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CNRS UMR 7079/Université Pierre et Marie Curie, Neuroendocrinologie de la Reproduction, 4 Place Jussieu 75230 Paris CEDEX 05, France
¹ INSERM U566/CEA/Université Paris 7, Unité Gamétogénése et Génotoxicité, DRR BP6, 92265 Fontenay-aux-Roses, France
² INSERM U135, Laboratoire d’Hormonologie et Biologie Moléculaire, Hôpital de Bicêtre, 94275 Le Kremlin Bicêtre, France

(Correspondence should be addressed to S Mhaouty-Kodja who is now at CNRS UMR 7148/Collège de France, 11 place Marcelin Berthelot, 75231 Paris CEDEX 05, France; Email: sakina.mhaouty-kodja{at}college-de-france.fr)

To examine whether norepinephrine, through activation of 1b-adrenergic receptor, regulates male fertility and testicular functions, we used 1b-adrenergic receptor knockout (1b-AR-KO) mice. In the adult stage (3–8 months), 73% of the homozygous males were hypofertile with relatively preserved spermatogenesis. Of the remaining males, 27% exhibited a complete infertility with a drastic reduction in testicular weight and spermatogenesis defect with germ cells entering a cell death pathway at meiotic stage. In both phenotypes, circulating levels of testosterone were highly reduced (–55 and –81% in hypofertile and infertile males respectively versus wild-type males). Consequently, circulating levels of LH were significantly elevated in 1b-AR-KO infertile mice. When incubated in vitro, the whole testes from infertile KO mice released significantly lower levels of testosterone (–40%). This, together with the fact that the mean absolute volume of Leydig cells per testis was not changed, suggests a compromised steroidogenic capacity of Leydig cells in infertile animals. In addition, RNA in situ hybridization study indicated an apparent higher expression of inhibin - and ßB-subunits in Sertoli cells of infertile 1b-AR-KO mice. This was correlated with a higher intra-testicular content of inhibin B (+220% above wild-type mice). Using specific primers, mRNA encoding 1b-AR was localized in early spermatocytes of wild-type testes. Our results indicate, for the first time, that 1b-AR signaling plays a critical role in the control of male fertility, spermatogenesis, and steroidogenic capacityof Leydig cells. It is thus hypothesized that the absence of 1b-AR alters either directly germ cells or indirectly Sertoli cell/Leydig cell communications in infertile 1b-AR-KO mice.