Huang H Y, Dai S P, Xie P G, Xu Y
Shanghai Institute of Physiology, Chinese Academy of Sciences.
Zhongguo Yao Li Xue Bao. 1992 Jan;13(1):51-4.
Slices of rat hippocampus, preincubated with [3H]norepinephrine ([3H]NE), were superfused and stimulated by addition of 3,4-diaminopyridine (3,4-DAP) for 10 min to the superfusion medium. 3,4-DAP-evoked [3H]NE release both in the absence and presence of extracellular Ca2+. 3,4-DAP-evoked Ca(2+)-independent release of [3H]NE was highly sensitive to sodium channel blocker, tetrodotoxin (TTX, 100% inhibition), suggesting that Na+ per se entered into nerve terminals but not depolarization of membrane followed by Ca2+ channel opening is necessary for 3,4-DAP-evoked Ca(2+)-independent release of [3H]NE. Phorbol ester PDB increased by 480% of control and polymyxin B (PMB) decreased 3,4-DAP-evoked [3H]NE release by 94% of control in the absence of extracellular Ca2+ indicating that the alterations of voltage-dependent Ca(2+)-currents into the cells are not involved in the mechanism of the modulation of 3,4-DAP-evoked [3H]NE release by protein kinase C.
用[3H]去甲肾上腺素([3H]NE)预孵育的大鼠海马切片,在灌流液中加入3,4 - 二氨基吡啶(3,4 - DAP)刺激10分钟。无论细胞外有无Ca2+,3,4 - DAP均可诱发[3H]NE释放。3,4 - DAP诱发的[3H]NE非Ca2+依赖性释放对钠通道阻滞剂河豚毒素(TTX,100%抑制)高度敏感,这表明Na+本身进入神经末梢,而非膜去极化后Ca2+通道开放,对于3,4 - DAP诱发的[3H]NE非Ca2+依赖性释放是必要的。在无细胞外Ca2+的情况下,佛波酯PDB使释放量比对照增加480%,而多粘菌素B(PMB)使3,4 - DAP诱发的[3H]NE释放量比对照减少94%,这表明进入细胞的电压依赖性Ca2+电流的改变不参与蛋白激酶C对3,4 - DAP诱发的[3H]NE释放的调节机制。