*; D005260:Female; D007031:Hypothalamus / Q000503:physiopathology*; D008141:Lordosis / Q000503:physiopathology*; D007986:Luteinizing Hormone / Q000378:metabolism*; D008297:Male; D051381:Rats; D017208:Rats, Wistar; D016194:Receptors, N-Methyl-D-Aspartate / Q000037:antagonists & inhibitors; D012726:Sexual Behavior, Animal
chemical_list: D016194:Receptors, N-Methyl-D-Aspartate; D004958:Estradiol; D007986:Luteinizing Hormone