In vitro regulation of immunoreactive beta-endorphin secretion from adult and fetal hypothalamus by sequential stimulation with corticotropin-releasing hormone.
In vitro regulation of immunoreactive beta-endorphin secretion from adult and fetal hypothalamus by sequential stimulation with corticotropin-releasing hormone.
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通过促肾上腺皮质激素释放激素的连续刺激，体外调节成人和胎儿下丘脑的免疫反应性β-内啡肽分泌。
DOI：
10.1016/0006-8993(92)91339-g
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发表时间：
1992
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;Weng,CF
先前的研究表明促肾上腺皮质激素释放激素(CRH)刺激下丘脑分泌β-内啡肽。我们验证了下丘脑组织对促肾上腺皮质激素释放激素(β-END)刺激的假说：(1)绵羊促肾上腺皮质激素释放激素的剂量，(2)促肾上腺皮质激素释放激素的刺激方式和顺序，(3)雄激素状态，(4)下丘脑年龄。对成年雄性大鼠和17日龄胎鼠的下丘脑进行了研究。在成人下丘脑，促肾上腺皮质激素释放激素刺激的免疫反应(IR)-β-End分泌10−7M组大于10−11M组，且呈剂量依赖性刺激。用10−11M促肾上腺皮质激素释放激素连续刺激20min，然后间隔40min不刺激促肾上腺皮质激素释放激素，可短暂刺激IR-β-END和IR-α-黑素细胞刺激素的分泌，后者是β-END的前体-阿片黑素皮质素前体。随后用10−6M促肾上腺皮质激素释放激素的刺激显示对刺激的脱敏，尽管钾诱导的去极化显示容易释放的IR-β-END。此外，在存在促肾上腺皮质激素释放激素的情况下，延长10−7M促肾上腺皮质激素释放1h或增加促肾上腺皮质激素释放激素浓度均可持续增加IR-β末端释放。双氢睾酮对去睾丸大鼠基础或促肾上腺皮质激素释放胰岛素样生长因子受体(IR-β-End)无影响。短时间(20min)或长时间(1h)暴露于促肾上腺皮质激素的胎儿下丘脑外植体的IR-β末端分泌模式与成人外植体相似。这些结果表明：(1)促肾上腺皮质激素释放激素(CRH)刺激的下丘脑IR-β-End分泌呈剂量依赖性；(2)CRH刺激下丘脑IR-β-End分泌的方式决定了对CRH刺激是否存在脱敏或持续反应；(3)去睾丸大鼠短期应用双氢睾酮不改变基础或CRH刺激的IR-β-End分泌；(4)绵羊CRH对胎儿下丘脑IR-β-End分泌的调节似乎与成人下丘脑相似。
Previous work has shown corticotropin-releasing hormone (CRH) stimulation of β-endorphin (END) secretion from hypothalamus. We tested the hypothesis that CRH stimulation of β-END (measured by radioimmunoassay) from hypothalamic explants is dependent on: (1) ovine CRH dose, (2) pattern and sequence of CRH stimulation, (3) androgen status, and (4) hypothalamic age. Hypothalami from adult male rats and day 17 fetal rats were studied. In adult hypothalami, CRH-stimulated immunoreactive (IR)-β-END secretion with 10−7M was greater than that with 10−11M CRH and showed dose-dependent stimulation. Serial stimulation for 20 min by 10−11M CRH followed by a 40 min interval without CRH stimulation resulted in a brief stimulation of secretion of IR-β-END and also secretion of IR-α-melanocyte-stimulating hormone (MSH), another peptide derive from pro-opiomelanocortin, the precursor of β-END. subsequent stimulatio with 10−6M CRH showed a desensitization to stimulation despite readily releasable pools of IR-β-END shown by potassium-induced depolarization. In addition, prolonged stimulation for 1 h with 10−7M CRH or increasing concentration of CRH produced a sustained increase in IR-β-END release as long as CRH was present. Dihydrotestosterone treatment had no effect on basal nor CRH-stimulated IR-β-END release in orchiectomized rats. The pattern of IR-β-END secretion from fetal hypothalamic explants exposed briefly (20 min) or for a prolonged period (1 h) to CRH was similar to that from adult explants. These results demonstrate that: (1) CRH-stimulated IR-β-END secretion from hypothalamus is dose-dependent; (2) the pattern of stimulation of hypothalamic IR-β-END release by CRH determines whether there is a desensitization or a sustained response to CRH stimulation; (3) short-term androgen treatment with dihydrotestosterone to orchiectomized rats does not alter basal nor CRH-stimulated IR-β-END secretion; and (4) regulation of IR-β-END secretion in fetal hypothalamus by ovine CRH appears similar to that observed in adult hypothalamus.