Ba2+ does not support synaptic vesicle retrieval in rat cerebrocortical synaptosomes

被引:26
作者
Cousin, MA [1 ]
Robinson, PJ [1 ]
机构
[1] Childrens Med Res Inst, Wentworthville, NSW 2145, Australia
基金
英国医学研究理事会;
关键词
endocytosis; exocytosis; barium; calcium; FM2-10; glutamate;
D O I
10.1016/S0304-3940(98)00610-7
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
To investigate whether any specific requirement for extracellular Ca2+ exists in the control synaptic vesicle retrieval, we examined the ability of the divalent cation Ba2+ to substitute for Ca2+ in both vesicle exocytosis and endocytosis. Ba2+ stimulated glutamate release from rat cerebrocortical synaptosomes. Ba2+-evoked release was inhibited by bafilomycin A1, indicating release was via exocytosis of synaptic vesicles. However, Ba2+ did not stimulate vesicle retrieval, monitored by a FM2-10-based retrieval assay. Therefore synaptic Vesicle retrieval in central nerve terminals has a specific requirement for extracellular Ca2+ and the Ca2+ receptor for retrieval has a different cation specificity to the Ca2+ receptor for exocytosis. (C) 1998 Elsevier Science Ireland Ltd. Ail rights reserved.
引用
收藏
页码:1 / 4
页数:4
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