Mechanism of apoptosis induction in amphibian spermatogonia by prolactin

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We have investigated about the mechanism of apoptosis induction in newt spermatogonia by prolactin. We clarified the following things.(1) Ovine prolactin (oPRL) administration into newts induced apoptotic cell death only in the last stage of spermatogonia (7th generation from primary spermatogonium) and co-administration of porcine follicle-stimulating hormone (pFSH) inhibited this cell death. In organ culture of testes fragments, it was demonstrated that PRL induces spermatogonial cell death by acting directly on the testis.(2) Transfer of newts to low temperature caused spermatogonial apoptosis and elevation of plasma PRL levels. Injection of anti-PRL serum into newt at low temperature almost completely rescued spermatogonia from degeneration for as long as 3 days. These results demonstrate that low temperature caused elevation of prolactin concentration in the newt blood, which induced cell death of spermatogonia just before meiosis.(3) Cycloheximide (CHX), a protein synthesis inhibitor, also induced apoptosis. zVAD -fmk, a broad caspase inhibitor, inhibited the apoptosis induced by PRL and CHX. On the other hand, these parameters were not suppressed by ICE inhibitor Ac-YVAD-CHO or by caspase-3 inhibitor Ac-DEVD-CHO, indicating that apoptotic morphological changes occurring when the 7th generation of spermatogonia dies are induced by some unknown caspases. We have isolated cDNA for newt caspase 3.(4) FSH activity is indispensable for accomplishment of the last mitosis of newt spermatogonia, because cell death of secondary spermatogonia just before meiosis occurred without pFSH in vitro. These results indicate that balance of the biological activity of PRL and FSH is the key factor for life-or-death of the last stage of spermatogonia and for decision whether spermatocytogenesis commence or not.