SPONTANEOUS CHANGES IN INTRACELLULAR CALCIUM-CONCENTRATION IN TYPE-I ASTROCYTES FROM RAT CEREBRAL-CORTEX IN PRIMARY CULTURE
SPONTANEOUS CHANGES IN INTRACELLULAR CALCIUM-CONCENTRATION IN TYPE-I ASTROCYTES FROM RAT CEREBRAL-CORTEX IN PRIMARY CULTURE
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DOI：
10.1002/glia.440050203
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发表时间：
1992-01-01
期刊：
影响因子：
6.2
通讯作者：
RUSSELL, JT
中科院分区：
文献类型：
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作者：
FATATIS, A;RUSSELL, JT
大鼠大脑皮层I型星形胶质细胞fura-2荧光测定显示，细胞内钙离子浓度发生了非常大的自发变化。这些尖峰状的变化范围从静止钙水平的50-250 nM到高达1-2 μ m。发现尖峰在频率和幅度上是不规则的，在融合培养中经常是同步的。同步事件表现为传播波，在许多细胞中传播。当细胞外钙浓度降低到低于微摩尔水平时，自发峰持续存在，这表明[Ca2+]i增加的来源是细胞内。河豚毒素处理星形胶质细胞并没有消除自发变化，尼莫地平和D-600也没有阻断电压依赖性钙通道。肌浆网钙诱导的钙释放通道阻滞剂Ryanodine也没有效果。这些[Ca2+]i的变化在性质上不同于激动剂诱导的振荡和去极化诱导的细胞内钙浓度的增加。使用25-100 mM [K+]o去极化导致细胞内钙浓度迅速上升，恢复到接近静息水平，这种反应对细胞外钙和电压门控制钙通道拮抗剂的去除很敏感。l -谷氨酸（0.5-100 mu- m）引起与某些细胞离散周期振荡相关的[Ca2+]i的大量增加。自发尖峰的细胞触发机制目前尚不清楚。我们得出结论，星形胶质细胞中[Ca2+]i的自发变化不同于激动剂诱导的和膜电位去极化诱导的变化。
Measurement of fura-2 fluorescence in type I astrocytes from rat cerebral cortex showed that the intracellular calcium ion concentration undergoes very large spontaneous changes. These spike-like changes ranged from resting levels of calcium of 50-250 nM to as high as 1-2-mu-M. The spikes were found to be irregular in frequency and amplitude and were frequently synchronous in confluent cultures. The synchronous events appeared as propagating waves that spread over many cells. The spontaneous spikes persisted when the extracellular calcium concentration was reduced to below micromolar levels suggesting that the source for the increases in [Ca2+]i was intracellular. Treatment of the astrocytes with tetrodotoxin did not abolish the spontaneous changes, nor did blockade of voltage-dependent calcium channels with nimodipine and D-600. Ryanodine, a blocker of the sarcoplasmic reticulum calcium-induced calcium release channel, was also without effect. These changes in [Ca2+]i were different in character from both agonist-induced oscillations and depolarization-induced increases in intracellular calcium concentration. Depolarization using 25-100 mM [K+]o resulted in a prompt rise in intracellular calcium concentration, which returned to near resting levels, and this response was sensitive to removal of extracellular calcium and voltage-gated calcium channel antagonists. L-glutamate (0.5-100-mu-M) caused large increases in [Ca2+]i that were associated with discrete periodic oscillations in some cells. The cellular trigger for the spontaneous spikes is currently not understood. We conclude that spontaneous changes in [Ca2+]i in astrocytes are distinct from agonist-induced and membrane potential depolarization-induced changes.