Abstract

Larval tiger salamanders induced to metamorphose with thyroxine were injected with oxytocin (100 mU/day) in order to assess the potential effect of neurohypophyseal contamination on the antimetamorphic activity of mammalian prolactin preparations. Unexpectedly, oxytocin caused a marked acceleration of tail fin regression and body weight loss and a slight acceleration of gill resorption. An additional experiment revealed that the decreases in tail height and body weight observed in the initial experiment were induced by oxytocin in animals that were not treated with thyroxine. Prolactin was only partially effective in blocking these effects of oxytocin. In animals induced to metamorphose and treated with oxytocin, prolactin, or both hormones, tail fin regression and weight loss were accelerated by oxytocin and antagonized by prolactin. Prolactin partially reversed the effects of oxytocin on tail height and body weight. In this experiment, oxytocin failed to accelerate gill resorption while prolactin inhibited this process. Oxytocin was without effect on prolactin inhibition of gill resorption. Incubation of tail tissue with oxytocin in vitro induced water loss compared to paired control tissue pieces and the addition of prolactin to the incubation medium caused only a slight inhibition of the oxytocin-induced water loss. These findings are discussed in relation to the hypothesis that the antimetamorphic action of prolactin is osmoregulatory in nature.

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