McDonald J K
Department of Anatomy and Cell Biology, Emory University School of Medicine, Atlanta, Georgia 30322.
Ann N Y Acad Sci. 1990;611:258-72. doi: 10.1111/j.1749-6632.1990.tb48937.x.
NPY acts both at the hypothalamus and the anterior pituitary gland to modulate reproductive hormone secretion. Within the hypothalamus, NPY stimulates LHRH secretion in the presence of physiological levels of estrogen and suppresses pulsatile LHRH release following ovariectomy. Intracerebroventricular injection of NPY antiserum blocks or delays the LH surge in steroid-primed ovariectomized rats, thereby adding support for a physiological role of NPY in the neuroendocrine events preceding ovulation. Blockade of alpha 2 adrenergic receptors decreases NPY-stimulated LH release in steroid-primed rats implying a potential noradrenergic mediation of NPY activity. Physiological levels of progesterone do not augment, and may actually suppress NPY-induced LHRH secretion in vitro from median eminences obtained from estrogen-primed ovariectomized rats. The physiological role of progesterone, if any, in modulating NPY effects on LHRH release remains to be determined. Little, if anything, is known about the NPY receptor in the median eminence or the intracellular mechanisms which transduce the NPY signal into activation of LHRH release in estrogen-treated ovariectomized rats although translocation of intracellular calcium is required. Equally puzzling is the mechanism of desensitization of the LHRH-releasing mechanisms of the median eminence of ovariectomized rats or the specific site of NPY suppression of pulsatile LHRH secretion. NPY is released into the hypothalamo-hypophysial portal circulation and this appears correlated with LHRH secretion before the LH surge. NPY affects LH and FSH release from anterior pituitary cells in vitro and enhances LHRH-induced LH secretion. Taken together, the studies described above suggest an important physiological role for NPY as a modulator of neuroendocrine activity which culminates in the preovulatory surge of LH.
神经肽Y（NPY）在下丘脑和垂体前叶发挥作用，调节生殖激素的分泌。在下丘脑内，NPY在生理水平雌激素存在的情况下刺激促黄体生成素释放激素（LHRH）的分泌，而在卵巢切除术后抑制LHRH的脉冲式释放。向脑室内注射NPY抗血清可阻断或延迟类固醇预处理的去卵巢大鼠的促黄体生成素（LH）峰，从而支持了NPY在排卵前神经内分泌事件中的生理作用。阻断α2肾上腺素能受体可降低类固醇预处理大鼠中NPY刺激的LH释放，这意味着NPY活性可能存在去甲肾上腺素能介导。孕酮的生理水平不会增强，实际上可能会抑制从雌激素预处理的去卵巢大鼠获得的正中隆起在体外由NPY诱导的LHRH分泌。孕酮在调节NPY对LHRH释放的影响方面的生理作用（如果有的话）仍有待确定。关于雌激素处理的去卵巢大鼠正中隆起中的NPY受体或介导NPY信号转化为LHRH释放激活的细胞内机制知之甚少，尽管细胞内钙的转运是必需的。同样令人困惑的是去卵巢大鼠正中隆起LHRH释放机制的脱敏机制或NPY抑制LHRH脉冲式分泌的特定部位。NPY释放到下丘脑 - 垂体门脉循环中，这似乎与LH峰前的LHRH分泌相关。NPY在体外影响垂体前叶细胞LH和促卵泡生成素（FSH）的释放，并增强LHRH诱导的LH分泌。综上所述，上述研究表明NPY作为神经内分泌活动的调节剂具有重要的生理作用，最终导致LH排卵前峰的出现。
