Onozuka M, Watanabe K, Nagata K, Imai S
Department of Anatomy (2nd Division), Gifu University School of Medicine, Japan.
Brain Res. 1994 Jul 11;650(2):336-40. doi: 10.1016/0006-8993(94)91802-3.
The inhibitory action of a glutamate agonist, quisqualate, in association with the intracellular signal transduction, was electrophysiologically examined in identified Euhadra neurons. Quisqualate dose-dependently induced a slow outward current (Quis current) which was blocked by tetraethylammonium. This current was suppressed by intracellular injection of Ca2+/calmodulin-dependent protein kinase II (CaMKII), and was enhanced by a CaMKII inhibitor, KN-62. However, no significant changes in the Quis current were observed when the catalytic subunit of protein kinase A (PKA) or the protein kinase C (PKC) fragment (530-558) was intracellularly applied; or using a PKA inhibitor, H-8, or a PKC inhibitor, staurosporine. These results suggest a novel mechanism linked to CaMKII, by which quisqualate induces an outward potassium current.
在已鉴定的日本欧哈德拉蜗牛神经元中，对谷氨酸激动剂quisqualate与细胞内信号转导相关的抑制作用进行了电生理学研究。quisqualate剂量依赖性地诱导出一种缓慢外向电流（quis电流），该电流可被四乙铵阻断。该电流被细胞内注射钙/钙调蛋白依赖性蛋白激酶II（CaMKII）所抑制，并被CaMKII抑制剂KN-62增强。然而，当细胞内应用蛋白激酶A（PKA）的催化亚基或蛋白激酶C（PKC）片段（530-558）时；或使用PKA抑制剂H-8或PKC抑制剂星形孢菌素时，quis电流未观察到显著变化。这些结果提示了一种与CaMKII相关的新机制，通过该机制quisqualate诱导外向钾电流。
