ENDOCRINE INFLUENCES ON THE DEVELOPMENT OF THE RUDIMENTARY GONAD OF FOWL1

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Abstract
Growth of the rudimentary right gonad of ovariecto-mized, domestic fowl can be inhibited with exogenous estrogen and, to a lesser extent, with androgen. It is possible to prevent the hypertrophy of the rudiment even with a quantity of estrogen that has no significant effect upon oviduct weight and which apparently lies below the estrogen threshold for oviduct stimulation. Estrogenic substance was demonstrated in the blood of young chicks. The adequacy of a "physiological" dose of estrogen coupled with the demonstration of its presence at an age of sexual "inactivity," lends strong support to the contention that estrogen is involved in the in vivo mechanism of rudiment inhibition. Following ovariectomy the sensitivity of the compensatory right gonad decreases with time, i.e., estrogen dosages increased in proportion to body weight lose their effectiveness. This observation helps to explain that compensatory gonads can, and ultimately do secrete considerable amounts of estrogen. Prolactin depresses rudiment hypertrophy in ovariectomized birds. The mode of action of prolactin, known to antagonistic to that of follicle stimulating hormone might be analogous in effect at least, to the mechanism of rudiment inhibition by estrogen. Hypophysectomy significantly depresses the weight of hypertrophied testicular rudiments as well as their androgen secretion. All attempts to accelerate the growth of compensatory gonads, or to maintain them in hypophysectomized poulards with mammalian gonadotropic hormones have failed.