Onozuka M, Furuichi H, Imai S, Fukami Y
Department of Anatomy, Gifu University School of Medicine, Japan.
Neurosci Lett. 1991 Mar 11;124(1):35-8. doi: 10.1016/0304-3940(91)90816-c.
The effect of Ca2+/calmodulin-dependent protein phosphorylation on K+ channels was examined in snail neurons, using several pharmacological agents, the voltage clamp method and the pressure injection technique. H-7, a general protein kinase inhibitor, reduced the delayed outward K+ current (IKD) which was suppressed by tetraethylammonium. Ca2+/calmodulin-dependent protein kinase II, when injected into neurons which had been treated with H-7, transiently restored the reduced IKD nearly to the pre-H-7 level. However, this restoration was blocked by W-7, a calmodulin inhibitor. In contrast, the catalytic subunit of cAMP-dependent protein kinase or protein kinase C injected into the H-7-treated neurons had little effect on the current. These findings suggest that Ca2+/calmodulin-dependent protein phosphorylation is involved in the opening process of K+ channels.
利用几种药理学试剂、电压钳法和压力注射技术，在蜗牛神经元中研究了Ca2+/钙调蛋白依赖性蛋白磷酸化对钾通道的影响。H-7是一种通用的蛋白激酶抑制剂，它降低了被四乙铵抑制的延迟外向钾电流（IKD）。当将Ca2+/钙调蛋白依赖性蛋白激酶II注入经H-7处理的神经元时，可使降低的IKD短暂恢复至接近H-7处理前的水平。然而，这种恢复被钙调蛋白抑制剂W-7阻断。相反，将cAMP依赖性蛋白激酶或蛋白激酶C的催化亚基注入经H-7处理的神经元对电流影响很小。这些发现表明，Ca2+/钙调蛋白依赖性蛋白磷酸化参与钾通道的开放过程。
