Neurotransmitter depletion by bafilomycin is promoted by vesicle turnover

被引：26

作者：

Cavelier, Pauline ^{[1
]}

Attwell, David ^{[1
]}

机构：

[1] UCL, Dept Physiol, London WC1E 6BT, England

来源：

NEUROSCIENCE LETTERS | 2007年 / 412卷 / 02期

基金：

英国惠康基金;

关键词：

glutamate; synaptic transmission; veratridine; potassium;

D O I：

10.1016/j.neulet.2006.10.040

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

Accumulation of neurotransmitter into synaptic vesicles is powered by the vacuolar proton ATPase. We show here that, in brain slices, application of the H(+)-ATPase inhibitors bafilomycin or concanamycin does not efficiently deplete glutamatergic vesicles of transmitter unless vesicle turnover is increased. Simulations of vesicle energetics suggest either that bafilomycin and concanamycin act on the H(+)-ATPase from inside the vesicle, or that the vesicle membrane potential is maintained after the H'-ATPase is inhibited. (c) 2006 Elsevier Ireland Ltd. All rights reserved.

引用

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页码：95 / 100

页数：6

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