The 3rd Korea-China-Japan Joint Symposium on Animal Reproduction (2014.06)바로가기
페이지
pp.4-4
저자
Xing-fa Han, Xian-yin Zeng
언어
영어(ENG)
URL
https://www.earticle.net/Article/A227387
원문정보
초록
영어
The present study was aimed to investigate the molecular mechanisms of active immunization against GnRH by focusing on effects of active immunization against GnRH on hypothalamic-pituitary-testicular axis. Adult male rats (n=36) were randomly and equally allocated into three groups: control (no treatment), surgically castrated, or immunized against 50 ug D-Lys6-GnRH-tandem-dimer peptide conjugated to ovalbumin in Specol adjuvant at 12 weeks of age (with a booster 8 weeks later). Blood samples (for antibody titers and hormone concentrations) were collected at 2-week intervals until rats were killed at 20 weeks of age. At decapitation, testes weight /volume and pituitary weight were recorded. Hypothalamus, pituitary and testis were collected to detect the mRNA expressions of reproduction-related genes with real-time fluorescence quantitative PCR, and the hypothalamus and testes were excised for tissue GnRH detection and morphological observation, respectively. Compared to intact controls, immunocastration reduced (p<0.05) serum concentrations of testosterone, LH and FSH, and the GnRH content in the median eminence, reduced the weight of the hypohysis (p<0.01), and induced testicular atrophy (suppression of spermatogenesis). Furthermore, mRNA expression of GnRH in the hypothalamus, GnRH receptor, LH-β and FSH-β in the pituitary, LH receptor and FSH receptor in the testes, and genes in sex steroid feedback loops (androgen receptor (AR), kisspeptin encoded gene (Kiss-1) and kisspeptin receptor (GPR54) in the hypothalamus were decreased in immunocastrated rats compared to intact controls (p<0.05). Similarly, surgical castration reduced GnRH in the median eminence as well as mRNA expression of GnRH, AR, Kiss-1 and GPR54 in the hypothalamus (p<0.05). These results suggest that active immunization against GnRH reduces GnRH synthesis in the hypothalamus by decreasing androgen-androgen receptor-Kisspeptin-GPR54 signaling pathways and causes dysfunction of the pituitarytesticular axis. Both the loss of GnRH synthesis and dysfunction of the pituitary- testicular axis seem to be mechanisms underlying immunocastration.