Lee Ji Eun, Kwak Jiyeon, Suh Chang Kook, Shin Jung Hoon
Department of Physiology and Biophysics, Inha University College of Medicine, 253 Yonghyun-dong, Nam-gu, Incheon 402-751, Korea.
J Biochem Mol Biol. 2006 Jan 31;39(1):91-6. doi: 10.5483/bmbrep.2006.39.1.091.
Previously, we have shown that nitric oxide (NO) directly activates the Maxi-K channels. In the present study, we have investigated whether NO has prolonged effects on the Maxi-K channels reconstituted in lipid bilayer. Application of S-nitroso-N-acetyl-D, L-penicillamine (SNAP), a NO donor, induced an immediate increase of open probability (Po) of Maxi-K channel in a dose-dependent manner. When SNAP was removed from the cytosolic solution, the Po did not simply returned to, but irreversibly decreased to a level lower than that of the control Po. At 0.2 mM, (Z)-[N-(3-Ammoniopropyl)-N-(n-propyl)amino] diazen-1-ium-1,2-diolate (PAPA-NO), another NO donor, produced a similar increase of Po and decrease of Po upon washout. The increasing effects of SNAP on Po were not blocked by either 50 U/ml superoxide dismutase (SOD) or 2 mM Nethylmaleimide (NEM) pre-treatments. However, NEM appears to be ineffective when applied after SNAP. These results suggest that NO can modulate Maxi-K channel via direct interaction and chemical modification, such as Snitrosylation in the brain.
此前，我们已经表明一氧化氮（NO）可直接激活大电导钙激活钾通道（Maxi-K通道）。在本研究中，我们研究了NO对脂质双分子层中重组的Maxi-K通道是否具有延长效应。应用NO供体S-亚硝基-N-乙酰-D，L-青霉胺（SNAP），可使Maxi-K通道的开放概率（Po）立即呈剂量依赖性增加。当从胞质溶液中去除SNAP时，Po并非简单地恢复到原来水平，而是不可逆地降低到低于对照Po的水平。在0.2 mM时，另一种NO供体（Z）-[N-（3-氨丙基）-N-（正丙基）氨基]重氮-1,2-二醇盐（PAPA-NO）也产生了类似的Po增加以及洗脱后Po降低的现象。SNAP对Po的增加作用不受50 U/ml超氧化物歧化酶（SOD）或2 mM N-乙基马来酰亚胺（NEM）预处理的阻断。然而，在SNAP之后应用NEM似乎无效。这些结果表明，在大脑中，NO可通过直接相互作用和化学修饰（如亚硝基化）来调节Maxi-K通道。
