Shin J H, Chung S, Park E J, Uhm D Y, Suh C K
Department of Physiology and Biophysics, Inha University College of Medicine, Inchon, South Korea.
FEBS Lett. 1997 Oct 6;415(3):299-302. doi: 10.1016/s0014-5793(97)01144-7.
Using the planar lipid bilayer technique, we tested whether NO directly activates calcium-activated potassium (Maxi-K) channels isolated from rat brain. We used streptozotocin (STZ) as NO donor, and the NO release was controlled with light. In the presence of 100-800 microM STZ, the Maxi-K channel activity increased up to 3-fold within several tens of seconds after the light was on, and reversed to the control level several minutes after shutting off the light. Similar activation was observed with other NO donors such as S-nitroso-N-acetylpenicillamine and sodium nitroprusside. The degree of activity increase was dependent upon the initial open probability (P[init]). When the P(init) was lower, the activity increase was greater. These results demonstrate that NO can directly affect the Maxi-K channel activity, and suggest that the Maxi-K channel might be one of the physiological targets of NO in brain.
我们运用平面脂质双层技术，测试了一氧化氮（NO）是否能直接激活从大鼠脑中分离出的钙激活钾通道（大电导钙激活钾通道，Maxi-K）。我们使用链脲佐菌素（STZ）作为NO供体，并通过光照来控制NO的释放。在存在100 - 800微摩尔STZ的情况下，光照开启后的几十秒内，Maxi-K通道活性增加高达3倍，关灯几分钟后又恢复到对照水平。使用其他NO供体如S-亚硝基-N-乙酰青霉胺和硝普钠时也观察到类似的激活现象。活性增加的程度取决于初始开放概率（P[init]）。当P(init)较低时，活性增加幅度更大。这些结果表明NO可直接影响Maxi-K通道活性，并提示Maxi-K通道可能是脑中NO的生理靶点之一。
