FSH-induced Sertoli cell proliferation in the developing rat is modified by beta-endorphin produced in the testis.

To probe the possible role of endogenous opiates in Sertoli cell proliferation during testicular development, the effect of interfering with beta-endorphin action either in vivo or in vitro was determined. The percent of Sertoli cells dividing was measured with quantitative autoradiography in [methyl 3H]-thymidine-exposed fetal testes maintained in organ culture with or without FSH, in the presence or absence of the opiate blocker naloxone. After 1 or 2 days in culture, naloxone enhanced the rise in Sertoli cell proliferation seen with FSH alone, while 2 days of incubation with naloxone alone markedly raised the percent of Sertoli cells dividing above that in untreated cultures. Moreover, when endorphin antiserum was injected directly into testes of pups and Sertoli cell proliferation in vivo measured 8 or 19 h later, there was a dramatic increase in the percent of Sertoli nuclei labeled by [methyl 3H]-thymidine compared to controls. These findings suggest that beta-endorphin produced within the testis is a paracrine modifier of the proliferative response of Sertoli cells to FSH. This implies that communication occurs between Leydig and Sertoli cells during development via endogenous testicular opiates.