Release of intracellular calcium and modulation of membrane currents by caffeine in bull‐frog sympathetic neurones.
Release of intracellular calcium and modulation of membrane currents by caffeine in bull‐frog sympathetic neurones.
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牛蛙交感神经元中细胞内钙的释放和咖啡因对膜电流的调节。
DOI：
10.1113/jphysiol.1992.sp018937
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发表时间：
1992
期刊：
影响因子：
--
通讯作者：
P. Adams
中科院分区：
文献类型：
--
作者：
N. Marrion;P. Adams
1.通过Fura-2信号的图像分析，在全细胞电压钳位牛蛙交感神经元中研究了钙的释放和隔离。2.将咖啡因（10 mM）应用于电压钳制在-38 mV的细胞，导致细胞内钙浓度（[Ca 2 +]i）迅速增加至平均值352 +/-33 nM，这激活了外向电流。在咖啡因持续存在的情况下，[Ca 2 +]i的上升缓慢下降至196 +/-20 nM的持续平台（高于对照水平112 nM），而外向电流迅速衰减。钙释放峰值在细胞边缘最高。3.两种钙诱导的钙释放抑制剂ryanodine和普鲁卡因可降低咖啡因诱导的细胞内钙升高。[Ca 2 +]i的剩余不可抑制的增加可能表明咖啡因可以从两种不同的细胞内储存中释放钙。4. ryanodine对咖啡因诱发的钙释放的抑制具有浓度和“使用依赖性”，因此只有在存在ryanodine的情况下第二次应用咖啡因时才能观察到完全的抑制作用。与此相反，普鲁卡因的作用没有表现出任何“使用依赖性”，不像兰尼定是完全可逆的。5.外向电流对大电导钙激活钾电流Ic的阻断剂敏感。从这个电流的方差分析表明，它至少部分地从自发的微型外向电流的总和。6.咖啡因释放钙的幅度和持续时间依赖于细胞内钙的静息水平和咖啡因暴露时间。这与释放的药理学一起表明，咖啡因通过敏化钙诱导的钙释放来增加细胞内钙。7.细胞内应用钌红可使诱发的[Ca ~（2+）]i增加幅度增强。这种作用通过线粒体解偶联剂羰基氰化物对三氟甲氧基苯腙（FCCP）的细胞外应用而不是通过FCCP或线粒体Ca 2+摄取的其他抑制剂的内部应用来模拟。这表明，诱发的[Ca 2 +]i增加主要由钌红敏感的螯合过程缓冲，而不是线粒体。
1. Calcium release and sequestration were studied in whole‐cell voltage‐clamped bull‐frog sympathetic neurones by image analysis of Fura‐2 signals. 2. Application of caffeine (10 mM) to cells voltage clamped at ‐38 mV caused a rapid increase in intracellular calcium concentration ([Ca2+]i) to a mean value of 352 +/‐ 33 nM, which activated an outward current. In the continued presence of caffeine the rise in [Ca2+]i slowly declined to a sustained plateau of 196 +/‐ 20 nM (112 nM above control levels), while the outward current rapidly decayed. Peak calcium release was highest at the edge of the cell. 3. The caffeine‐evoked intracellular calcium increase was reduced by two inhibitors of calcium‐induced calcium release, ryanodine and procaine. The residual non‐suppressible increase in [Ca2+]i may indicate that caffeine can release calcium from two pharmacologically distinct intracellular stores. 4. Inhibition of the caffeine‐evoked release of calcium by ryanodine was both concentration and ‘use dependent’ so that the full inhibitory effect was only observed when caffeine was applied for the second time in the presence of ryanodine. In contrast, the action of procaine did not show any ‘use dependence’ and unlike ryanodine was fully reversible. 5. The outward current was sensitive to blockers of the large conductance calcium‐activated potassium current, Ic. Analysis of variance from this current indicated that it arose at least partly from summation of spontaneous miniature outward currents. 6. The magnitude and duration of calcium release by caffeine was dependent on the resting level of intracellular calcium and the caffeine exposure time. This, together with the pharmacology of the release, suggests that caffeine increases intracellular calcium by sensitizing calcium‐induced calcium release. 7. The evoked [Ca2+]i increase was enhanced in amplitude by intracellular application of Ruthenium Red. This effect was mimicked by extracellular application of the mitochondrial uncoupler carbonyl cyanide p‐trifluoromethoxyphenyl‐hydrazone (FCCP) but not by internal application of FCCP or other inhibitors of mitochondrial Ca2+ uptake. This suggests that the evoked increase in [Ca2+]i is predominantly buffered by a Ruthenium Red‐sensitive sequestration process which is not mitochondrial.
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DOI：
10.1016/0006-291x(87)91467-7
发表时间：
1987-02
影响因子：
3.1
作者：
K. Hwang;K. Saida;C. van Breemen
通讯作者：
K. Hwang;K. Saida;C. van Breemen
影响因子：
3.6
作者：
I. Pessah;R. Stambuk;J. Casida
通讯作者：
I. Pessah;R. Stambuk;J. Casida
影响因子：
--
作者：
Gunter,TE;Wingrove,DE;Banerjee,S;Gunter,KK
通讯作者：
Gunter,KK
肌浆网钙释放通道的 Ryanodine 敏感性。
影响因子：
4
作者：
Nagasaki,K;Fleischer,S
通讯作者：
Fleischer,S
壁细胞胆碱能刺激后细胞内 Ca 储存的释放和重新加载。
DOI：
10.1152/ajpcell.1988.254.4.c498
发表时间：
1988
期刊：
The American journal of physiology
影响因子：
--
作者：
Negulescu,PA;Machen,TE
通讯作者：
Machen,TE