MECHANISMS OF NEUROENDOCRINE REGULATION

调查的重点是监管的机制 应激时的下丘脑和垂体功能。免疫组织化学 研究表明，虽然急性压力会导致显著释放 促肾上腺皮质激素释放激素(CRH)和加压素(VP)，慢性 应激伴随着TE小细胞中加压素的增加 系统。确定VP在脑垂体变化中的作用 在慢性应激过程中观察到的反应性， 慢性渗透压下丘脑-垂体-肾上腺轴的研究 刺激，一种强烈的VP分泌刺激。缺水48天 HR引起血浆VP、VP mRNA及免疫活性VP显著升高 在大细胞神经元中。尽管脑下垂体Vp升高， 在正常情况下，ACTH对CRH注射或急性应激的反应降低 在肾上腺切除的大鼠中也是如此，表明ACTH减少 这些反应不是由于糖皮质激素的反馈。这些研究表明 小细胞，而不是大细胞VP系统起作用 在慢性应激过程中控制ACTH的分泌。关于中国石油天然气集团公司 促肾上腺皮质激素释放激素受体调节与促肾上腺皮质激素功能的关系 CRH受体和POMC mRNA的变化之间无相关性 脑垂体前叶或中间叶的水平或多肽释放 长期应激的老鼠。这表明，压力诱导的变化 垂体反应性不是由垂体促肾上腺皮质激素释放激素的变化引起的 感受器。促肾上腺皮质激素对一种新型药物的超敏反应 刺激措施，尽管血浆皮质酮持续增加，表明 慢性阻塞性肺疾病糖皮质激素反馈机制的变化 压力。糖皮质激素受体检测显示差异 慢性应激后受体浓度的变化 垂体和海马区减少，下丘脑室旁核增加， NTS。慢性应激肾上腺切除大鼠接受皮质酮治疗 替代，显示糖皮质激素受体没有变化，但 ACTH对一种新的应激反应的超敏反应表明 糖皮质激素受体的改变不是导致这种改变的原因 反馈。

Investigation has focused on the mechanism of regulation of the hypothalamic and pituitary function during stress. Immunohistochemical studies revealed that while acute stress causes marked release of corticotropin releasing hormones (CRH) and vasopressin (VP), chronic stress is accompanied by increases in vasopressin in te parvicellular system. To determine the role of VP on the changes in pituitary responsiveness observed during chronic stress, the function of the hypothalamic-pituitary-adrenal axis was studied during chronic osmotic stimulation, a potent stimulus of VP secretion. Water deprivation for 48 hr caused marked increases in plasma VP, VP mRNA and immunoreactive VP in magnocellular neurones. In spite of the increases in VP, pituitary ACTH responses to CRH injection or acute stress were reduced, in intact as well as in adrenalectomized rats, indicating that the reduced ACTH responses were not due to glucocorticoid feedback. These studies show that the parvicellular, but not the magnocellular VP system plays a role in the control of ACTH secretion during chronic stress. Studies on the relationship between CRH receptor regulation and corticotroph function showed no correlation between changes in CRH receptor and POMC mRNA levels or peptide release in anterior or intermediate pituitary of chronically stressed rats. This indicates that stress-induced changes in pituitary responsiveness are not due to changes in pituitary CRH receptors. The hypersensitivity of the ACTH responses to a novel stimulus, despite sustained increases in plasma corticosterone, suggest an alteration of the glucocorticoid feedback mechanism during chronic stress. Measurement of glucocorticoid receptors showed differential changes in receptor concentration following chronic stress, with decreases in the pituitary and hippocampus and increases in the PVN, and NTS. Chronically stressed adrenalectomized rats receiving corticosterone replacement, showed no changes in glucocorticoid receptors, but hypersensitivity of the ACTH response to a novel stress indicating that glucocorticoid receptor changes are not responsible for the altered feedback.