Follicle-stimulating hormone is required for the initial phase of spermatogenic restoration in adult rats following gonadotropin suppression.
The role of follicle-stimulating hormone (FSH) in adult rat spermatogenesis is unclear. Although exogenous testosterone (T) restores spermatogenesis following gonadotropin-releasing hormone (GnRH) immunization or T plus estradiol (TE) treatments, an assessment of the independent action of T and FSH was not possible, as exogenous T treatment maintains serum FSH levels. We have used passive immunization against FSH to determine whether T alone is capable of reinitiating spermatogenesis after chronic and acute FSH withdrawal. Adult rats received T-filled Silastic implants 6 cm (T6) or 8 cm (T24) in length for 7 days in combination with either a polyclonal sheep antisera raised against rat FSH (FSHAb, 2 mg/kg SC daily) or control sheep immunoglobulin (ConAb) after either GnRH immunization (12 weeks) or TE treatment (9 weeks). The neutralizing capacity of the FSHAb was determined using a FSH in vitro bioassay; this analysis demonstrated that administration of FSHAb in vivo reduced FSH levels by >90%. Testes were fixed and germ cell number per testis quantified using the optical dissector. GnRH immunization reduced spermatogonia, pachytene spermatocytes, and round spermatids to 50, 13, and <1% of normal, respectively. T6 and T24 Silastic implants with the inclusion of the FSHAb did not increase the number of spermatogonia, pachytene spermatocytes, and round spermatids (50, 15, and 1% of normal, respectively). T6+ConAb treatment increased spermatogonial, pachytene spermatocyte, and round spermatid numbers to 74, 30, and 3% of normal, respectively (P < 0.05). No further increases were seen with T24 implants. TE treatment suppressed pachytene spermatocytes and round spermatids to 33 and 1% of normal, respectively (P < 0.05). T6+FSHAb treatment did not increase the number of pachytene spermatocytes and round spermatids (36 and 8%, respectively), whereas T6+ConAb treatment increased pachytene spermatocyte and round spermatid number to 50 and 28% of normal, respectively (P < 0.05). T24+FSHAb treatment increased the number of pachytene spermatocyte and round spermatids (56 and 22% of normal, respectively; P < 0.05), whereas T24+ConAb treatment increased these cells forms to 79 and 31% of normal, respectively. In conclusion, T alone is unable to restore spermatogenic cell populations in the setting of chronic FSH withdrawal. Although acute FSH withdrawal markedly impairs the restoration process, higher doses of T can partially compensate for the lack of FSH. These data suggest that FSH is important for the initial phase of spermatogenic restoration.
Meachem
S J
SJ
Prince Henry's Institute of Medical Research, Monash University, Clayton, Victoria, Australia.
Wreford
N G
NG
Stanton
P G
PG
Robertson
D M
DM
McLachlan
R I
RI
D000818:Animals; D005640:Follicle Stimulating Hormone / Q000276:immunology / Q000502:physiology*; D006062:Gonadotropins / Q000037:antagonists & inhibitors*; D007116:Immunization, Passive; D008297:Male; D009929:Organ Size; D051381:Rats; D017207:Rats, Sprague-Dawley; D013091:Spermatogenesis / Q000502:physiology*; D013094:Spermatozoa / Q000166:cytology; D013737:Testis / Q000378:metabolism / Q000502:physiology; D013739:Testosterone / Q000097:blood / Q000378:metabolism
D006062:Gonadotropins; D013739:Testosterone; D005640:Follicle Stimulating Hormone