Role for diacylglycerol in mediating the actions of ACh on M-current in gastric smooth muscle cells.
Role for diacylglycerol in mediating the actions of ACh on M-current in gastric smooth muscle cells.
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二酰基甘油在介导 ACh 对胃平滑肌细胞 M 电流作用中的作用。
DOI：
10.1152/ajpcell.1992.263.6.c1274
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发表时间：
1992
期刊：
影响因子：
--
通讯作者：
WalshJr,JV
中科院分区：
文献类型：
--
作者：
Clapp,LH;Sims,SM;Singer,JJ;WalshJr,JV
第二信使二酰基甘油（DAG）在介导毒蕈碱抑制m电流（一种由乙酰胆碱（ACh）抑制的电压门控K+电流）中的作用，在新鲜分离的蟾蜍胃平滑肌细胞中进行了研究。电流记录使用单电极电压钳采用传统的微电极。细胞外应用1,2-二辛烷酰- cn -甘油（DiC8），一种合成DAG，是蛋白激酶C （PKC）的有效激活剂，可逆地抑制m电流。代表m电流下K+通道的电压依赖性闭合的电流松弛也被DiC8减少，尽管抑制并不总是像ACh那样完全。相比之下，另一种DAG类似物，1,2-二辛烷酰-3-硫甘油酯，其结构与DiC8密切相关，但不激活PKC，未能抑制m电流。此外，β激动剂异丙肾上腺素诱导的m电流，其机制显然是由腺苷3',5'-环磷酸腺苷介导的（S. M. Sims， L. H. Clapp， J. V. Walsh, Jr.和J. J. Singer）。植物生理学报，17(1):291,1990)。ACh和DiC8均抑制内源性和异丙肾上腺素诱导的m电流，而不改变m电流失活的时间过程，这表明这些药物通过减少可打开的通道数量起作用。这些结果证明了毒蕈碱对m电流的调节是由DAG介导的。
The role of the second messenger diacylglycerol (DAG) in mediating muscarinic suppression of M-current, a type of a voltage-gated K+ current that is suppressed by acetylcholine (ACh), was examined in freshly isolated smooth muscle cells from toad stomach. Currents were recorded using a single electrode voltage clamp employing conventional microelectrodes. Extracellular application of 1,2-dioctanoyl-sn-glycerol (DiC8), a synthetic DAG that is a potent activator of protein kinase C (PKC), reversibly suppressed M-current. Current relaxations, representing the voltage-dependent closure of K+ channels underlying M-current, were also decreased by DiC8, although suppression was not always as complete as it was with ACh. In contrast, another DAG analogue, 1,2-dioctanoyl-3-thioglycerol, which has a structure closely related to DiC8 but does not activate PKC, failed to inhibit M-current. Furthermore, M-current induced by the beta-agonist isoproterenol, by a mechanism apparently mediated by adenosine 3',5'-cyclic monophosphate (S. M. Sims, L. H. Clapp, J. V. Walsh, Jr., and J. J. Singer. Pflugers Arch. 417: 291, 1990), was also suppressed by DiC8. Both ACh and DiC8 were found to suppress endogenous and isoproterenol-induced M-current without altering the time course of M-current deactivation, suggesting that these agents act by decreasing the number of channels available to be opened. These results provide evidence that muscarinic regulation of M-current is mediated by DAG.
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DOI：
10.1093/infdis/153.5.848
发表时间：
1986
期刊：
The Journal of infectious diseases
影响因子：
--
作者：
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