title: Heterotopic transplantation as a model to study the regulation of spermatogenesis; some histomorphological considerations about sperm decline in man.
abstract: A novel animal model (syngeneic neonatal testicular graft transplanted under the skin of the outer ear in adult inbred Fischer rats that had been castrated, hypophysectomised, and/or subjected to hormonal replacement therapy) was developed to study regulation of spermatogenesis and Sertoli cell number. Given that Sertoli cell number and testicular size are important in determining spermatozoan production rates, this model was first used to study Sertoli cell proliferation, testicular size, and establishment of germ cells. The specific objectives were to determine the developmental pattern of Sertoli cell numbers in transplanted testes and the effect of number of testes transplanted, sex of hosts, pituitary hormonal removal, and replacement on Sertoli cell number, hormonal status of the host, and establishment of germ cells. A few tubules had complete spermatogenesis at 90 days posttransplantation, indicating that Sertoli cells in some of these tubules were functional. Leydig cell structure appeared to be normal, but the density of these interstitial cells was greater than that in testes of intact rats. Although the weight of the seminal vesicles and prostate were maintained in the castrated host with transplants, both serum FSH and LH concentrations were higher than intact control rats. Leukocytic infiltration of testes was not observed in intact rats or in rats receiving neonatal testes. Although transplanted testes showed a delay in reaching the plateau value for Sertoli cell number per testis and although the value reached was lower than in intact testes, the developmental pattern of Sertoli cell proliferation (early division of cells followed by stabilized number of cells) in transplanted testes was similar to that in intact rats. Hypophysectomy reduced the growth of testicular grafts, and hormonal replacement via retransplantation to pituitary intact hosts enhances Sertoli cell proliferation and testicular growth. When two on four testes were transplanted into castrated males or ovariectomized female hosts for 65 days, there was no difference in the graft weights or Sertoli cell numbers between sexes of hosts. Four transplanted testes per rat produced more total testicular parenchyma and a greater number of Sertoli cells per testis than did two testes regardless of sex of the host. Transplantation of six or eight testes produced more total Sertoli cells/host than that found in testes of intact rats. Using hormonal therapy in hypophysectomized hosts, the testicular parenchymal weight was greater for pituitary-intact hosts and FSH-LH combination than the control media. There was no statistically significant difference among the media control, LH, FSH, and GH. This testicular transplant model has shown that the period of Sertoli cell proliferation can be delayed by hypophysectomy, that Sertoli cell number can be influenced by endogenous and exogenous hormones, and that a major component in regulation of testicular size is at the level of the testis. Hence, this model should facilitate study of experimental endocrine manipulation control and potential experimental intervention to increase Sertoli cell number, testicular size, and spermatogenesis. Regarding human sperm count decline in recent years, there appears to be no significant decline in Sertoli cell number or spermatogenic potential in a group of North American men. However, there was a significant decline in volume/man of Leydig cells and volume/man of Leydig cell cytoplasm.
authors.affiliation: Department of Veterinary Anatomy and Public Health, Texas A&M University, College Station, USA.
authors.forename: L
authors.initials: L
authors.lastname: Johnson
authors.forename: G U
authors.initials: GU
authors.lastname: Falk
authors.forename: L C
authors.initials: LC
authors.lastname: Suggs
authors.forename: D J
authors.initials: DJ
authors.lastname: Henderson
authors.forename: G E
authors.initials: GE
authors.lastname: Spoede
authors.forename: S W
authors.initials: SW
authors.lastname: Brown
authors.forename: T A
authors.initials: TA
authors.lastname: McGowen
authors.forename: H
authors.initials: H
authors.lastname: Meguerditchian
authors.forename: J J
authors.initials: JJ
authors.lastname: Barnard
mesh_terms: D000328:Adult; D000367:Age Factors; D000818:Animals; D002369:Castration; D004195:Disease Models, Animal; D005260:Female; D006801:Humans; D007016:Hypophysectomy; D007248:Infertility, Male / Q000503:physiopathology* / Q000628:therapy*; D007985:Leydig Cells / Q000502:physiology; D008297:Male; D051381:Rats; D011916:Rats, Inbred F344; D012708:Sertoli Cells / Q000502:physiology*; D013076:Sperm Count; D013091:Spermatogenesis / Q000502:physiology*; D013737:Testis / Q000637:transplantation*