Age-related and testicular regression-induced changes in adenosine 3',5'-monophosphate responses in cultured hamster Sertoli cells.
Sertoli cells prepared from adult hamsters with maximally regressed testes responded to FSH with an increased accumulation of intracellular cAMP similar to that of Sertoli cells from an immature animal. That is, the age-dependent decline in responsiveness of Sertoli cells to FSH was reversed during testicular regression. To determine whether this testicular regression-induced restoration of FSH responsiveness was mechanistically a reversal of the age-dependent decline in response, the ability of cholera toxin, forskolin, catecholamines, and pertussis toxin to stimulate cAMP accumulation in Sertoli cells cultured from hamsters undergoing testicular regression was assessed and compared to the responses of Sertoli cells from 18- and 36-day-old hamsters. The age-related decline in responsiveness was evident not only with FSH but also when cells were stimulated with isoproterenol, cholera toxin, forskolin, or pertussis toxin singly or in combination. While the FSH response of Sertoli cells from regressed testes was restored to values indicative of an immature Sertoli cell, the response of the cultured cells to cholera toxin, forskolin, catecholamines, or pertussis toxin either singly or in combination suggested that the adenylate cyclase system of Sertoli cells from regressed testes was unchanged from its "adult" activity. Thus, our original hypothesis that testicular regression/recrudescence was a mirror image of sexual maturation was an oversimplification. However, since FSH is the physiological regulator of Sertoli cell function, and its response is restored to levels found in the immature animal during testicular regression and declines to adult levels during testicular recrudescence, our original hypothesis that testicular recrudescence mimics sexual maturation (i.e. the animal goes through "puberty" each time it goes through a regression/recrudescence cycle) is still tenable. However, at the molecular level, differences in mechanism exist.
Heindel
J J
JJ
Department of Biology, University of Mississippi, University 38677.
D000255:Adenosine Triphosphate / Q000378:metabolism; D037361:Adenylate Cyclase Toxin; D000375:Aging; D000818:Animals; D002478:Cells, Cultured; D002772:Cholera Toxin / Q000494:pharmacology; D005576:Colforsin / Q000494:pharmacology; D006224:Cricetinae; D000242:Cyclic AMP / Q000378:metabolism*; D004305:Dose-Response Relationship, Drug; D004357:Drug Synergism; D005640:Follicle Stimulating Hormone / Q000494:pharmacology; D007545:Isoproterenol / Q000494:pharmacology; D008297:Male; D008647:Mesocricetus; D037342:Pertussis Toxin; D012016:Reference Values; D012708:Sertoli Cells / Q000187:drug effects / Q000378:metabolism*; D013737:Testis / Q000502:physiology*; D013997:Time Factors; D010566:Virulence Factors, Bordetella / Q000494:pharmacology
D037361:Adenylate Cyclase Toxin; D010566:Virulence Factors, Bordetella; D005576:Colforsin; D000255:Adenosine Triphosphate; D005640:Follicle Stimulating Hormone; D002772:Cholera Toxin; D000242:Cyclic AMP; D037342:Pertussis Toxin; D007545:Isoproterenol