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This version published online on July 10, 2003
Endocrinology, doi:10.1210/en.2003-0409
A more recent version of this article appeared on September 1, 2003
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Submitted on April 1, 2003
Accepted on June 30, 2003

Male Reproductive Function is not affected in Prolactin Receptor Deficient Mice

Nadine Binart1*, Nathalie Melaine1, Charles Pineau1, Henri Kercret1, Anne Marie Touzalin1, Prune Imbert-Bolloré1, Paul A. Kelly1, and Bernard Jégou1

1 Hormone Targets, Inserm U584 Faculté de Médecine Necker-Enfants Malades, 75015 Paris, France (N.B., P.I-B., P.A.K.), GERM- Inserm U 435 Université de Rennes 1, 35042 Rennes Cedex, Bretagne, France (N. M., C. P., H. K., A. M. T., B. J.)

* To whom correspondence should be addressed. E-mail: binart{at}necker.fr.

Mice with a targeted disruption of the prolactin (PRL) receptor (R) gene were used to study the physiological role of PRL in the control of the male reproductive function. Fertility parameters as well as body and reproductive organ weights (epididymis and testes) were unaffected in PRLR KO mice. Testicular histology and sperm reserves were also normal. Compared with wild-type animals, KO mice had no significant difference in basal plasma LH, FSH levels and testosterone levels and the weight of seminal vesicles and prostate was unaffected. Moreover, no alteration was detected in hCG-induced testosterone levels. It is concluded that the absence of PRL signaling is not detrimental to male testicular function and to fertility in the mouse.






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