AN INVESTIGATION OF THE REFRACTORY PERIOD OF REPRODUCTION IN MALE BIRDS BY MEANS OF EXOGENOUS PROLACTIN AND FOLLICLE STIMULATING HORMONE

Abstract

SUMMARY At the end of the breeding season wild birds become refractory to photostimulation, and at the same time there is cessation of spermatogenesis, production of cholesterol-positive tubular lipids, tubular collapse and an overall reduction in size of the testis. These natural events can be duplicated by hypophysectomy or prolactin injection. Just before the onset of such changes the males of at least some wild species produce prolactin. It is shown in pigeons that exogenous prolactin is probably without direct effect on the avian testis, operating merely by inhibiting adenohypophysial activity. However, since in pluralbrooded wild species such collapse is delayed until the last clutch of the season has been fertilized and the males of some of these also brood the eggs, it seems likely that, in nature, prolactin can only temporarily depress, and not inhibit, the output of gonadotrophin. The seasonal inhibition of adenohypophysial function, and the resultant metamorphosis of the testis, is probably essentially under neural control with external stimuli ultimately involved. As regards the termination of the refractory period, it is demonstrated that very small quantities (0·6 i.u.) of exogenous follicle stimulating hormone will clear the tubules of experimentally produced (by hypophysectomy) 'post-nuptial' lipids and cholesterol almost immediately after their appearance. This is interpreted as confirmatory evidence that it is the anterior pituitary, and not the testis, that becomes seasonally refractory. The time taken for the rhythmical annual recovery of adenohypophysial function is probably one of the most important events in the regulation of avian breeding seasons and migration.