Allopregnanolone Alters the Luteinizing Hormone, Prolactin, and Progesterone Serum Levels Interfering with the Regression and Apoptosis in Rat Corpus Luteum

别孕甾酮 内分泌学 内科学 催乳素 黄体期 黄体 促黄体激素 发情周期 排卵 早晨 荷包牡丹碱 卵巢 黄体溶解 放射免疫分析 激素 生物 神经活性类固醇 化学 医学 敌手 受体 γ-氨基丁酸受体
作者
Myriam Raquel Laconi,Carlos J Chávez,Juan C. Cavicchia,M.R. Fóscolo,Zulema Y. Sosa,Roberto Yunes,Rodrigo Cabrera
出处
期刊:Hormone and Metabolic Research [Georg Thieme Verlag KG]
卷期号:44 (08): 632-638 被引量:16
标识
DOI:10.1055/s-0032-1314834
摘要

Steroids synthesized in the central nervous system are termed "neurosteroids". They are synthesized and metabolized in several brain areas. The objective of this work was to determine if 1 intracerebroventricular allopregnanolone injection in rats can interfere in luteal regression in a close relationship with modifications in LH, progesterone, and prolactin serum concentrations. Allopregnanolone was injected during proestrus morning and the animals were sacrificed on oestrous morning. Ovulation test and histological analysis were performed in the oestrus morning with light and electron microscopy. Serum prolactin, LH, and progesterone levels were measured by radioimmunoassay. The allopregnanolone injection significantly decreased luteinizing hormone serum level and the number of oocytes on oestrus. Progesterone and prolactin serum levels were increased after this injection. The inhibition of apoptotic figures due to allopregnanolone administration was detected in the already formed corpora lutea belonging to the previous ovary cycle and it was significantly lower than in vehicle group (control). When the GABA(A) antagonist (bicuculline) was administered alone or previously to allopregnanolone, no effect on the ovulation rate was observed. No changes in the apoptotic cell numbers were observed with respect to those of vehicle group. These results show that the effect of centrally injected allopreganolone over reproductive function could be due to a centrally originated LH mediated effect over ovarian function that affects luteal regression, through the inhibition of apoptosis and stimulation of progesterone and prolactin release.
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