Skip to main content

Thank you for visiting nature.com. You are using a browser version with limited support for CSS. To obtain the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles and JavaScript.

  • Letter
  • Published:

Gonadotrophin-releasing hormone deficiency in a mutant mouse with hypogonadism

Abstract

FAMILIAL hypogonadism in man, due to an isolated deficiency of gonadotrophin secretion, has been well documented1–6, but difficult to investigate because of the lack of a suitable animal model4. We report here the genetic and endocrinological background of a mutant strain of mouse in which the testes and ovaries fail to develop postnatally. The primary cause of this seems to be a deficiency in hypothalamic gonadotrophin-releasing hormone (GnRH) with a consequent reduction in pituitary content and circulating levels of luteinising hormone (LH) and follicle-stimulating hormone (FSH). By analogy with the Brattleboro rat (genetic defect in vasopressin synthesis) this mutant should prove useful for studying the synthesis of hypothalamic releasing hormones as well as the role of the hypothalamic–gonadotrophin system in sexual differentiation, puberty, folliculogenesis and spermatogenesis. The mutant has been named hypogonadal, symbol hpg.

This is a preview of subscription content, access via your institution

Access options

Buy this article

Prices may be subject to local taxes which are calculated during checkout

Similar content being viewed by others

References

  1. Kallman, F. J., Schoenfeld, W. A. & Barrera, S. E. Am. J. ment. Defic. 48, 203–236 (1944).

    Google Scholar 

  2. Nowakowski, H. & Lenz, W. Rec. Progr. Horm. Res. 17, 53–89 (1961).

    CAS  PubMed  Google Scholar 

  3. Ewer, R. W. J. clin. Endocr. Metab. 28, 783–788 (1968).

    Article  CAS  Google Scholar 

  4. Naftolin, F., Harris, G. W. & Bobrow, M. Nature 232, 496–497 (1971).

    Article  ADS  CAS  Google Scholar 

  5. Santen, R. J. & Paulsen, C. A. J. clin. Endocr. Metab. 36, 47–54 (1973).

    Article  CAS  Google Scholar 

  6. Boyar, R. M., Wu, R. H. K., Kapen, S., Hellman, L., Weitzman, E. D. & Finkelstein, J. W. J. clin. Endocr. Metab. 43, 1268–1275 (1976).

    Article  CAS  Google Scholar 

  7. Cattanach, B. M., Williams, C. E. & Bailey, H. Cytogenetics 11, 412–423 (1972).

    Article  CAS  Google Scholar 

  8. Chester-Jones, I. Br. med. Bull. 11, 156–158 (1955).

    Article  Google Scholar 

  9. Brown-Grant, K. in Regulation and Control in Living Systems (ed. Kalmus, H.) 176–255 (Wiley, London, 1966).

    Google Scholar 

  10. Nett, T. M., Akbar, A. M., Niswender, G. D., Hedlund, M. J. & White, W. F. J. clin. Endocr. Metab. 36, 880–885 (1973).

    Article  CAS  Google Scholar 

  11. Chiappa, S. A. & Fink, G. J. Endocr. 72, 195–210 (1977).

    Article  CAS  Google Scholar 

  12. Niswender, G. D., Midgley, A. R., Jr, Montoe, S. E. & Reichert, L. E. Jr, Proc. Soc. exp. Biol. Med. 128, 807–811 (1968).

    Article  CAS  Google Scholar 

  13. Daane, T. A. & Parlow, A. F. Endocrinology 88, 653–663 (1971).

    Article  CAS  Google Scholar 

Download references

Author information

Authors and Affiliations

Authors

Rights and permissions

Reprints and permissions

About this article

Cite this article

CATTANACH, B., IDDON, C., CHARLTON, H. et al. Gonadotrophin-releasing hormone deficiency in a mutant mouse with hypogonadism. Nature 269, 338–340 (1977). https://doi.org/10.1038/269338a0

Download citation

  • Received:

  • Accepted:

  • Published:

  • Issue Date:

  • DOI: https://doi.org/10.1038/269338a0

This article is cited by

Comments

By submitting a comment you agree to abide by our Terms and Community Guidelines. If you find something abusive or that does not comply with our terms or guidelines please flag it as inappropriate.

Search

Quick links

Nature Briefing

Sign up for the Nature Briefing newsletter — what matters in science, free to your inbox daily.

Get the most important science stories of the day, free in your inbox. Sign up for Nature Briefing