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Localization of Gonadotropin-Releasing Hormone (GnRH) Gonadotropin-Inhibitory Hormone (GnIH) Kisspeptin and GnRH Receptor and Their Possible Roles in Testicular Activities From Birth to Senescence in Mice

机译:促性腺激素释放激素(GnRH)促性腺激素抑制激素(GnIH)亲吻促动素和GnRH受体及其在睾丸活动可能的角色从出生到衰老小鼠本地化

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摘要

The changes in distribution and concentration of neuropeptides, gonadotropin-releasing hormone (GnRH), gonadotropin-inhibitory hormone (GnIH), kisspeptin, and gonadotropin-releasing hormone receptor (GnRH-R) were evaluated and compared with reproductive parameters, such as cytochrome P450 side-chain cleavage (P450 SCC) enzyme activity, androgen receptors (AR) in the testis and serum testosterone levels, from birth to senescence in mice. The results showed the localization of these molecules mainly in the interstitial and germ cells as well as showed significant variations in immunostatining from birth to senescence. It was found that increased staining of testicular GnRH-R coincided with increased steroidogenic activity during pubertal and adult stages, whereas decreased staining coincides with decreased steroidogenic activity during senescence. Similar changes in immunostaining were confirmed by Western/slot blot analysis. Thus, these results suggest a putative role of GnRH during testicular pubertal development and senescence. Treatment with a GnRH agonist ([DTrp6, Pro9-NEt] GnRH) to mice from prepubertal to pubertal period showed a significant increase in steroidogenic activity of the mouse testis and provided further support to the role of GnRH in testicular pubertal maturation. The significant decline in GnRH-R during senescence may be due to a significant increase in GnIH synthesis during senescence causing the decrease in GnRH-R expression. It is considered that significant changes in the levels of GnRH-R may be responsible for changes in steroidogenesis that causes either pubertal activation or senescence in testis of mice. Furthermore, changes in the levels of GnRH-R may be modulated by interactions among GnRH, GnIH, and kisspeptin in the testis.
机译:评价了神经肽,促性腺激素释放激素(GnRH),促性腺激素抑制激素(GnIH),kisseptin和促性腺激素释放激素受体(GnRH-R)的分布和浓度变化,并将其与生殖参数(例如细胞色素P450)进行了比较从出生到衰老,小鼠的侧链裂解(P450 SCC)酶活性,睾丸中的雄激素受体(AR)和血清睾丸激素水平。结果显示这些分子主要定位于间质和生殖细胞中,并且从出生到衰老的免疫抑制作用均显示出显着差异。发现在青春期和成年期睾丸GnRH-R的染色增加与类固醇生成活性增加同时发生,而衰老过程中染色的减少与类固醇生成活性下降同时发生。 Western /狭缝印迹分析证实了免疫染色的类似变化。因此,这些结果暗示了GnRH在睾丸青春期发育和衰老过程中的推定作用。从青春期前到青春期用GnRH激动剂([DTrp 6 ,Pro 9 -NEt] GnRH)治疗小鼠,小鼠睾丸和小鼠睾丸激素的活性显着增加。为GnRH在睾丸青春期成熟中的作用提供了进一步的支持。衰老过程中GnRH-R的显着下降可能是由于衰老过程中GnIH合成的显着增加导致GnRH-R表达下降。据认为,GnRH-R水平的显着变化可能是引起小鼠睾丸青春期激活或衰老的类固醇生成变化的原因。此外,GnRH-R水平的变化可以通过睾丸中GnRH,GnIH和Kisspeptin之间的相互作用来调节。

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