Yen S S, Quigley M E, Reid R L, Ropert J F, Cetel N S
Am J Obstet Gynecol. 1985 Jun 15;152(4):485-93. doi: 10.1016/s0002-9378(85)80162-9.
Substantial evidence now exists to indicate that the endogenous hypothalamic opioidergic mechanism(s) represents one of the important controlling systems for release of gonadotropin-releasing hormone. Modulations of frequency and amplitude of the secretory activity of gonadotropin-releasing hormone appears to be mediated through an inhibitory action of endogenous opioids, and the functional coupling of the opioidergic and gonadotropin-releasing hormone systems is an ovarian steroid-dependent event. There is also evidence to implicate suprahypothalamic mechanism(s) that enhance endogenous opioid inhibition of secretion of gonadotropin-releasing hormone. Although exogenous opioid peptides and their synthetic analogs consistently induce the secretion of prolactin, blockade of opioid receptors in humans by naloxone failed to elicit a decrement in the levels of prolactin under a variety of conditions. On the contrary, naloxone induced a remarkable increment in the secretion of prolactin via an increased frequency of pulsatile release which is synchronized with pulses of luteinizing hormone. These observations suggest that a common neuroendocrine mechanism is involved in the opioidergic control of the secretion of both luteinizing hormone and prolactin in women.
现有大量证据表明，内源性下丘脑阿片肽机制是促性腺激素释放激素释放的重要控制系统之一。促性腺激素释放激素分泌活动的频率和幅度调节似乎是通过内源性阿片肽的抑制作用介导的，并且阿片肽系统与促性腺激素释放激素系统的功能耦合是一个依赖卵巢类固醇的事件。也有证据表明存在下丘脑以上的机制，这些机制会增强内源性阿片肽对促性腺激素释放激素分泌的抑制作用。尽管外源性阿片肽及其合成类似物始终会诱导催乳素的分泌，但在各种情况下，纳洛酮对人体阿片受体的阻断并未导致催乳素水平下降。相反，纳洛酮通过增加与促黄体生成素脉冲同步的脉冲释放频率，诱导催乳素分泌显著增加。这些观察结果表明，一种共同的神经内分泌机制参与了女性中阿片肽对促黄体生成素和催乳素分泌的控制。
