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¹ Monash Institute of Medical Research, Monash University, 27–31 Wright Street, Clayton, Victoria 3168, Australia
² Australian Research Council Centre of Excellence in Biotechnology and Development, Monash Medical Centre, Melbourne, Victoria, Australia

(Requests for offprints should be addressed to M P Hedger; Email: mark.hedger{at}med.monash.edu.au)

(T Hayashi is now at Department of Urology, Saitama Medical University, 1981 Tsujido, Kamoda, Kawagoe, Saitama 350-8550, Japan)

Production and regulation of activin A and inhibin B during the cycle of the seminiferous epithelium were investigated in adult rats. Immunohistochemistry localised the activin ß_A-subunit to the Sertoli cell cytoplasm, with much weaker expression in spermatocytes and spermatids. Both activin A and inhibin B, measured by ELISA were secreted by, seminiferous tubule fragments over 72 h in culture. Activin A was secreted in a cyclic manner with peak secretion from tubules isolated at stage VIII. Tubules collected during stage VI produced the least activin A. Inhibin B secretion was highest from stage IX-I tubules and lowest from stage VII tubules. Addition of interleukin-1ß (IL-1ß) had relatively little effect on activin A or inhibin B secretion in culture. In contrast, the peak secretion of activin A by stage VIII tubules was blocked by co-incubation with an excess of human recombinant IL-1 receptor antagonist, whereas inhibin B secretion increased slightly. Dibutyryl cAMP stimulated activin A secretion by late stage VII and VIII tubules and stimulated inhibin B across all stages. These data indicate that activin A and inhibin B are cyclically regulated within the seminiferous epithelium, with endogenous IL-1 (presumably IL-1 produced by the Sertoli cells), responsible for a peak of activin A production subsequent to sperm release at stage VIII. These data provide direct evidence that production of activin A and inhibin B by the Sertoli cell is locally modulated by IL-1 , in addition to FSH/cAMP, under the influence of the developing spermatogenic cells.

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