...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>The European Journal of Neuroscience >Rapid modulatory effect of estradiol on acetylcholine-induced Ca signal is mediated through cyclic-GMP cascade in LHRH-releasing GT1-7 cells.
【24h】

Rapid modulatory effect of estradiol on acetylcholine-induced Ca signal is mediated through cyclic-GMP cascade in LHRH-releasing GT1-7 cells.

机译：雌二醇对乙酰胆碱诱导的Ca信号的快速调节作用是通过LHRH释放GT1-7细胞中的环GMP级联介导的。

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Hypothalamic luteinizing hormone-releasing hormone neurons (LHRH) form the final pathway for the central control of reproduction through the release of LHRH into the pituitary-hypothalamic system. We previously found that LHRH-producing GT1-7 cells respond to acetylcholine (ACh) with an increase in intracellular calcium ([Ca(2+)](i)) through activation of muscarinic receptors. This effect is acutely modulated by 17beta-estradiol in a manner compatible with specific membrane binding sites. Because increasing evidence suggests that second messengers are involved in the rapid action of estradiol, the aim of the present study was to identify the pathway underlying estrogen actions on ACh-induced Ca(2+) signals. 8-Bromoguanosine 3',5'-cyclic monophosphate (10 microm) and C-type natriuretic peptide (10 microm) mimicked the effect of estradiol. On the contrary, neither dibutyryl cAMP (100 microm), forskolin (100 nm or 10 microm), or sodium nitroprusside (10 microm) induced any modification of [Ca(2+)](i) in response to ACh. The effect of estradiol on calcium transients was totally blocked by two different cGMP-dependent protein kinase (PKG) inhibitors. In addition, phosphorylation of inositol 1,4,5-triphosphate (IP(3)) receptor was rapidly induced by estradiol but totally blocked when the cells were pretreated with a PKG inhibitor. We conclude that physiological concentrations of estradiol reduce ACh-induced Ca(2+) transients via a mechanism involving a membrane-associated guanylate cyclase, which finally induces a PKG-dependent IP(3) receptor phosphorylation that modifies calcium release from the endoplasmic reticulum.
机译：下丘脑促黄体生成激素释放激素神经元（LHRH）通过将LHRH释放到垂体-下丘脑系统中而形成了中央控制生殖的最终途径。我们先前发现，产生LHRH的GT1-7细胞通过激活毒蕈碱受体而对乙酰胆碱（ACh）的反应与细胞内钙（[Ca（2 +）]（i））的增加有关。此作用由17β-雌二醇以与特定膜结合位点兼容的方式剧烈调节。因为越来越多的证据表明第二信使参与了雌二醇的快速作用，所以本研究的目的是确定雌激素作用于ACh诱导的Ca（2+）信号的基础通路。 8-溴鸟苷3'，5'-环一磷酸（10微米）和C型利钠肽（10微米）模仿了雌二醇的作用。相反，二丁酰基cAMP（100微米），福司可林（100 nm或10微米）或硝普钠（10微米）均未响应ACh引起[Ca（2 +）]（i）的任何修饰。两种不同的cGMP依赖性蛋白激酶（PKG）抑制剂完全阻断了雌二醇对钙瞬变的影响。此外，雌二醇可快速诱导肌醇1,4,5-三磷酸（IP（3））受体的磷酸化，但当用PKG抑制剂预处理细胞后，磷酸化完全被阻断。我们得出结论，雌二醇的生理浓度通过涉及膜相关鸟苷酸环化酶的机制降低ACh诱导的Ca（2+）瞬变，该机制最终诱导PKG依赖性IP（3）受体磷酸化，从而修饰钙从内质网释放。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号