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\m=.\6i.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.At the end of the breeding season of wild birds the interstitial cells become exhausted, the seminiferous tubules collapse, and their contents undergo a massive steatogenesis involving the production of cholesterol [Marshall, 1949]. It has long been known that both hypophysectomy [Hill & Parkes, 1934] and injections of prolactin [Riddle & Bates, 1933] will stop spermatogenesis and lead to collapse of the testis. Further, it has been demonstrated by Coombs & Marshall [1956] and Lofts & Marshall [1956] that such changes are accompanied by the cholesterol-producing metamor¬ phosis described above.At the period of collapse and steatogenesis the bird becomes unresponsive to experimental photostimulation and enters a refractory period during which sexual behaviour is extinguished. For several months, the duration depending on the species, reproduction is impossible. It is probable that the essential cause of the metamor¬ phosis of the testis is a seasonal, post-nuptial reduction in the output of gonado¬ trophins [Marshall, 1952], but it has been a matter of doubt whether the testis, in addition to the adenohypophysis, becomes refractory.