CRITICAL INTRACELLULAR CA2+ CONCENTRATION FOR ALL-OR-NONE CA2+ SPIKING IN SINGLE SMOOTH-MUSCLE CELLS
CRITICAL INTRACELLULAR CA2+ CONCENTRATION FOR ALL-OR-NONE CA2+ SPIKING IN SINGLE SMOOTH-MUSCLE CELLS
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DOI：
10.1002/j.1460-2075.1993.tb06224.x
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发表时间：
1993-12-15
期刊：
影响因子：
11.4
通讯作者：
KASAI, H
中科院分区：
文献类型：
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作者：
LINO, M;YAMAZAWA, T;KASAI, H
神经递质最初通过肌醇1，4，5-三磷酸(InsP3)受体从细胞内钙库中动员钙离子，诱导平滑肌细胞收缩。在这里，我们研究了单个平滑肌细胞中参与钙动员的分子的作用。激动剂刺激的平滑肌细胞胞浆内钙离子([Ca~(2+)]_i)缓慢升高后，随着局部[Ca~(2+)]_i达到约160 nM的临界浓度，又出现了一波快速的再生钙释放波。在再生的钙释放过程中，既不需要磷脂酶C的反馈调节，也不需要咖啡因敏感的钙离子诱导的钙释放。这些结果表明，InsP3诱导的钙释放依赖于钙离子的反馈控制在再生钙释放的产生中起主导作用。由此导致的整个细胞内的钙释放是一个要么全有要么全无的事件，即当激动剂浓度高于阈值时，[Ca~(2+)]i达到恒定峰值。这一发现表明，一种可能的数字模式参与了对平滑肌收缩的神经控制。
Neurotransmitters induce contractions of smooth muscle cells initially by mobilizing Ca2+ from intracellular Ca2+ stores through inositol 1,4,5-trisphosphate (InsP3) receptors. Here we studied roles of the molecules involved in Ca2+ mobilization in single smooth muscle cells. A slow rise in cytoplasmic Ca2+ ([Ca2+]i) in agonist-stimulated smooth muscle cells was followed by a wave of rapid regenerative Ca2+ release as the local [Ca2+]i reached a critical concentration of approximately 160 nM. Neither feedback regulation of phospholipase C nor caffeine-sensitive Ca2+-induced Ca2+ release was found to be required in the regenerative Ca2+ release. These results indicate that Ca2+-dependent feedback control of InsP3-induced Ca2+ release plays a dominant role in the generation of the regenerative Ca2+ release. The resulting Ca2+ release in a whole cell was an all-or-none event, i.e. constant peak [Ca2+]i was attained with agonist concentrations above the threshold value. This finding suggests a possible digital mode involved in the neural control of smooth muscle contraction.