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Male Reproductive Function Is Not Affected in Prolactin Receptor-Deficient Mice

Hormone Targets, Institut National de la Santé et de la Recherche Médicale Unité 584 (N.B., P.I-B., P.A.K.), Faculté de Médecine Necker-Enfants Malades, 75015 Paris, France; and Groupe d’Etude de la Reproduction chez le Mâle-Institut National de la Santé et de la Recherche Médicale Unité 435 (N.M., C.P., H.K., A.M.T., B.J.), Université de Rennes 1, 35042 Rennes Cedex, Bretagne, France

Address all correspondence and requests for reprints to: Dr. Nadine Binart, Hormone Targets, Institut National de la Santé et de la Recherche Médicale Unité 584, Faculté de Médecine Necker-Enfants Malades, 156 rue de Vaugirard, 75015 Paris, France. E-mail: binart{at}necker.fr.

Abstract

Mice with a targeted disruption of the prolactin (PRL) receptor 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 PRL receptor knockout mice. Testicular histology and sperm reserves were also normal. Compared with wild-type animals, knockout mice had no significant difference in basal plasma LH, FSH, and testosterone levels, and the weight of seminal vesicles and prostate was unaffected. Moreover, no alteration was detected in human chorionic gonadotropin-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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