Recrudescence of spermatogenesis in the dog following downregulation using a slow release GnRH agonist implant.
The present study examined the degree to which downregulation with a GnRH agonist impaired spermatogenesis and the time course of morphological and hormonal changes that occurred during recrudescence of spermatogenesis. Using a control group (group 1, n = 5) of dogs, the effect of a removable slow release GnRH-agonist implant was investigated in beagle dogs (group 2, n = 30). The implant was removed after 5 months (week 0) and three to four dogs were castrated at weeks 0, 3, 6, 9, 12, 15, 18, 21 and 24. The degree of downregulation and recrudescence of spermatogenesis was assessed by evaluation of 200 tubular cross-sections, resulting in an assigning of dogs of group 2 to testis developmental groups (DG) according to the most developed germ cell observed: DG A, spermatocytes; DG B, round spermatids; DG C, elongating spermatids and DG D, elongated spermatids. Downregulation led to an arrest of spermatogenesis at the level of spermatogonia/primary spermatocytes. The time course of recrudescence showed high individual variations and the number of dogs falling into DG A, B, C and D was 4, 3, 6 and 17 respectively. Spermatogenesis in group 2, DG D was not different from group 1 (control). In DG A, mean area of Leydig-cell nuclei was lower (p < 0.001) than in the other DG and group 1 and resembled that of juvenile dogs (group 3, n = 3); nuclei of Sertoli cells had changed from more flat/polygonal (group 1, group 2, DG C and D) to round/ovoid and had moved to a more luminal position. As indicated by basal testosterone (T), luteinizing hormone (LH) and follicle stimulating hormone (FSH) concentrations at implant removal, full downregulation had been obtained. Testosterone, LH and FSH concentrations [X(g) (DF), ng/ml] increased (p < 0.05) from implant removal to DG B [T: 0.1 (1.24) vs 2.12 (2.31); LH: 0.2 (2.15) vs 1.11 (1.7); FSH: 0.37 (3.50) vs 6.37 (1.68)] and were more or less constant thereafter indicating that onset of spermatogenesis was related to an increase of plasma T occurring in a very narrow time window. Following GnRH implantation, the size of the testes and the prostate decreased by approximately 55% (p < 0.001), they increased to sizes similar to pre-treatment values following implant removal.
Goericke-Pesch
S
S
Clinic for Obstetrics, Gynecology and Andrology of Large and Small Animals, Justus-Liebig-University, Giessen, Germany. sandra.pesch@vetmed.uni-giessen.de
Spang
A
A
Schulz
M
M
Ozalp
G
G
Bergmann
M
M
Ludwig
C
C
Hoffmann
B
B
D000818:Animals; D000988:Antispermatogenic Agents / Q000494:pharmacology*; D003692:Delayed-Action Preparations; D004285:Dogs; D004334:Drug Administration Schedule; D004343:Drug Implants; D007987:Gonadotropin-Releasing Hormone / Q000819:agonists*; D008297:Male; D017274:Nafarelin / Q000031:analogs & derivatives* / Q000494:pharmacology; D012741:Sexual Maturation; D013076:Sperm Count / Q000662:veterinary; D013091:Spermatogenesis / Q000187:drug effects*; D013737:Testis / Q000166:cytology / Q000187:drug effects
D000988:Antispermatogenic Agents; D003692:Delayed-Action Preparations; D004343:Drug Implants; C483115:azaglycylnafarelin; D017274:Nafarelin; D007987:Gonadotropin-Releasing Hormone