Vitamin A deficiency results in a decrease in number of large basophils (presumed gonadotropes) in male Lophortyx californicus and a decrease in large basophil cell diameters in females. Decrease in functional activity (as judged by number and size) of this cell type may be partially responsible for the observed effects of vitamin A deficiency on reproduction. Gonads of nondeficient birds respond positively to gonadotropins. The testes of vitamin Adeficient birds produce androgens, but spermatogenesis was subnormal. The hormone-producing component of ovaries of vitamin Adeficient birds responds to gonadotropins, but follicular development does not occur. Vitamin A deficiency in the California Quail appears to act both at the pituitary (and/or hype thalamic) level and at the gonadal level to result in decreased reproductive competence, Study of the effect of vitamin A on bird reproduction has been restricted to galliforms of economic importance. The general effects of vitamin A deficiency in these species include reduced egg production, decreased hatchability of eggs, and impairment of spermatogenesis (see most recently: Reid et al., '65; Shellenberger and Lee, '66). In California Quail vitamin A deficiency also results in decreased egg production and impaired spermatogenesis; however, hatchability was not affected.The manner in which vitamin A deficiency reduces reproductive competence has not been elucidated. In the generally accepted scheme of avian reproduction, the hypothalamus, when properly stimulated, produces factors resulting in the production and release of gonadotropins by the hypophysis. The hypophysial gonadotropins, in turn, induce gonadal maturation. Vitamin A deficiency could act at the hypothalamic and/or hypophysial level to result in decreased production and secretion of gonadotropins. Vitamin A deficiency could also act at the gonadal level, preventing the gonad from responding to gonadotropins. The present experiments were carried out to increase the understanding of the effects of vitamin A deficiency of pituitary cytology and on the response of gonads to gonadotropins.