| Sex hormones (including androgens and estrogens) are involved in regulating the secreting function of pituitary hormones in adult animals and in development of central nervous system. However, the actions of sex hormones on the neural-endocrine system and related mechanisms are unclear. The present study was performed to investigated the effects of sex hormones on the cell proliferation and differentiation of embryonic chick pituitary cells and peripheral neurons in vivo and in vitro, we injected specific corresponding receptor inhibitor in vivo to investigate the related mechanisms of sex hormones on the peripheral neurons. In addition, we detected the changes of ER expression in the pituitary gland of chick embryo and sheep fetus to compare the mechanisms of actions of estrogen on pituitary endocrine cells. The results include five parts as followings:1. The results reveal that both testosterone and estradiol promoted proliferation of cells in both normal DRG and the Froriep's ganglia. By contrast, estradiol significantly increased the number of apoptotic cells, while testosterone strongly inhibited apoptosis. These actions of sex steroids on DRG development were dose-dependent, and C5DRG and C2DRG showed different sensitivities to the applied sex steroids.2. The present results demonstrated that specific ER and AR inhibitors (tamoxifen and flutamide) did not influence the effects of 5μg E2 and 5μg T on C2 and C5DRG significantly and no AR, ER and aromotase immunoreactivity were observed in C2 and C5DRG at St 18 and 23. The results suggest that both estradiol and testosterone can modulate DRG development through an epigenetic mechanism, and testosterone acts on the DRG development may not be transformed to estradiol.3. The results show that proliferating cell nuclear antigen immuno-reactivity (PCNA-IR) is consistently detected throughout the Rathke's pouch (RP) and anterior pituitary gland (AP) during the development of chick embryo. As development progressed, the percentages of PCNA+ cells in AP decline gradiently, to 22% in newly hatched chicken. As for laying hens and adult cockerels, unlike in chick embryos, PCNA-IR is mainly located in the cephalic lobe of pars distalis. Dual-labeled IHC results demonstrated that PCNA-IR is dominantly distributed in lactotrophs. Exogenous E2 administration increases the number of BrdU+ cells and mitotic cells in RP. 10nM E2 also increase percentage of PCNA+ cells in culturing AP cells at E10.5.4. A few ERa immunopositive (ERa+) cells were first detected at E6.5, after which ERa+ cells were consistently detected throughout the anterior pituitary gland, although the density of ERa+ cells in the caudal lobe of the pars details was higher than in the cephalic lobe. Double labeling of the ERa and pituitary hormones showed that the dominant cell types expressing ERa are luteinizing hormone (LH) immunopositive (LH+) gonadotrophs; the propotion of ERa+ cells expressing LH increased throughout incubation. In addition, a small propotion of thyrotrophs and lactotrophs expressed ERa respectively at the later stages of embryonic development, but no somatotrophs and corticotrophs expressed ERaduring the embryonic period. 5ug exogenous estradiol can bring an advanced expression of ERa at E6 after 24 hours administration. The percentage of ERa was approximately 24% in the anterior pituitary gland of adult chicken, and there was no significant difference between laying hens and adult cockerels. Double-immunolabeled results showed no thyrotrophs, lactotrophs, samototrophs and corticotrophs expressed ERa, and quite a number of LH+ cells contained ERa+ in the adult chickens. In addition, the percentage of dual-labeled cells accounting for ERa+ and LH+ cells in adult cockerels significantly differed with that of the laying hens. AR is mainly found in LH positive gonadotrophs and thyrotrophs, few corticotrophs contain AR immunoreactivity, and no AR immunoreactivity is observed in lactotrophs and samototrophs. AR and ERa do not co-localize in the same cells of anterior p...
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