...
  • 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 >Control of secretion by mitochondria depends on the size of the local (Ca2+) after chromaffin cell stimulation.
【24h】

Control of secretion by mitochondria depends on the size of the local (Ca2+) after chromaffin cell stimulation.

机译：线粒体对分泌的控制取决于嗜铬细胞刺激后局部（Ca2 +）的大小。

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

In chromaffin cells, plasma membrane calcium (Ca2+) channels and mitochondria constitute defined functional units controlling the availability of Ca2+ nearby exocytotic sites. We show here that, when L-/N-type Ca2+ channels were inhibited with nisoldipine and omega-conotoxin GVIA, cytosolic [Ca2+] ([Ca2+]c) peaks measured in fura-4F-loaded cells were reduced by 36%; however, mitochondrial Ca2+ uptake was unaffected and secretion was potentiated by protonophores as in control cells. By contrast, when non L-type Ca2+ channels were inhibited with omega-conotoxin MVIIC, [Ca2+]c peaks induced by high K+ were reduced by 73%, mitochondrial Ca2+ uptake was abolished, and secretion was not modified by protonophores. However, if Ca2+ entered only through L-type channels activated by FPL64176, high K+ stimulation induced fast mitochondrial Ca2+ uptake and catecholamine secretion was strongly increased and potentiated by protonophores. These results confirm the close association of catecholamine secretion to mitochondrial Ca2+ uptake, and indicate the sharp threshold of local [Ca2+]c (about 5 microM) required for triggering fast mitochondrial Ca2+ uptake that is able to modulate secretion. The entry of Ca2+ through L-type channels generated local [Ca2+]c increases just below that, inducing little mitochondrial Ca2+ uptake unless FPL64176 was present. By contrast, Ca2+ entry through P/Q-type channels fully activated mitochondrial Ca2+ uptake. Control of secretion by mitochondria therefore depends critically on the ability of the stimulus to create large local [Ca2+]c microdomains.
机译：在嗜铬细胞中，质膜钙（Ca2 +）通道和线粒体构成确定的功能单元，控制附近胞吐部位Ca2 +的可用性。我们在这里表明，当尼索地平和ω-芋螺毒素GVIA抑制L- / N型Ca2 +通道时，在呋喃4F加载的细胞中测得的胞质[Ca2 +]（[Ca2 +] c）峰降低了36％;然而，线粒体对Ca2 +的吸收并没有受到影响，质子体也能像控制细胞一样增强分泌。相比之下，当用ω-芋螺毒素MVIIC抑制非L型Ca2 +通道时，高K +诱导的[Ca2 +] c峰减少了73％，线粒体Ca2 +的吸收被消除，质子体不改变分泌。但是，如果Ca2 +仅通过FPL64176激活的L型通道进入，则高K +刺激诱导线粒体Ca2 +的快速吸收，儿茶酚胺的分泌会大大增加并被质子体增强。这些结果证实了儿茶酚胺分泌与线粒体Ca2 +摄取密切相关，并表明触发能够调节分泌的快速线粒体Ca2 +摄取所需的局部[Ca2 +] c尖锐阈值（约5 microM）。 Ca2 +通过L型通道的进入产生的局部[Ca2 +] c刚好低于该水平，除非存在FPL64176，否则几乎不引起线粒体Ca2 +的吸收。相比之下，通过P / Q型通道进入的Ca2 +完全激活了线粒体Ca2 +的吸收。因此，线粒体对分泌的控制主要取决于刺激物产生较大的局部[Ca2 +] c微结构域的能力。

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