Huang H Y, Xie P G, Huang Y Z
Shanghai Institute of Physiology, Chinese Academy of Sciences.
Zhongguo Yao Li Xue Bao. 1994 Jul;15(4):354-7.
Slices of rat hippocampus, preincubated with [3H] norepinephrine ([3H]NE) were superfused with Ca(2+)-free medium containing desipramine 1 mumol.L-1, Li+ (40-80 mmol.L-1) evoked [3H]NE release in a concentration dependent manner. It was enhanced by 4 beta-phorbol 12,13-dibutyrate (PDB) and inhibited by tetrodotoxin. Ca(2+)-chelator BAPTA-AM did not attenuate this Li-evoked [3H]NE release. After application of 3,4-diaminopyridine to evoke [3H]NE release and PDB to enhance this release, the Li(+)-evoked [3H]NE release was significantly inhibited. The findings suggest that the liberation of internal Ca2+ stores was not involved in this release process.
用[3H]去甲肾上腺素([3H]NE)预孵育的大鼠海马切片,在含有1μmol.L-1地昔帕明的无钙培养基中进行灌流,锂离子(40 - 80 mmol.L-1)以浓度依赖的方式诱发[3H]NE释放。它被4β-佛波醇12,13-二丁酸酯(PDB)增强,被河豚毒素抑制。钙螯合剂BAPTA-AM并没有减弱这种锂诱发的[3H]NE释放。在应用3,4-二氨基吡啶诱发[3H]NE释放并使用PDB增强这种释放后,锂(+)诱发的[3H]NE释放被显著抑制。这些发现表明,细胞内钙库的释放不参与这个释放过程。