Testicular weight, tubular diameter and number of Sertoli cells in rats are decreased after early prepubertal administration of an LHRH-antagonist; the quality of spermatozoa is not impaired.
To suppress gonadotropin secretion during the sensitive period in development of the testes, immature male rats were treated with an antagonist of luteinizing hormone-releasing hormone (LHRH; ORG. 30276) from postnatal days 6-15. Previously, it has been demonstrated that this treatment results in delayed pubertal development, decreased testicular weight, impaired fertility and adult sexual behavior. In the present experiments it was investigated whether the decreased testicular weight was correlated with morphological changes in the testis. Also, by using an artificial insemination technique, the biological activity of spermatozoa of adult male rats, treated during early prepuberty with the LHRH antagonist (LHRH-A), was tested. The present results demonstrated a decrease in the diameter of the testicular tubuli of LHRH-A-treated rats. The number of Sertoli cells per tubular cross-section was also smaller. But qualitatively no differences could be observed in the testis. All stages of maturation of the seminiferous epithelium were equally frequently represented in LHRH-A-treated males compared with controls. Artificial insemination using spermatozoa obtained from the epididymis of LHRH-A-treated rats, resulted in a pregnancy rate of 100%, similar to the control rate. From the present data, we conclude that the infertility in adult male rats, treated with an antagonist to LHRH during prepubertal life, does not result from malfunction in the maturational processes in the germinal cells and the testes as a whole, despite the observation of changes in the testicular morphology. The infertility of LHRH-A-treated male rats can be explained by the observed impairment of sexual behavior. We suggest, that a central action of the antagonist of LHRH when administered to immature male rats may lead to permanent changes in the development of sexual behavior.
van den Dungen
H M
HM
Department of Obstetrics and Gynaecology, Vrije Universiteit, Amsterdam, The Netherlands.
van Dieten
J A
JA
van Rees
G P
GP
Schoemaker
J
J
D000818:Animals; D002452:Cell Count; D005260:Female; D005640:Follicle Stimulating Hormone / Q000097:blood / Q000378:metabolism; D007987:Gonadotropin-Releasing Hormone / Q000031:analogs & derivatives / Q000037:antagonists & inhibitors* / Q000494:pharmacology; D007248:Infertility, Male / Q000209:etiology*; D007315:Insemination, Artificial; D007986:Luteinizing Hormone / Q000097:blood / Q000378:metabolism; D008297:Male; D009929:Organ Size; D051381:Rats; D011919:Rats, Inbred Strains; D012708:Sertoli Cells / Q000502:physiology*; D012741:Sexual Maturation; D013094:Spermatozoa / Q000187:drug effects / Q000502:physiology* / Q000648:ultrastructure; D013737:Testis / Q000187:drug effects / Q000502:physiology* / Q000648:ultrastructure
D007987:Gonadotropin-Releasing Hormone; C042691:LHRH, N-acetyl-(4-chlorophenylalanyl)(1)-(4-chlorophenylalanyl)(2)-tryptophyl(3)-arginyl(6)-alanine(10)-; D007986:Luteinizing Hormone; D005640:Follicle Stimulating Hormone