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分化中的大鼠嗜铬细胞瘤细胞胞质钙对钙通道和细胞内钙库的依赖性

Dependence of cytosolic calcium in differentiating rat pheochromocytoma cells on calcium channels and intracellular stores.

作者信息

Reber B F, Reuter H

机构信息

Department of Pharmacology, University of Bern, Switzerland.

出版信息

J Physiol. 1991 Apr;435:145-62. doi: 10.1113/jphysiol.1991.sp018502.

Abstract
  1. The rat clonal pheochromocytoma cell line (PC12) was used to study changes in the free intracellular Ca2+ concentration [( Ca2+]i) that are related to the distribution of L-type (dihydropyridine-sensitive) and N-type (omega-conotoxin-sensitive) calcium channels during nerve growth factor (NGF)-induced outgrowth of neurites. Changes in [Ca2+]i during K+ depolarization were recorded by means of Fura-2 single-cell microfluorimetry. 2. The basal [Ca2+]i of cells at rest was not altered by long-term treatment with NGF, neither in the cell bodies nor in the growth cones. K+ depolarization of the cells caused a rise in [Ca2+]i. 3. The dihydropyridine (DHP) nifedipine alone, or together with omega-conotoxin (omega-CgTX), were similarly effective in inhibiting the K(+)-induced increase in [Ca2+]i in untreated and NGF-treated cell bodies, arguing for a preferential distribution of L-type Ca2+ channels in this cell area. By contrast, after 6-7 days exposure to NGF the K(+)-induced initial transient rise of [Ca2+]i in growth cones was very sensitive to omega-CgTX, whereas nifedipine affected only the sustained rise. 4. PC12 cells also contain caffeine- and inositol trisphosphate (IP3)-sensitive intracellular Ca2+ stores. Addition of 30 mM-caffeine caused a fast transient rise in [Ca2+]i. The extent of filling of the caffeine-sensitive pool affected basal [Ca2+]i. These Ca2+ storage sites were empty under normal culture conditions. However, a single K+ depolarization caused filling of the stores, followed by spontaneous depletion (50% in about 5 min) after wash-out of high [K+]o. When the caffeine-sensitive stores were empty, the rise in [Ca2+]i was attenuated during submaximal depolarization. Caffeine-sensitive Ca2+ stores were also present in some growth cones, though with much smaller capacities than in cell bodies. 5. Mobilization of Ca2+ from the IP3-sensitive store, by bradykinin exposure, was found to be independent of the caffeine-sensitive pool. There was no apparent 'cross-talk' between both Ca2+ pools. 6. We conclude that changes in [Ca2+]i in cell bodies depend on both membrane Ca2+ channels and intracellular Ca2+ stores. During NGF-induced differentiation there is a predominance of N-type Ca2+ channels in growth cones, while Ca2+ stores are of minor importance in these structures.
摘要
  1. 采用大鼠克隆嗜铬细胞瘤细胞系(PC12)来研究在神经生长因子(NGF)诱导神经突生长过程中,与L型(二氢吡啶敏感型)和N型(ω-芋螺毒素敏感型)钙通道分布相关的细胞内游离钙离子浓度[Ca2+]i的变化。通过Fura-2单细胞显微荧光测定法记录K+去极化过程中[Ca2+]i的变化。2. 长期用NGF处理,无论是细胞体还是生长锥,静止细胞的基础[Ca2+]i均未改变。细胞的K+去极化导致[Ca2+]i升高。3. 二氢吡啶(DHP)硝苯地平单独使用或与ω-芋螺毒素(ω-CgTX)联合使用,在未处理和NGF处理的细胞体中,对抑制K+诱导的[Ca2+]i升高同样有效,这表明L型钙通道在该细胞区域优先分布。相比之下,在暴露于NGF 6 - 7天后,生长锥中K+诱导的[Ca2+]i初始瞬时升高对ω-CgTX非常敏感,而硝苯地平仅影响持续升高。4. PC12细胞还含有对咖啡因和肌醇三磷酸(IP3)敏感的细胞内钙储存库。添加30 mM咖啡因会导致[Ca2+]i快速瞬时升高。咖啡因敏感池的充盈程度影响基础[Ca2+]i。在正常培养条件下,这些钙储存位点是空的。然而,单次K+去极化会导致储存库充盈,在洗去高浓度[K+]o后,随后会自发耗竭(约5分钟内耗竭50%)。当咖啡因敏感储存库为空时,在次最大去极化过程中[Ca2+]i的升高会减弱。咖啡因敏感的钙储存库在一些生长锥中也存在,但其容量比细胞体中的小得多。5. 通过暴露于缓激肽从IP3敏感储存库中动员Ca2+,发现与咖啡因敏感池无关。两个钙池之间没有明显的“串扰”。6. 我们得出结论,细胞体中[Ca2+]i的变化取决于膜钙通道和细胞内钙储存库。在NGF诱导的分化过程中,生长锥中N型钙通道占主导,而钙储存在这些结构中不太重要。

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