A study on the mechanism of intracellular Ca^<2+> release in neurones and its physiological functions.

神经元细胞内Ca^2释放机制及其生理功能的研究。

• 批准号: 04454139
• 负责人: KUBA Kenji
• 金额: $ 1.73万
• 依托单位: Saga Medical School
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for General Scientific Research (B)
• 财政年份: 1992
• 资助国家: 日本
• 起止时间: 1992 至 1993
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-04454139/
• 关键词: Intracellular Ca^<2+>; Ca^<2+> -induced Ca^<2+> release; Ca^<2+> influx; Bullfrog sympathetic ganglion cells; Rabbit otic ganglion cells; Cylic ADP-ribose; Mitochondria Cyclosporin-A; サイクロスポリンA; Ca^<2+>誘起性Ca^<2+>遊離; cyclic ADP-ribose; Ca^<2+>感受性

The mechanism of intracellular Ca^<2+> release and its physiological functions were studied in cultured bullfrog sympathetic and rabbit otic ganglion cells, using fura-2 or indo-1 fluorescence redording techniques with a photomultiplier or confocal laser-scanning microscope and shole cell patch clamp techniques. Ryanodine-sensitive Ca^<2+> -induced Ca^<2+> release (CICR) in bullfrog sympathetic neurones were voltage-dependently activated throughout the cytoplasm by Ca^<2+> influx produced by a depolarizing voltage pulse (> 100 ms), but only in the submembrane regions by Ca^<2+> influx caused by action potentials (> 10 Hz, 100 pulses). Under the effects of intracellular cyclic ADP-ribose, tetanic action potentials activated propagating CICR.iIn cultured rabbit otic ganglion cells, when the extracellular Ca^<2+> was reduced to a level < 0.1 mM, a small Ca^<2+> entry produced by a high K^+ -induced depolarization caused a propagating Ca^<2+> release from mitochondria which was blocked by cyclosprin A.These two mechanisms may operate in ceurones in situ depending on the extracellular Ca^<2+> levels that would be altered by activities of neighboring neurones.

采用光电倍增管或共聚焦激光扫描显微镜的fura-2或indo-1荧光记录技术和孔细胞膜片钳技术，研究了培养的牛蛙交感神经细胞和兔耳神经节细胞内Ca^<2+>释放的机制及其生理功能。牛蛙交感神经细胞中Ca^<2+>敏感的Ca^<2+>诱导的Ca^<2+>释放（CICR）是由去极化电压脉冲（> 100 ms）产生的Ca^<2+>内流在整个细胞质中电压依赖性激活的，但仅在膜下区域由动作电位（> 10 Hz， 100脉冲）引起的Ca^<2+>内流激活。在胞内环adp核糖的作用下，破伤风动作电位激活了增殖的CICR。在培养的兔神经节细胞中，当细胞外Ca^<2+>降低到< 0.1 mM时，由高K^+诱导的去极化产生的小Ca^<2+>进入引起线粒体内Ca^<2+>的增殖释放，并被环sprin a阻断。这两种机制可能在神经元中起作用，这取决于细胞外Ca^<2+>的水平，而细胞外Ca^<2+>的水平会被邻近神经元的活动改变。

项目成果

Hua Shao-Ying: "Excitation-induced Ca^<2+> dynamics in sympathetic neurons measured with conventional epifluorescence and confocal UV laser-scanning microscopes." Jpn. J.Physiol.43 suppl. 1. S513-S160 (1993)

Hua Shao-Ying：“用传统落射荧光和共焦紫外激光扫描显微镜测量交感神经元中兴奋诱导的 Ca^2 动态。”

Kitakoga Osamu: "Bradykinin-induced ion currents in cultured rat trigeminal ganglion cells" Neuroscience Research. 16. 79-93 (1993)

Kitakoga Osamu：“培养的大鼠三叉神经节细胞中缓激肽诱导的离子电流”神经科学研究。

Hua Shao-Ying: "Characteristics of Ca^<2+> release induced by Ca^<2+> influx in cultured bullfrog sympathetic neurones." J.Physiology(Lond.). 464. 245-272 (1993)

华少英：“培养牛蛙交感神经元Ca^2流入诱导Ca^2释放的特征”。

能見光雄: "最新医学からのアプローチ(7)イオンチャネル・2 細胞機能への関与とその異常" メジカルビュー社, 198 (1993)

Mitsuo Nomi：“最新医学的方法（7）离子通道2参与细胞功能及其异常”Medical View Publishing，198（1993）

Mitsuo Nohmi: "Basal Ca^<2+> and the oscillation of Ca^<2+> in caffeine-treated bullfrog sympathetic neurones." Journal of Physiology (London). 450. 513-528 (1992)

Mitsuo Nohmi：“咖啡因处理的牛蛙交感神经元中的基础 Ca^<2> 和 Ca^<2> 振荡。”