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
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
收藏
页码:905 / 915
页数:11
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