Suppr超能文献

通过抗体介导破坏SNAP-25功能抑制七鳃鳗网状脊髓突触中的神经递质释放。

Inhibition of neurotransmitter release in the lamprey reticulospinal synapse by antibody-mediated disruption of SNAP-25 function.

作者信息

Löw P, Norlin T, Risinger C, Larhammar D, Pieribone V A, Shupliakov O, Brodin L

机构信息

The Nobel Institute for Neurophysiology, Department of Neuroscience, Karolinska Institutet, Stockholm/Sweden.

出版信息

Eur J Cell Biol. 1999 Nov;78(11):787-93. doi: 10.1016/S0171-9335(99)80029-6.

Abstract

Exocytosis - syntaxin - synaptobrevin - SNARE synaptic vesicle The lamprey giant reticulospinal synapse can be used to manipulate the molecular machinery of synaptic vesicle exocytosis by presynaptic microinjection. Here we test the effect of disrupting the function of the SNARE protein SNAP-25. Polyclonal SNAP-25 antibodies were shown in an in vitro assay to inhibit the binding between syntaxin and SNAP-25. When microinjected presynaptically, these antibodies produced a potent inhibition of the synaptic response. Ba2+ spikes recorded in the presynaptic axon were not altered, indicating that the effect was not due to a reduced presynaptic Ca2+ entry. Electron microscopic analysis showed that synaptic vesicle clusters had a similar organization in synapses of antibody-injected axons as in control axons, and the number of synaptic vesicles in apparent contact with the presynaptic plasma membrane was also similar. Clathrin-coated pits, which normally occur at the plasma membrane around stimulated synapses, were not detected after injection of SNAP-25 antibodies, consistent with a blockade of vesicle cycling. Thus, SNAP-25 antibodies, which disrupt the interaction with syntaxin, inhibit neurotransmitter release without affecting the number of synaptic vesicles at the plasma membrane. These results provide further support to the view that the formation of SNARE complexes is critical for membrane fusion, but not for the targeting of synaptic vesicles to the presynaptic membrane.

摘要

胞吐作用 - syntaxin - 突触小泡蛋白 - SNARE突触小泡 七鳃鳗的巨大网状脊髓突触可用于通过突触前显微注射来操控突触小泡胞吐作用的分子机制。在此,我们测试破坏SNARE蛋白SNAP - 25功能的效果。在体外实验中,多克隆SNAP - 25抗体可抑制syntaxin与SNAP - 25之间的结合。当突触前显微注射这些抗体时,它们对突触反应产生了强效抑制。突触前轴突中记录到的Ba2 + 峰未改变,这表明该效应并非由于突触前Ca2 + 内流减少所致。电子显微镜分析显示,在注射抗体的轴突突触中,突触小泡簇的组织方式与对照轴突相似,并且与突触前质膜明显接触的突触小泡数量也相似。注射SNAP - 25抗体后未检测到通常出现在受刺激突触周围质膜上的网格蛋白包被小窝,这与囊泡循环受阻一致。因此,破坏与syntaxin相互作用的SNAP - 25抗体可抑制神经递质释放,而不影响质膜上突触小泡的数量。这些结果进一步支持了以下观点:SNARE复合物的形成对于膜融合至关重要,但对于突触小泡靶向突触前膜并非如此。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验