Release of prostaglandin E2 from the hypothalamus depends on extracellular Ca2+ availability: relation to LHRH release.
Release of prostaglandin E2 from the hypothalamus depends on extracellular Ca2+ availability: relation to LHRH release.
复制标题
下丘脑前列腺素 E2 的释放取决于细胞外 Ca2 的可用性：与 LHRH 释放的关系。
DOI：
10.1159/000124018
复制
发表时间：
1984
影响因子：
4.1
通讯作者：
Negro-Vilar,A
中科院分区：
文献类型：
--
作者：
Ojeda,SR;Negro-Vilar,A
本实验旨在研究细胞外Ca2+在下丘脑正中隆起（ME）释放前列腺素E2（PGE2）过程中的作用。还评估了 LHRH 释放的变化。 ME 片段与不同浓度 K+ 的孵育诱导 PGE2 和 LHRH 释放的剂量相关增加。 K+ 的作用取决于培养介质中Ca2+ 的浓度。 0.1 mM 的 Ca2+ 浓度足以使 PGE2 和 LHRH 释放对 K+ 产生显着反应。通过从培养介质中省略 Ca2+ 并用 EDTA 或 EGTA 螯合剩余的 Ca2+，最大 K+ 浓度 (56 mM) 的影响几乎完全消除。在不同浓度 (1–50 µM) 下测试的 Ca2+ 离子载体 A23187 以 Ca2+ 依赖性方式显着增加了 ME 中 PGE2 和 LHRH 的释放。 0.25 mM 的 Ca2+ 浓度允许对离子载体产生最大的 LHRH 反应，但仅允许部分 (50%) PGE2 反应。用 Verapamil（一种 Ca2+ 进入阻滞剂）阻断 Ca2+ 通道，以剂量依赖性方式阻止 K+ 对 PGE2 和 LHRH 释放的影响。结果表明，ME 神经末梢释放的 PGE2 取决于细胞外 Ca2+ 的浓度，并表明 PGE2 释放是由流向末梢的 Ca2+ 增加启动的。此外，数据进一步证明 LHRH 的释放在很大程度上是通过 Ca2+ 电压依赖性通道的 Ca2+ 流入的函数。
The present experiments were performed to investigate the role of extracellular Ca2+in the process of prostaglandin E2(PGE2) release from the median eminence (ME) of the hypothalamus. Changes in the release of LHRH were also evaluated. Incubation of ME fragments with different concentrations of K+induced a dose-related increase in PGE2and LHRH release. The effect of K+depended upon the Ca2+concentration in the incubation medium. A Ca2+concentration of 0.1 mM was sufficient to permit a significant response in both PGE2and LHRH release to K+. The effect of a maximal K+concentration (56 mM)was almost completely obliterated by omitting Ca2+from the incubation medium and by chelating the remaining Ca2+with EDTA or EGTA. The Ca2+ionophore A23187, tested at different concentrations (1–50 µM)significantly increased the release of both PGE2and LHRH from the ME in a Ca2+-dependent manner. A Ca2+concentration of 0.25 mM allowed maximal LHRH response to the ionophore, but permitted only a partial (50%) PGE2response. Blockade of Ca2+channels with Verapamil, a Ca2+entry blocker, prevented the effect of K+on both PGE2and LHRH release in a dose-dependent manner. The results demonstrate that release of PGE2from ME nerve terminals depends upon the concentration of extracellular Ca2+and suggest that PGE2release is initiated by an increase in Ca2+influx to the terminals. In addition, the data provide further evidence that release of LHRH is, to a significant extent, a function of Ca2+influx through Ca2+voltage-dependent channels.