title: Sex-differences in adrenocortical responsiveness during development in rats.
abstract: It is known that the stress hyporesponsive period (SHRP), which seems to be related to an immature hypothalamo-pituitary-adrenal (HPA) regulatory system, occurs during the first 2 weeks after birth in rats. In the present study, we investigated the effects of sex-steroid hormones on adrenocortical responsiveness to adrenocorticotropic hormone (ACTH) in neonatal rats. The levels of cyclic adenosine 3',5'-monophosphate (cAMP), corticosterone, and adenylate cyclase activity increased with the dose of ACTH in adrenal cells of males and females in vitro. The ACTH responsiveness in adrenal cells increased with age (7-35 days of age), that is, the loss in responsiveness to ACTH just after birth began to recover in 14-35-day-old rats, but the responsiveness in 14-day-old rats was attenuated in males compared with females. Although castration markedly augmented the responsiveness in male rats, testosterone-replacement in the castrated male rats inhibited the enhancement. Furthermore, the responsiveness in 14-day-intact female rats was suppressed by treatment with testosterone. Expression levels of ACTH receptor mRNA in adrenals increased with age in the female rat, but not in the male. Castration enhanced the level of ACTH receptor mRNA to three-fold of that in intact male rats at 14 days of age, but replacement treatment with testosterone in castrated male rats lowered the elevated levels. Testicular androgens are thought to evoke a gender-specific response in neonates, and the temporal decrease of adrenal ACTH-responsiveness might be due to the topically immature adrenal system as well as the central nervous system in mammals.
authors.affiliation: Medical Research Institute, Tokyo Medical and Dental University, 1-5-45 Yushima Bunkyo-ku, Tokyo 113-8510, Japan.
authors.forename: Shintarou
authors.initials: S
authors.lastname: Yoshimura
authors.forename: Shinobu
authors.initials: S
authors.lastname: Sakamoto
authors.forename: Hideki
authors.initials: H
authors.lastname: Kudo
authors.forename: Shuji
authors.initials: S
authors.lastname: Sassa
authors.forename: Akihiko
authors.initials: A
authors.lastname: Kumai
authors.forename: Ryohei
authors.initials: R
authors.lastname: Okamoto
mesh_terms: D000262:Adenylyl Cyclases / Q000378:metabolism; D000311:Adrenal Glands / Q000187:drug effects* / Q000378:metabolism; D000324:Adrenocorticotropic Hormone / Q000494:pharmacology*; D000818:Animals; D000831:Animals, Newborn; D002369:Castration; D003345:Corticosterone / Q000378:metabolism; D000242:Cyclic AMP / Q000378:metabolism; D004305:Dose-Response Relationship, Drug; D004958:Estradiol / Q000494:pharmacology; D005260:Female; D066298:In Vitro Techniques; D008297:Male; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D018043:Receptors, Corticotropin / Q000235:genetics; D012737:Sex Factors; D013739:Testosterone / Q000494:pharmacology; D013997:Time Factors
chemical_list: D012333:RNA, Messenger; D018043:Receptors, Corticotropin; D013739:Testosterone; D004958:Estradiol; D000324:Adrenocorticotropic Hormone; D000242:Cyclic AMP; D000262:Adenylyl Cyclases; D003345:Corticosterone