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3,4-二氨基吡啶诱导鸡胚前脑培养神经元中磷酸肌醇的水解。

3,4-Diaminopyridine induced hydrolysis of phosphoinositide in cultured neurons from embryo chick forebrain.

作者信息

Dong Z, Zhu P H

机构信息

Shanghai Institute of Physiology, Chinese Academy of Sciences.

出版信息

Neuropharmacology. 1995 Mar;34(3):297-302. doi: 10.1016/0028-3908(94)00148-l.

Abstract

The effect of 3,4-diaminopyridine (DAP) on phosphoinositide hydrolysis in cultured neurons from embryo chick forebrain has been studied. DAP produced a dose- and time-dependent accumulation of inositol phosphates. At 1 mM DAP a maximal effect was obtained. In Ca2+ free medium, DAP-activated turnover of phosphoinositide was reduced, but was still significant. Blocking Ca2+ entry with 200 microM Cd2+ also did not abolish the DAP-induced accumulation of inositol phosphates. As a comparison the effect of high K+ exposure was investigated. High K+ enhanced phosphoinositide hydrolysis, and this effect was also reduced by excluding Ca2+ influx. Moreover, DAP had no additional effect on the high K(+)-induced hydrolysis of phosphoinositide. Using oxonol-V, a depolarization of the membrane potential was seen in the neurons bathed in DAP containing medium. It is suggested that the depolarization may play a role in DAP-activated phosphoinositide turnover in cultured neurons of the embryo chick forebrain, but that Ca2+ entry is not necessary for this effect.

摘要

研究了3,4-二氨基吡啶(DAP)对鸡胚前脑培养神经元中磷酸肌醇水解的影响。DAP可引起肌醇磷酸酯呈剂量和时间依赖性积累。在1 mM DAP时可获得最大效应。在无Ca2+培养基中,DAP激活的磷酸肌醇周转减少,但仍很显著。用200 μM Cd2+阻断Ca2+内流也不能消除DAP诱导的肌醇磷酸酯积累。作为对照,研究了高钾暴露的影响。高钾增强了磷酸肌醇水解,排除Ca2+内流也可降低此效应。此外,DAP对高钾诱导的磷酸肌醇水解没有额外影响。使用氧杂萘酚-V,在含有DAP的培养基中培养的神经元中可见膜电位去极化。提示去极化可能在DAP激活鸡胚前脑培养神经元的磷酸肌醇周转中起作用,但此效应并不需要Ca2+内流。

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