Keirstead S A, Miller R F
Department of Physiology, University of Minnesota, Minneapolis 55455, USA.
Glia. 1995 May;14(1):14-22. doi: 10.1002/glia.440140104.
Calcium imaging techniques were used to study intracellular free calcium ion regulation in isolated Müller cells in response to changes in extracellular potassium concentration and to caffeine and ryanodine. Müller 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 Müller 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 Müller cell and moves toward the endfoot. A similar calcium wave can be evoked in Müller 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 Müller 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.
采用钙成像技术研究了分离的Müller细胞中细胞内游离钙离子的调节情况，以响应细胞外钾离子浓度、咖啡因和ryanodine的变化。从成年虎螈（Ambystoma tigrinum）视网膜中分离出Müller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，细胞外钾离子升高会引起Müller细胞整个长度内细胞内钙（[Ca2+]i）的增加。相反，在没有细胞外钙的情况下，细胞外钾离子升高会引发[Ca2+]i的长时间延迟、波浪状增加，该增加始于Müller细胞的顶端区域并向终足移动。当Müller细胞暴露于咖啡因或ryanodine时，也会引发类似的钙波，这两种物质会导致许多细胞类型从细胞内储存中释放钙。这些数据表明，[Ca2+]i可能通过细胞外途径以及对ryanodine敏感的细胞内释放机制在Müller细胞中发生改变。[Ca2+]i这些变化的功能后果仍有待阐明。
