LH and testosterone cause the development of seminiferous tubule contractile activity and the appearance of testicular oxytocin in hypogonadal mice.
Immunoreactive oxytocin is present in the testis and it has been shown that this hormone increases the contractility of seminiferous tubules. We have investigated the relationship between testicular oxytocin, tubular movements and the effects of LH and testosterone using, as a model, the hypogonadal (hpg/hpg) mouse, which is deficient in hypothalamic LH-releasing hormone (LHRH). Whilst both testicular oxytocin and seminiferous tubule movements, resembling those seen in the rat, can be found in normal adult mice, neither can be found in hypogonadal mice. After 2 weeks of treatment with LH (200 ng to 100 micrograms daily) low levels of testicular oxytocin and tubular movements were observed. Treatment with large doses of testosterone for 2-12 weeks led to higher concentrations of testicular oxytocin and tubular movements resembling those seen in the normal adult mouse. The results support the evidence that testicular oxytocin modulates seminiferous tubule movements. We suggest that testosterone may play a part in the accumulation of oxytocin in the testis.
D000818:Animals; D007006:Hypogonadism / Q000378:metabolism*; D007986:Luteinizing Hormone / Q000494:pharmacology*; D008297:Male; D051379:Mice; D008817:Mice, Mutant Strains; D009068:Movement / Q000187:drug effects; D010121:Oxytocin / Q000378:metabolism*; D012671:Seminiferous Tubules / Q000187:drug effects; D013737:Testis / Q000378:metabolism*; D013739:Testosterone / Q000494:pharmacology*
D013739:Testosterone; D010121:Oxytocin; D007986:Luteinizing Hormone