POSSIBLE MECHANISM FOR THE FIRST RESPONSE TO SHORT CAPTIVITY STRESS IN THE WATER FROG, RANA-ESCULENTA

To clarify the endocrine mechanism involved in the short captivity str ess in the water frog, Rana esculenta, the activity of 9-ketoreductase , the enzyme which converts prostaglandin E(2) (PGE(2)) into prostagla ndin F-2 alpha (PGF(2 alpha)), and aromatase, which converts testoster one into oestradiol-17 beta, were studied. Adult male and female frogs were sacrificed 0, 1.5, 3, 6, 12, 24, 48, 72, 168 and 336 h after cap ture in the field. PGE(2), PGF(2 alpha), progesterone, testosterone, o estradiol-17 beta and corticosterone plasma levels were detected by RI A at each time point. 9-Ketoreductase (conversion of [H-3]PGE(2) into [H-3]PGF(2 alpha)) and aromatase (conversion of [H-3]testosterone into [H-3]oestradiol-17 beta) activities in the brain, testis, ovary and i nterrenal were also determined at each time point. After capture, leve ls of plasma PGF(2 alpha) increased (male: 228%; female: 288%) and PGE (2) decreased (male: 68%; female: 81%) at 1.5 h, oestradiol-17 beta in creased (male: 399%; female: 425%) and testosterone decreased (male: 8 7%; female. 83%) at 6 h, and corticosterone increased (male: 421%; fem ale. 426%) at 72 h. 9-Ketoreductase activity in the brain was enhanced at 1.5 h after capture (male: 249%; female: 262%); aromatase activity increased at 6 h in the testis (261%), ovary (273%) and interrenal (m ale: 227%; female. 267%). These results indicate that short captivity stress could induce an increase in plasma PGF(2 alpha) through activat ion of brain 9-ketoreductase. In turn, PGF(2 alpha) might enhance the levels of circulating oestradiol-17 beta through activation of gonadal and interrenal aromatase.