Heterologous Desensitization of Opioid-stimulated Ca2+ Increase by Bradykinin or ATP in NG108-15 Cells (*)
Heterologous Desensitization of Opioid-stimulated Ca2+ Increase by Bradykinin or ATP in NG108-15 Cells (*)
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NG108-15 细胞中缓激肽或 ATP 对阿片类药物刺激的 Ca2+ 增加的异源脱敏作用 (*)
DOI：
10.1074/jbc.270.28.16630
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发表时间：
1995
期刊：
影响因子：
--
通讯作者：
T. Liu
中科院分区：
文献类型：
--
作者：
S. Chueh;S. Song;T. Liu
亮氨酸-脑啡肽（Leucine-enkephalin, Leu-EK）通过磷酸肌苷级联引起NG108-15细胞胞浆内Ca2+浓度（[Ca2+]i）的增加，EC50为1.2 μM。慢性用[D-Ala2，D-Leu5]脑啡肽处理细胞引起时间依赖性同源脱敏。与Leu-EK相比，在细胞外Ca2+、ATP和缓激肽的存在下，肌醇1,4,5-三磷酸（IP3）的生成显著增加；然而，在ATP刺激后，细胞内Ca2+池的大小增加，而缓激肽使细胞内池减少。因此，如果首先加入缓激肽诱导[Ca2+]i增加，细胞失去了对Leu-EK的[Ca2+]i反应，而如果在加入ATP后加入Leu-EK，反应不变。当Leu-EK与缓激肽或ATP同时加入时，IP3产生有加性反应；然而，[Ca2+]i的上升达到与缓激素或ATP单独诱导的水平相同。在缺乏细胞外Ca2+的情况下，细胞内池的补充是不可能的，ATP对leu - ek诱导的[Ca2+]i增加表现出类似于缓激肽的抑制作用。先前用Leu-EK处理的细胞有轻微的异源性脱敏，但对ATP的反应没有影响。我们的研究结果表明，共享的细胞内Ca2+池对阿片样物质、缓激肽和p2 -嘌呤受体激动剂敏感；然而，一种确定的4,5-二磷酸磷脂酰肌醇池或一种特定的磷脂酶C负责每种受体。
Leucine-enkephalin (Leu-EK) dose-dependently elicited an increase in cytosolic Ca2+ concentration ([Ca2+]i) with an EC50 of 1.2 μM via the phosphoinositide cascade in NG108-15 cells. Chronic treatment of cells with [D-Ala2,D-Leu5]enkephalin caused time-dependent homologous desensitization. In the presence of extracellular Ca2+, ATP as well as bradykinin stimulated significantly higher increases in inositol 1,4,5-trisphosphate (IP3) generation than did Leu-EK; however, the magnitude of intracellular Ca2+ pools increased after ATP stimulation, whereas bradykinin depleted intracellular pools. Hence, cells lost their [Ca2+]i response to Leu-EK if bradykinin was first added to induce a [Ca2+]i increase, whereas the response was unchanged if Leu-EK was added after addition of ATP. When Leu-EK was added simultaneously with bradykinin or ATP, an additive response was observed in IP3 generation; however, the rise in [Ca2+]i reached the same level as that induced by bradykinin or ATP alone. In the absence of extracellular Ca2+ in which the replenishment of intracellular pools was not possible, ATP displayed an inhibitory effect similar to that of bradykinin on the Leu-EK-induced [Ca2+]i increase. Prior treatment of cells with Leu-EK slightly heterologously desensitized the action of bradykinin, but had no effect on the ATP response. Our results suggest that a shared intracellular Ca2+ pool is sensitive to the opioid, bradykinin and P2-purinoceptor agonists; however, a defined pool of phosphatidylinositol 4,5-bisphosphate or a specific phospholipase C is responsible for each receptor.
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神经母细胞瘤-神经胶质瘤杂交 NG108-15 细胞中脑啡肽和生长抑素阻断钙通道。
DOI：
10.1073/pnas.83.24.9832
发表时间：
1986
影响因子：
11.1
作者：
Tsunoo,A;Yoshii,M;Narahashi,T
通讯作者：
Narahashi,T
影响因子：
3.6
作者：
P. Law;D. Hom;H. Loh
通讯作者：
P. Law;D. Hom;H. Loh
慢性D-Ala、2D-Leu5-脑啡肽或百日咳毒素治疗对神经母细胞瘤x神经胶质瘤NG108-15杂交细胞中δ阿片受体高亲和力状态的影响。
DOI：
--
发表时间：
1991
期刊：
The Journal of pharmacology and experimental therapeutics
影响因子：
--
作者：
Law,PY;Hom,DS;Loh,HH
通讯作者：
Loh,HH
分化的 NG108-15 细胞上血管紧张素受体的共价交联分析。
DOI：
10.1016/0006-291x(90)90505-h
发表时间：
1990
影响因子：
3.1
作者：
Carrithers,MD;Koide,KA;Raman,VK;Masuda,S;Weyhenmeyer,JA
通讯作者：
Weyhenmeyer,JA
δ-阿片受体与多种 G 蛋白的相互作用：抑制腺苷酸环化酶和激活 G 蛋白的激动剂效力之间不存在关系。
影响因子：
3.6
作者：
Prather,PL;Loh,HH;Law,PY
通讯作者：
Law,PY