CHOLECYSTOKININ INCREASES INTRACELLULAR CA2+ CONCENTRATION IN CULTURED STRIATAL NEURONS
CHOLECYSTOKININ INCREASES INTRACELLULAR CA2+ CONCENTRATION IN CULTURED STRIATAL NEURONS
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DOI：
10.1016/0143-4179(91)90102-o
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发表时间：
1991-03-01
期刊：
影响因子：
2.9
通讯作者：
NOMOTO, T
中科院分区：
文献类型：
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作者：
MIYOSHI, R;KITO, S;NOMOTO, T
尽管已证实胰腺CCK受体与磷脂酰肌醇的代谢有关，但CCK受体激活后在中枢神经系统中发生的事件尚未引起太多关注。本文用Fura-2荧光分光光度法检测了CCK多肽对单个培养的大鼠纹状体神经元细胞内钙离子浓度([Ca~(2+)]i)的影响。CCK多肽呈剂量依赖性单相升高[Ca~(2+)]i。CCK多肽升高[Ca~(2+)]_i的效价顺序为：雨蛙素>；CCK-8>；CCK-8>；CCK-4。在钙离子耗竭的介质中，雨蛙素的作用被完全阻断。此外，欧米茄-芋螺毒素GVIA可完全抑制雨蛙素的作用，而硝苯地平和维拉帕米均不影响其作用。我们的结果表明，在培养的大鼠纹状体神经元中，CCK受体偶联于N型电压敏感的钙通道。
Although it has been established that pancreatic cholecystokinin (CCK) receptors are coupled to phosphatidylinositol turnover, the events which follow activation of CCK receptors in the central nervous system have not received much attention. In this paper, changes in intracellular Ca2+ concentration ([Ca2+]i) in response to CCK peptides were measured in single cultured rat striatal neuron by fura-2 fluorometry. CCK peptides dosedependently increased [Ca2+]i in a monophasic manner. The order of the potencies of CCK peptides to increase [Ca2+]i was as follows: caerulein > CCK-8 > CCK-8 > CCK-4. The effect of caerulein was completely blocked in a Ca2+ -depleted medium. In addition, omega-conotoxin GVIA completely inhibited the effect of caerulein, while neither nifedipine nor verapamil affected it. Our results indicate that CCK receptors couple to N-type voltage-sensitive Ca2+ channels in cultured rat striatal neurons.