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Corticosterone, Adrenal, and the Pituitary-Gonadal Axis in Neonatal Rats: Effect of Maternal Separation and Hypoxia.
Endocrinology ( IF 3.8 ) Pub Date : 2020-05-27 , DOI: 10.1210/endocr/bqaa085
Ashley L Gehrand 1 , Jonathan Phillips 1 , Kevin Malott 1 , Hershel Raff 1, 2, 3, 4
Affiliation  

Hypoxia, a common stressor in prematurity, leads to sexually dimorphic, short- and long-term effects on the adult hypothalamic-pituitary-adrenal (HPA) and hypothalamic-pituitary-gonadal (HPG) axes. We hypothesized that these effects are due to stress-induced increases in testosterone during early postnatal life. We evaluated this phenomenon by systematically assessing the short-term effects of normoxic or hypoxic separation on male and female pups at birth, postnatal hours (H) 2, 4, and 8, and postnatal days (PD) 2 to 7. Our findings were (a) hypoxic separation led to a large increase in plasma corticosterone from 4H-PD4, (b) neither normoxic nor hypoxic separation affected critical adrenal steroidogenic pathway genes; however, a significant decrease in baseline Cyp11a1, Mc2r, Mrap, and Star adrenal expression during the first week of neonatal life confirmed the start of the adrenal stress hyporesponsive period, (c) a luteinizing hormone/follicle-stimulating hormone–independent increase in plasma testosterone occurred in normoxic and hypoxic separated male pups at birth, (d) testicular Cyp11a1, Lhcgr, and Star expression was high at birth and decreased thereafter suggesting a hyporesponsive period in the testes, and (e) elevated estrogen in the early neonatal period occurred independently of gonadotropin stimulation. We conclude that a large corticosterone response to hypoxia during the first 5 days of life occurs as an adaptation to neonatal stress, that the testosterone surge during the first hours after birth occurs independently of gonadotropins but is associated with upregulation of the steroidogenic pathway genes in the testes, and that high postnatal estrogen production also occurs independently of gonadotropins.

中文翻译:

新生大鼠的皮质酮,肾上腺和垂体-性腺轴:母体分离和缺氧的影响。

缺氧是早产的常见压力源,会对成年下丘脑-垂体-肾上腺(HPA)和下丘脑-垂体-性腺(HPG)轴产生性二态,短期和长期影响。我们假设这些影响是由于出生后早期的压力导致睾丸激素增加。我们通过系统地评估常氧或低氧分离对出生,产后小时(H)2、4和8以及产后天(PD)2至7的雄性和雌性幼仔的短期影响,评估了这一现象。 (a)低氧分离导致4H-PD4血浆皮质酮大量增加,(b)常氧分离和低氧分离均未影响关键的肾上腺类固醇生成途径基因;但是,基线Cyp11a1Mc2r新生儿出生后第一周的MrapStar肾上腺表达证实了肾上腺应激低反应期的开始,(c)在出生时常氧和低氧的雄性幼崽中,黄体生成激素/促卵泡激素依赖性血浆睾丸激素的升高,(d)睾丸Cyp11a1LhcgrStar在出生时,其表达水平很高,此后降低,提示睾丸反应低下;(e)新生儿早期雌激素升高与促性腺激素刺激无关。我们得出的结论是,生命的前5天,皮质酮对缺氧的反应很大,这是对新生儿压力的适应,出生后头几个小时的睾丸激素激增独立于促性腺激素而发生,但与激素中的类固醇生成途径基因的上调有关。睾丸,并且高产后雌激素的产生也独立于促性腺激素。
更新日期:2020-06-23
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