Migratory arrest of gonadotropin-releasing hormone neurons in transgenic mice

S. Radovick, S. Wray, E. Lee, D. K. Nicols, Y. Nakayama, B. D. Weintraub, H. Westphal, G. B. Cutler, F. E. Wondisford

Research output: Contribution to journalArticlepeer-review

Abstract

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.

Original languageEnglish (US)
Pages (from-to)3402-3406
Number of pages5
JournalProceedings of the National Academy of Sciences of the United States of America
Volume88
Issue number8
DOIs
StatePublished - 1991

Keywords

  • Kallmann syndrome
  • T antigen
  • hypogonadism
  • hypothalamus
  • infertility

ASJC Scopus subject areas

  • General

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