Delidow B C, Baldocchi R A, Nicoll C S
Department of Physiology, University of California, Berkeley 94720.
Gen Comp Endocrinol. 1988 Jun;70(3):418-24. doi: 10.1016/0016-6480(88)90116-5.
Hormonal control of amphibian development involves thyroid hormones (TH), which promote metamorphosis, and prolactin (PRL), which antagonizes the effects of TH and promotes larval growth. Although the liver is not considered to be a regulator of developmental processes such as metamorphosis, it secretes a PRL-synergizing factor (synlactin) in response to PRL. We explored the possibility that the liver may participate in the antimetamorphic actions of PRL in Rana catesbeiana. Bullfrog tadpoles, in which release of endogenous PRL was suppressed by injections of bromocryptine to induce metamorphic changes including tail regression, received hormone-containing implants in various sites. PRL implants in the spleen to deliver hormone directly to the liver via the hepatic portal drainage not only prevented tail regression but actually caused a substantial increase in the height of the tail fin. PRL implanted in other sites or GH implanted in the spleen was much less effective. The liver of animals with intrasplenic PRL implants secreted more synlactin in vitro than that of tadpoles with subcutaneous PRL implants. Young grass frogs were injected with ovine (o) GH or oPRL to determine effects on hepatic synlactin secretion. Although the GH stimulated body growth it did not induce the liver to secrete synlactin. By contrast, PRL treatment did stimulate hepatic secretion of synlactin without stimulating body growth. These results indicate that the liver of pre- and postmetamorphic animals can be stimulated by PRL to secrete synlactin. Furthermore, the antimetamorphic actions of PRL in tadpoles appears to be mediated, at least in part, by an action on the liver. Synlactin may mediate this hepatic effect.
