Suppr超能文献

ω-芋螺毒素和Cd2+刺激细胞内电压门控Ca2+通道池向质膜募集。

omega-Conotoxin and Cd2+ stimulate the recruitment to the plasmamembrane of an intracellular pool of voltage-operated Ca2+ channels.

作者信息

Passafaro M, Clementi F, Pollo A, Carbone E, Sher E

机构信息

Department of Medical Pharmacology, University of Milan, Italy.

出版信息

Neuron. 1994 Feb;12(2):317-26. doi: 10.1016/0896-6273(94)90274-7.

Abstract

125I-omega-conotoxin binding to neuroblastoma cells at 37 degrees C continuously increased, reaching a plateau after 6-8 hr; this was up to 6 times higher than that observed at lower temperatures. The same effect was induced by short pulses with omega-conotoxin followed by a chase period at 37 degrees C in control medium. Cd2+ also induced up-regulation of surface 125I-omega-conotoxin-binding sites. Fura-2 and patch-clamp experiments showed that the recruited binding sites corresponded to functional voltage-operated Ca2+ channels. Permeabilization experiments revealed a large intracellular pool of 125I-omega-conotoxin-binding sites, whose recruitment to the plasmamembrane was prevented by brefeldin A and nocodazole. These data suggest that specific stimuli might induce voltage-operated Ca2+ channel translocation to plasmamembrane and, in this way, modulate presynaptic events.

摘要

125I-ω-芋螺毒素在37℃下与神经母细胞瘤细胞的结合持续增加,6-8小时后达到平台期;这比在较低温度下观察到的结合量高出6倍。用ω-芋螺毒素短脉冲处理后,在37℃的对照培养基中进行追踪培养,也能诱导相同的效应。Cd2+也能诱导表面125I-ω-芋螺毒素结合位点的上调。Fura-2和膜片钳实验表明,新募集的结合位点对应于功能性电压门控Ca2+通道。透化实验揭示了细胞内存在大量125I-ω-芋螺毒素结合位点,布雷菲德菌素A和诺考达唑可阻止这些位点募集到质膜上。这些数据表明,特定刺激可能诱导电压门控Ca2+通道转位到质膜,从而调节突触前事件。

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验