Vasotocin induces final oocyte maturation and ovulation through the production of a maturation-inducing steroid in the catfish Heteropneustes fossilis

The study reports for the first time vasotocin (VT) induction of final oocyte maturation and ovulation through the production of the maturation-inducing steroid 17, 20β-dihydroxy-4-pregnen-3-one (MIS, 17, 20β-DP). Post-vitellogenic follicles of the catfish Heteropneustes fossilis were incubated with different concentrations of VT (1, 10, 100 and 1000 nM) for different time periods. Germinal vesicle breakdown [GVBD, as a marker of final oocyte maturation (FOM)] and ovulation were scored. In another series of experiments, the follicles were incubated with VT alone or in combination with VT receptor (V1 and V2) antagonists, and GVBD and ovulation were increased with progesterone, 17-hydroxy-4-pregnene-3, 20-dione (17-P) and 17, 20β-DP levels. VT stimulated both GVBD and ovulation in a concentration and time-dependent manner, and the responses were inhibited to varying degrees in groups incubated with the VT receptor antagonists. The V1 antagonist inhibited the responses by 2- to 3-fold and more than the V2 antagonist, and the combination was more potent than the separate incubation. Progestins increased time-dependently in the VT groups and the fold increase was greater for the MIS. The VT-induced steroid stimulation was significantly inhibited to near the control levels in co-incubations with both V1 and V2 receptor antagonists, in the order 17, 20β-DP > 17-P > P4. The inhibition by the V1 receptor antagonist was greater than that with the V2 blocker, and followed the same order of inhibition described above. The results suggest that VT induces FOM and ovulation mainly through the V1 receptors.

► Vasotocin stimulates final oocyte maturation and ovulation.
► It involves the induction of the maturation-inducing steroid 17, 20β-DP.
► The vasotocin effects are mediated mainly through VT1 receptors.
► VT2 receptor has only a minor role in these processes.