Luteinising hormone releasing hormone (LHRH), produced by the hypothalamus, stimulates gonadotropin production by the pituitary1–3. Paradoxically, chronic treatment with large doses of LHRH or its agonists causes a decline in testicular steroidogenesis and testicular LH/human chorionic gonadotropin (hCG) receptors; they also cause a decrease in the weight of testes, seminal vesicles and ventral prostate4–7. There are three possible mechanisms for the inhibitory action of LHRH and its agonists. At the pituitary level, prolonged action of LHRH or its agonists may make the pituitary refractory to further stimulation by LHRH, with a decrease in serum gonadotropins and subsequent atrophy of the male reproductive organs8,9. It is also possible that pharmacological doses of LHRH stimulate the release of a large amount of LH, which in turn ‘desensitises’ the testis to further LH10–14. We have tested a third possibility, namely that LHRH and its agonists act directly on the testis. We report here that LHRH and LHRH agonists cause a decrease in testicular LH/hCG receptors and inhibit testicular steroidogenesis in hypophysectomised male rats, indicating a direct effect on the Leydig cells. This is consistent with our demonstration that LHRH and its agonists act independently of the pituitary to inhibit ovarian steroidogenesis in cultured rat granulosa cells and in hypophysectomised female rats in vivo15.