Kalra S P, Allen L G, Sahu A, Kalra P S, Crowley W R
Department of Obstetrics and Gynecology, University of Florida College of Medicine, Gainesville 32610.
J Steroid Biochem. 1988;30(1-6):185-93. doi: 10.1016/0022-4731(88)90092-1.
We report that the two classes of regulatory neuropeptides, neuropeptide Y (NPY) and endogenous opioid peptides (EOP), modulate luteinizing hormone (LH) release in diverse fashion in gonad-intact rats. Each neuropeptide acts at two loci, the hypothalamus and pituitary, to excite (NPY) or inhibit (EOP) LH release. At the hypothalamic level, NPY stimulates luteinizing hormone releasing hormone (LHRH) release, a response mediated by alpha 2-adrenoreceptors and amplified in the presence of adrenergic agonists. At the pituitary level, NPY acts in concert with LHRH to amplify the LH response. In contrast, EOP inhibit LHRH release by decreasing the supply of excitatory adrenergic signals in the vicinity of LHRH neurons in the preoptic-tuberal pathway, and at the pituitary level, they decrease LH release in response to LHRH. Further, the gonadal steroidal milieu facilitates NPY neurosecretion and postsynaptic expression of NPY in concert with adrenergic system; a similar clear-cut facilitatory effect of gonadal steroids on EOP secretion is not yet obvious. Our additional studies imply that the EOP system has the potential to increase sensitivity towards gonadal steroids and that to induce the preovulatory LH surge the neural clock may decrease the inhibitory EOP tone prior to the critical period on proestrus. This antecedent neural event allows the excitatory adrenergic and NPY signals to evoke LHRH secretion at a higher frequency approximating that seen in ovariectomized rats. Further studies are under way to delineate the steroid-induced subcellular events that integrate the action of these regulatory peptides in the control of the episodic LHRH secretion pattern which sustains basal and cyclic gonadotropin release in the rat.
我们报告，两类调节性神经肽，即神经肽Y（NPY）和内源性阿片肽（EOP），在性腺完整的大鼠中以不同方式调节促黄体生成素（LH）的释放。每种神经肽作用于两个位点，即下丘脑和垂体，以兴奋（NPY）或抑制（EOP）LH释放。在下丘脑水平，NPY刺激促黄体生成素释放激素（LHRH）释放，该反应由α2 - 肾上腺素能受体介导，并在肾上腺素能激动剂存在时放大。在垂体水平，NPY与LHRH协同作用以放大LH反应。相比之下，EOP通过减少视前 - 结节途径中LHRH神经元附近兴奋性肾上腺素能信号的供应来抑制LHRH释放，并且在垂体水平，它们响应LHRH而减少LH释放。此外，性腺甾体环境与肾上腺素能系统协同促进NPY神经分泌和NPY的突触后表达；性腺甾体对EOP分泌的类似明显促进作用尚不明显。我们的进一步研究表明，EOP系统有可能增加对性腺甾体的敏感性，并且为了诱导排卵前LH峰，神经时钟可能在发情前期关键期之前降低抑制性EOP张力。这一先前的神经事件允许兴奋性肾上腺素能和NPY信号以更高频率诱发LHRH分泌，接近在去卵巢大鼠中观察到的频率。正在进行进一步研究以描绘甾体诱导的亚细胞事件，这些事件整合了这些调节肽在控制大鼠基础和周期性促性腺激素释放的间歇性LHRH分泌模式中的作用。
