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MIGRATORY ARREST OF GONADOTROPIN-RELEASING-HORMONE NEURONS IN TRANSGENIC MICE

被引：200
作者：
RADOVICK, S
WRAY, S
LEE, E
NICOLS, DK
NAKAYAMA, Y
WEINTRAUB, BD
WESTPHAL, H
CUTLER, GB
WONDISFORD, FE
机构：
[1] CASE WESTERN RESERVE UNIV,UNIV HOSP CLEVELAND,DEPT INTERNAL MED,CLEVELAND,OH 44106
[2] CASE WESTERN RESERVE UNIV,UNIV HOSP CLEVELAND,DEPT PEDIAT,CLEVELAND,OH 44106
[3] NICHHD,BETHESDA,MD 20892
[4] NINCDS,BETHESDA,MD 20892
[5] NCI,OFF RES SERV,BETHESDA,MD 20892
[6] NIDDKD,BETHESDA,MD 20892
来源：
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA | 1991年 / 88卷 / 08期
关键词：
T-ANTIGEN; INFERTILITY; KALLMANN SYNDROME; HYPOGONADISM; HYPOTHALAMUS;
D O I：
10.1073/pnas.88.8.3402
中图分类号：
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号：
07 ; 0710 ; 09 ;
摘要：
Gonadotropin-releasing hormone (GnRH) is important in reproduction, although the mechanism of central hypogonadism in humans remains unclear. Because the GnRH neuron originates from the olfactory placode and migrates to the hypothalamus during development,central hypogonadism in humans could be caused by failure in normal migration of GnRH neurons to the hypothalamus. We report that in transgenic mice expression of the simian virus 40 T antigen, driven by the promoter of human GnRH gene, resulted in central hypogonadism due to an arrest in neuronal migration during development and tumor formation along the migratory pathway. This system appears to be an important animal model of hypogonadotropic hypogonadism in humans. Additionally, olfactory bulb tumors from these animals were dispersed, and a GnRH-secreting neuronal cell line (GN cell line) was established.
引用
收藏
页码：3402 / 3406
页数：5
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