Effect of defolliculation and 17 alpha-hydroxy, 20 beta-dihydroprogesterone on cyclic AMP level in full-grown oocytes of the rainbow trout, Salmo gairdneri.

The changes in cAMP were followed in trout oocytes incubated in vitro after defolliculation performed by either enzymatic or manual dissection. Both defolliculation methods induced a highly significant rise in oocyte cAMP level (4.5 times the basal level of control [follicle-enclosed oocytes], after 6 h). Treatment of defolliculated oocytes with 17 alpha-hydroxy, 20 beta-dihydroprogesterone (17 alpha, 20 beta-OH-P) (10(-6) M), which induced oocyte maturation (germinal vesicle breakdown [GVBD]) was able, first, to interrupt the increase of oocyte cAMP level promoted by defolliculation and then to lower this level significantly down to values that still remained higher than folliculated controls. Very low concentrations of 17 alpha, 20 beta-OH-P (1.38-55.6 10(-9) M), or physiological doses of testosterone (0.35 10(-6) M, in the range found in vivo before ovulation) were able to induce a similar decrease of oocyte cAMP level without inducing GVBD. Under the same experimental conditions estradiol (0.35 10(-6) M) exhibited no action. These results suggest that some factor(s) originating in the follicle (FIF), inhibit the oocytes' tendency to accumulate cAMP before the final surge of 17 alpha, 20 beta-OH-P. This factor might be a follicular steroid such as testosterone or nonmaturing concentrations of 17 alpha, 20 beta-OH-P. Moreover our data favour the hypothesis that the final surge of 17 alpha, 20 beta-OH-P could induce distinct intraoocyte mechanisms: the first induces an irreversible blockage of cAMP level before the inhibitory action of the FIF is suppressed by ovulation, and the second mechanism leads to GVBD.