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机构地区:[1]中国科学院上海生理研究所
出 处:《中国药理学报》1994年第4期354-357,共4页Acta Pharmacologica Sinica
基 金:Stiftung Volkswagenwerk;Germany;National Natural Science Foundation of China;№ 39070328.
摘 要:在细胞外无钙条件下,Li^+能诱发海马脑片释放去甲肾上腺素(NE)。佛波醇基酯(PDB)能加强这一诱发释放,而河豚毒素能抑制它,Ca^(2+)螯合剂BAPTA-AM对它无作用。如先用3,4-二氨基吡啶诱发NE释放,并用PDB加强这一释放,则Li^+诱发NE释放的作用被抑制。结果提示:内源性Ca^+释放并不参与Li^+诱发NE释放的机制。Slices of rat hippocampus, preincubated with [3 H ] norepinephrine ([3H]NE) were superfused with Ca2+-free medium containing desipramine 1 μmol·L-1 Li+(40-80 mmol·L1) evoked [3H]NE release in a concentration dependent manner. It was enhanced by 4β-phorbol 12 , 13-dibutyrate (PDB) and inhibited by tetrodotoxin. Ca2+-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 in volved in this release process.
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