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

来源：

NEUROSCIENCE LETTERS | 1998年 / 253卷 / 01期

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

页码：1 / 4

页数：4

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