sexes with delayed puberty had normal LH and FSH release when tested, suggesting that hypothalamic or higher centres are involved in the initiation of puberty.In patients with "functionless" pituitary tumours or those with active acromegaly, impaired LH release was often seen, though FSH reserve under the test conditions appeared intact. The ability of the pituitary to release gonadotrophins occurred in many patients independently of the functional pituitary reserve for other hormones. The three patients with pituitarydependent Cushing's disease each showed a different type of response-normal, impaired, or exaggerated. Impaired or absent TSH responses to TRH were seen in these three patients and this is characteristic of this condition .When the 15 patients with amenorrhoea and galactorrhoea were investigated it was clear that basal gonadotrophin levels were normal or high in nine, and that normal or even exaggerated responses could occur after administration of the decapeptide. The response did not correlate with basal prolactin levels nor the levels achieved after administration of TRH. The cause of amenorrhoea in these women was clearly not due to inability to synthesize the gonadotrophins but was probably the result of failure of their cyclical release. Hyperprolactinaemia may be responsible, at least in part, for this functional abnormality, since when the prolactin levels were reduced with bromergocryptine galactorrhoea ceased and normal menstruation resumed; potency returned in male patients similarly treated . Whether prolactin interferes at the hypothalamic-pituitary level or has a direct action on the gonads remains to be elucidated.Gonadotrophin releasing hormone responsiveness was present in every patient with anorexia nervosa, and here again it is probably the failure of cyclical release rather than inability to synthesize gonadotrophins which is the major factor in the initiation and perpetuation of the amenorrhoea. Patients with primary gonadal failure showed the expected exaggerated response to the decapeptide.In view of the fact that in most patients with hypogonadotrophic hypogonadism, of whatever cause, LH and FSH secretion can be induced with the synthetic decapeptide LH/FSH-RH, it is evident that the pituitaries of these patients contain LH and FSH. It would therefore appear that it is the impairment of release which is the primary cause of the hypogonadism rather than pituitary gonadotroph destruction in these patients.