CHOLECYSTOKININ INDUCES A DECREASE IN CA-2+ CURRENT IN SNAIL NEURONS THAT APPEARS TO BE MEDIATED BY PROTEIN-KINASE-C
CHOLECYSTOKININ INDUCES A DECREASE IN CA-2+ CURRENT IN SNAIL NEURONS THAT APPEARS TO BE MEDIATED BY PROTEIN-KINASE-C
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DOI：
10.1038/325809a0
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发表时间：
1987-02-26
期刊：
影响因子：
64.8
通讯作者：
GERSCHENFELD, HM
中科院分区：
文献类型：
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作者：
HAMMOND, C;PAUPARDINTRITSCH, D;GERSCHENFELD, HM
三种不同类型的蛋白激酶已被证明可以调节可兴奋组织中的Ca 2+电流。环腺苷酸依赖性蛋白激酶介导去甲肾上腺素对心肌细胞Ca 2+电流的作用1，2。环GMP-依赖性蛋白激酶介导确定的蜗牛神经元中的降钙素诱导的Ca 2+电流调制3。还发现Ca 2 +/二酰基甘油依赖性蛋白激酶（蛋白激酶C）调节神经元的Ca 2+电流4，5。然而，尚未发现神经递质通过激活蛋白激酶C来调节Ca ~（2+）电流。我们现在报道胆囊收缩素，一种广泛存在于软体动物神经元中的神经肽6，7，8，调节已鉴定的蜗牛神经元9中的Ca 2+电流，这种作用似乎是由蛋白激酶C介导的。具体而言，硫酸胆囊收缩素八肽26-33（CCK 8），蛋白激酶C的激活剂，和蛋白激酶C的细胞内注射，都缩短了钙依赖性动作电位，并降低了这些细胞中的钙电流的幅度。所有这些效应在实验期间都是不可逆的。此外，细胞内注射低浓度的蛋白激酶C，这是无效的本身，提高了有效性的低浓度的CCK 8的Ca 2+电流。
Three distinct classes of protein kinases have been shown to regulate Ca2+current in excitable tissues. Cyclic AMP-dependent protein kinase mediates the action of noradrenaline on the Ca2+current of cardiac muscle cells1,2. Cyclic GMP-dependent protein kinase mediates the serotonin-induced modulation of the Ca2+current in identified snail neurons3. The Ca2+/diacylglycerol-dependent protein kinase (protein kinase C) has also been found to regulate Ca2+currents of neurons4,5. However, no neurotrans-mitter has yet been shown to regulate Ca2+current through the activation of protein kinase C. We now report that cholecystokinin, a widely occurring neuropeptide6which is present in molluscan neurons7,8, modulates the Ca2+current in identified neurons9of the snailHelix aspersa, and that this effect appears to be mediated by protein kinase C. Specifically, sulphated cholecystokinin octapeptide 26–33 (CCK8), activators of protein kinase C, and intracellular injection of protein kinase C, all shorten the Ca2+-dependent action potential and decrease the amplitude of the Ca2+current in these cells. All these effects are not reversible within the duration of the experiments. Moreover, intracellular injections of low concentrations of protein kinase C, which are ineffective by themselves, enhance the effectiveness of low concentrations of CCK8 on the Ca2+current.