Corticotropin-releasing hormone and dexamethasone do not alter secretion of immunoreactive beta-endorphin from dissociated fetal hypothalamic cell cultures.
Corticotropin-releasing hormone and dexamethasone do not alter secretion of immunoreactive beta-endorphin from dissociated fetal hypothalamic cell cultures.
复制标题
促肾上腺皮质激素释放激素和地塞米松不会改变离体胎儿下丘脑细胞培养物中免疫反应性β-内啡肽的分泌。
DOI：
10.1016/0006-8993(90)91744-2
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发表时间：
1990
期刊：
影响因子：
2.9
通讯作者：
Weng,CF
中科院分区：
文献类型：
--
作者：
Kapcala,LP;Juang,HH;Weng,CF
促肾上腺皮质激素释放激素（CRH）和糖皮质激素是下丘脑-垂体-肾上腺（HPA）轴的主要调节因子，HPA轴控制垂体分泌β-内啡肽和其他前阿黑皮素（POMC）衍生肽。虽然先前的工作已经表明，CRH刺激分泌β-内啡肽从成人下丘脑外植体，和糖皮质激素可以抑制基础和刺激分泌的POMC衍生肽从垂体，糖皮质激素的作用下丘脑β-内啡肽分泌是未知的。研究了CRH和地塞米松（一种强效糖皮质激素）对分离的胎儿下丘脑细胞分泌免疫反应性（IR）β-内啡肽的影响。CRH（10−9-10− 6 M）不刺激下丘脑细胞分泌IR-β-内啡肽，下丘脑细胞在钾诱导的去极化时释放IR-β-内啡肽。然而，CRH确实刺激胎儿下丘脑外植体分泌IR-β-内啡肽，这与分离的下丘脑细胞培养物来源的下丘脑组织相似。将细胞暴露于地塞米松（10− 6 M）并不抑制IR-β-内啡肽的基础或钾刺激释放。这些结果表明：（1）培养中分离的胎儿下丘脑细胞不表现出与刺激IR-β-内啡肽分泌偶联的功能性CRH受体;（2）下丘脑细胞暴露于地塞米松不会抑制基础或去极化诱导的IR-β-内啡肽释放;和（3）由于体外条件和/或细胞结构关系。
Corticotropin-releasing hormone (CRH) and glucocorticoids are major regulators of the hypothalamic-pituitary-adrenal (HPA) axis controlling secretion of β-endorphin and other pro-opiomelanocortin (POMC)-derived peptides from pituitary. Although previous work has shown that CRH stimulates secretion of β-endorphin from adult hypothalamic explants, and that glucocorticoids can inhibit basal and stimulated secretion of POMC-derived peptides from pituitary, the role of glucocorticoids on hyopthalamic β-endorphin secretion is not known. Studies were performed to assess the effects of CRH and dexamethasone, a potent glucocorticoid, on secretion of immunoreactive (IR) β-endorphin from dissociated fetal hypothalamic cell cultures. CRH (10−9–10−6M) did not stimulate secretion of IR-β-endorphin from hypothalamic cells which did release IR-β-endorphin upon potassium-induced depolarization. However, CRH did stimulate IR-β-endorphin secretion from fetal hypothalamic explants which were similar to hypothalamic tissue from which dissociated hypothalamic cell cultures were derived. Exposure of cells to dexamethasone (10−6M) did not inhibit basal nor potassium-stimulated release of IR-β-endorphin. These results indicate that: (1) dissociated fetal hypothalamic cells in culture do not exhibit a functional CRH receptor coupled to stimulation of IR-β-endorphin secretion; (2) exposure of hypothalamic cells to dexamethasone does not inhibit basal nor depolarization-induced release of IR-β-endorphin; and (3) dissociated fetal hypothalamic cells may have limited utility in elucidating specific regulatory relationships because of in vitro conditions and/or cytoarchitectural relationships.