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.

Summary. Seasonal changes in the behaviour, sexual cycle, moult and external environment of the Rook (Corvus f. frugilegus) were studied in relation to each other over a period of twelve years in the climatically mild Truro area of South‐west England where the species is sedentary and undergoes a prolonged autumnal sexual season. There is an internal rhythm of reproduction, based on cyclical changes in the gonads (and no doubt in the adenohypophysis) which controls the primary (autumnal) sexual season. This is extinguished during the winter. The secondary, productive, “spring” sexual season is under the control of external stimuli. Both sexes begin the “spring” gametogenesis early in February when the weather is still as cold as in mid‐winter, sunshine is not considerably increased, and food is still relatively difficult to find. Reproductive behaviour is inhibited by unusually cold weather, but in the mild Cornwall climate initial ovulations fell within the period 8th‐16th March during five years. The breeding season is “timed” to coincide with the seasonal harvest of earthworms (on which the young are fed) which begins before ovulation. The date of ovulation, and therefore actual reproduction (as distinct from the onset of gametogenesis), may be governed by a combination of factors including temperature, sunshine and food availability. The species breeds up to three weeks later following a line East across the colder European land‐mass. At no period of the year is either ovary or testis without quantities of cholesterol. In the testis this is contained in the lipid Leydig cells and when these become seasonally exhausted at the end of spermatogenesis there is a massive cholesterol‐positive steatogenesis in the seminiferous tubules. This tubule material disappears at the onset of the following gametogenesis, by which time the new generation of Leydig cells has become heavily charged with cholesterol and is again in a process of secretion. During the immediate postnuptial period the spermatogenetic mechanism is temporarily thrown completely out of action (Pl. 1, fig. 2). The ovary, on the other hand, is never without some active follicles. Secretory components of the ovary (i.e. those structures that exhibit an unmistakable gain, followed by depletion, of cholesterol‐positive lipids) are as follows: Ex‐follicular gland‐cells (Text‐fig. 4–F, G, H). These possibly arise from fibroblasts that migrate from the theca to the lumen of the atretic follicle. As the follicle disintegrates they are freed in groups into the stroma in which they are dispersed by pressures exerted by the enlargement of neighbouring follicles. These are already present in the stroma of young only three months old. (These are perhaps ostrogenic in function). Female interstitial cells (Text‐fig. 4‐O). These are morphologically like the above, but arise from connective tissue‐cells in the ovarian stroma and therefore seem to be homologous with male Leydig cells. Glandular cells, similar in appearance to the two types above, occasionally ari...

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