Abstract
The process of spermatogenesis was studied in mutant hypogonadal (hpg) male mice treated with equine chorionic gonadotropin (eCG) or gonadotropin releasing hormone (GnRH) for 60 days. Untreated adult hpg male mice had very small gonads (5.7 ± 0.6, n=7, mean ± SEM) and no mature spermatozoa due to a genetic deficiency of GnRH. Testicular weights increased to 55.7 ± 5.6 mg in eCG (5 IU/day) injected mice (n=7) and 30.0 ± 3.8 mg in GnRH (1 μg/day) injected mice after 60 days. Similar increases were seen in seminal vesicles. In eCG-administered mice, matured spermatozoa appeared in epididymides after 45 days of treatment. A lower dose of eCG (2.5 IU/day) or GnRH (1 μg/day) were less effective for stimulation of spermatogenesis. Although the propotion of hpg mouse sperm fertilized embryos that developed to the blastocyst stage (18%) was lower than the proportion of normal mouse sperm fertilized embryos (43%), at least some of the hpg mouse sperm fertilized embryos produced viable offspring through embryo transfer. The present study proved that chronic eCG or GnRH administration could stimulate spermatogenesis in hpg males, and cauda epididymal spermatozoa were fertile when obtained from eCG-injected mutant mice. These results intimated that hpg male mice provide valuable information for clarifying the endocrine and paracrine control processes of spermatogenesis.
