Hormonal and cellular brain mechanisms regulating the amplexus of male and female water frog (Rana esculenta).
The role of nitric oxide (NO) synthase, prostaglandin E2-9-ketoreductase, and aromatase brain activities in regulating frog amplexus was assessed in the water frog (Rana esculenta). Plasma concentrations of testosterone were higher, and concentrations of 17beta-oestradiol lower, in amplexing males than in unamplexing males; while concentrations of testosterone and PGE2 were lower, and those of 17beta-oestradiol and PGF2alpha higher, in amplexing females compared to unamplexing females. Hormone release rescued from frog brains in vitro mirrored plasma hormone measures. Brain aromatase activity was lower in amplexing males; NO synthase was lower and PGE2-9-ketoreductase and aromatase were higher in amplexing females. In male brains, PGE2-9-ketoreductase inhibitor decreased PGF2alpha release and increased that of PGE2; aromatase inhibitor decreased 17beta-oestradiol and increased testosterone release. In female brains, NO donor and PGE2-9-ketoreductase inhibitor increased testosterone and PGE2 release and decreased that of 17beta-oestradiol and PGF2alpha; NO synthase inhibitor decreased testosterone release and PGE2 and increased 17beta-oestradiol and PGF2alpha release; PGF2alpha decreased testosterone release and increased 17beta-oestradiol release; aromatase inhibitor decreased 17beta-oestradiol release and increased testosterone release. In female brains, NO donor and PGE2-9-ketoreductase inhibitor decreased PGE2-9-ketoreductase and aromatase activities; PGF2alpha increased aromatase activity; NO synthase inhibitor increased PGE2-9-ketoreductase and aromatase activity. The data suggest that, in amplexing female brains, external and/or internal stimuli inhibit NO synthase, decreasing NO and activating PGE2-9-ketoreductase; in turn, PGF2alpha increases aromatase activity and 17beta-oestradiol release; while, in amplexing male brains, stimuli inhibit aromatase activity, thereby increasing testosterone production.
Gobbetti
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Department of Molecular, Cellular, and Animal Biology, University of Camerino, Camerino MC, Italy. goze@camserv.unicam.it
Zerani
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D000818:Animals; D001141:Aromatase / Q000378:metabolism*; D047072:Aromatase Inhibitors; D001921:Brain / Q000201:enzymology* / Q000502:physiology; D015237:Dinoprost / Q000097:blood; D015232:Dinoprostone / Q000097:blood; D004791:Enzyme Inhibitors / Q000494:pharmacology; D004958:Estradiol / Q000097:blood; D005260:Female; D006911:Hydroxyprostaglandin Dehydrogenases / Q000037:antagonists & inhibitors / Q000378:metabolism*; D008297:Male; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors / Q000378:metabolism*; D011893:Rana esculenta / Q000502:physiology*; D012726:Sexual Behavior, Animal / Q000502:physiology*; D013739:Testosterone / Q000097:blood
D047072:Aromatase Inhibitors; D004791:Enzyme Inhibitors; D013739:Testosterone; D004958:Estradiol; D015237:Dinoprost; D006911:Hydroxyprostaglandin Dehydrogenases; C035858:prostaglandin-E2 9-reductase; D019001:Nitric Oxide Synthase; D001141:Aromatase; D015232:Dinoprostone