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细胞内钙库参与3,4-二氨基吡啶诱发的[3H]去甲肾上腺素释放。

Involvement of intracellular Ca2+ stores in 3,4-diaminopyridine-evoked [3H]norepinephrine release.

作者信息

Huang H Y, Zhou C W

机构信息

Shanghai Institute of Physiology, Chinese Academy of Sciences, China.

出版信息

Zhongguo Yao Li Xue Bao. 1996 Jul;17(4):302-5.

PMID:9812707
Abstract

AIM

To study the mechanism for 3, 4-diaminopyridine (DAP) evoking external Ca(2+)-independent release of [3H] norepinephrine ([3H] NE).

METHODS

Rat hippocampal slices were preincubated with [3H] NE and superfused with medium. [3H] NE release was determined.

RESULTS

Under Ca(2+)-free conditions, DAP evoked [3H] NE release. In rats pretreated by reserpine, the effect of DAP was no longer detectable. Ca2+ chelator BAPTA-AM potently inhibited DAP-evoked [3H] NE release. Desipramine 100-500 mumol.L-1 strongly induced [3H] NE release in a concentration-dependent manner, whereas caffeine 30-70 mmol.L-1 was slightly effective on [3H]NE release. The blocker of Ca(2+)-induced Ca2+ releasable stores, dantrolene sodium did not attenuate DAP-evoked [3H]NE release.

CONCLUSION

In the absence of extracellular Ca2+, DAP evokes exocytotic release of [3H]NE from synaptic vesicles through liberation of internal Ca2+ from inositol 1, 4, 5-trisphosphate-sensitive Ca2+ stores.

摘要

目的

研究3,4 - 二氨基吡啶(DAP)引发[3H]去甲肾上腺素([3H]NE)非依赖细胞外钙的释放机制。

方法

将大鼠海马切片用[3H]NE预孵育,然后用培养基进行灌流。测定[3H]NE的释放情况。

结果

在无钙条件下,DAP可引发[3H]NE的释放。在经利血平预处理的大鼠中,不再能检测到DAP的作用。钙离子螯合剂BAPTA - AM能有效抑制DAP引发的[3H]NE释放。100 - 500μmol·L-1的地昔帕明以浓度依赖的方式强烈诱导[3H]NE释放,而30 - 70mmol·L-1的咖啡因对[3H]NE释放的作用较弱。钙离子诱导的钙离子释放储存的阻滞剂丹曲林钠并未减弱DAP引发的[3H]NE释放。

结论

在细胞外无钙离子的情况下,DAP通过从肌醇1,4,5 - 三磷酸敏感的钙离子储存中释放内部钙离子,引发突触小泡中[3H]NE的胞吐释放。

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Zhongguo Yao Li Xue Bao. 1996 Jul;17(4):302-5.
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