Belchetz P E, Plant T M, Nakai Y, Keogh E J, Knobil E
Science. 1978 Nov 10;202(4368):631-3. doi: 10.1126/science.100883.
In rhesus monkeys with hypothalamic lesions that abolish gonadotropic hormone release by the pituitary gland, the constant infusion of exogenous gonadotropin-releasing hormone (GnRH) fails to restore sustained gonadotropin secretion. In marked contrast, intermittent administration of the synthetic decapeptide once per hour, the physiological frequency of gonadotropin release in the monkeys, reestablishes pituitary gonadotropin secretion. This phenomenon is attributable to the pattern of GnRH delivery rather than to the amounts of this hormone to which the cells of the pituitary are exposed. Moreover, the initiation of continuous GnRH administration in animals with lesions and in which gonadotropin secretion is reestablished by intermittent GnRH replacement can result in a "desensitization" or "down regulation" of the processes responsible for gonadotropin release.
在患有下丘脑损伤的恒河猴中，这种损伤会消除垂体释放促性腺激素，持续输注外源性促性腺激素释放激素（GnRH）无法恢复持续的促性腺激素分泌。与之形成鲜明对比的是，每小时间歇性给予一次合成十肽（这是猴子体内促性腺激素释放的生理频率），可重建垂体促性腺激素分泌。这种现象归因于GnRH的给药模式，而非垂体细胞所接触到的该激素的量。此外，在患有损伤且通过间歇性GnRH替代已重建促性腺激素分泌的动物中，开始持续给予GnRH会导致负责促性腺激素释放的过程出现“脱敏”或“下调”。
