IMPAIRMENT OF SYNTAXIN BY BOTULINUM NEUROTOXIN C-1 OR ANTIBODIES INHIBITS ACETYLCHOLINE-RELEASE BUT NOT CA2+ CHANNEL ACTIVITY

被引：54

作者：

MOCHIDA, S ^{[1
]}

SAISU, H ^{[1
]}

KOBAYASHI, H ^{[1
]}

ABE, T ^{[1
]}

机构：

[1] NIIGATA UNIV,BRAIN RES INST,DEPT NEUROCHEM,NIIGATA 951,JAPAN

来源：

NEUROSCIENCE | 1995年 / 65卷 / 03期

关键词：

D O I：

10.1016/0306-4522(94)00508-3

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

The involvement of syntaxin, an omega-conotoxin-sensitive Ca2+ channel-associated protein, in acetylcholine release was studied at synapses formed between rat sympathetic neurons in culture. Transmission at these synapses involved omega-conotoxin-sensitive Ca2+ channels because a dose-dependent inhibition was observed when omega-conotoxin was bath-applied. Confocal microscope examination of immunofluorescent staining showed that syntaxin had a similar distribution to synaptic vesicle-associated membrane proteins, synaptophysin and vesicle-associated membrane protein/synaptobrevin-2, indicating that syntaxin molecules are concentrated in the presynaptic terminals. Botulinum neurotoxin C-1 applied extracellularly or intracellularly into presynaptic neurons blocked synaptic transmission. Introduction of a monoclonal antibody, or polyclonal antibodies, to syntaxin into the presynaptic neuron depressed the evoked release of acetylcholine without affecting Ca2+ influx through Ca2+ channels. These results suggest that syntaxin plays an important role in release of neurotransmitter by a nerve impulse and that this mechanism is downstream of Ca2+ influx.

引用

页码：905 / 915

页数：11

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