CALCIUM WAVES IN DISSOCIATED RETINAL GLIAL (MULLER) CELLS ARE EVOKED BY RELEASE OF CALCIUM FROM INTRACELLULAR STORES
CALCIUM WAVES IN DISSOCIATED RETINAL GLIAL (MULLER) CELLS ARE EVOKED BY RELEASE OF CALCIUM FROM INTRACELLULAR STORES
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DOI：
10.1002/glia.440140104
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发表时间：
1995-05-01
期刊：
影响因子：
6.2
通讯作者：
MILLER, RF
中科院分区：
文献类型：
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作者：
KEIRSTEAD, SA;MILLER, RF
使用钙成像技术来研究分离的 Muller 细胞中细胞内游离钙离子对细胞外钾浓度以及咖啡因和兰尼丁的变化的反应。从成年虎蝾螈 (Ambystoma tigrinum) 视网膜中分离出 Muller 细胞，并使用钙指示剂 Fura-2 和视频成像显微镜技术进行研究。我们的结果表明，在细胞外钙存在的情况下，细胞外钾的升高会引起整个 Muller 细胞长度内细胞内钙 ([Ca2+](i)) 的增加。相反，在缺乏细胞外钙的情况下，细胞外钾的升高可以触发 [Ca2+](i) 的长潜伏期、波状增加，该增加从 Muller 细胞的顶端区域开始并向足底移动。当米勒细胞接触咖啡因或兰尼定时，会在米勒细胞中引起类似的钙波，这些物质会导致许多细胞类型的细胞内储存释放钙。这些数据表明，Muller 细胞中的 [Ca2+](i) 可能通过细胞外途径以及兰尼碱敏感的细胞内释放机制发生改变。 [Ca2+](i) 的这些变化的功能后果仍有待阐明。 (C) 1995 Wiley-Liss, Inc.
Calcium imaging techniques were used to study intracellular free calcium ion regulation in isolated Muller cells in response to changes in extracellular potassium concentration and to caffeine and ryanodine. Muller cells were dissociated from the adult tiger salamander (Ambystoma tigrinum) retina and studied using the calcium indicator Fura-2 and video imaging microscopy techniques. Our results demonstrate that elevation of extracellular potassium in the presence of extracellular calcium evokes an increase in intracellular calcium ([Ca2+](i)) throughout the length of the Muller cell. In contrast, in the absence of extracellular calcium, elevation of extracellular potassium can trigger a long latency, wave-like increase in [Ca2+](i) that begins in the apical region of the Muller cell and moves toward the endfoot. A similar calcium wave can be evoked in Muller cells when they are exposed to caffeine or ryanodine, agents that cause release of calcium from intracellular stores in many cell types. These data suggest that [Ca2+](i) may be altered in Muller cells through an extracellular pathway as well as through a ryanodine-sensitive intracellular release mechanism. The functional consequences of these changes in [Ca2+](i) remain to be elucidated. (C) 1995 Wiley-Liss, Inc.