Neurotransmitter depletion by bafilomycin is promoted by vesicle turnover
Neurotransmitter depletion by bafilomycin is promoted by vesicle turnover
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DOI：
10.1016/j.neulet.2006.10.040
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发表时间：
2007-01-29
影响因子：
2.5
通讯作者：
Attwell, David
中科院分区：
文献类型：
--
作者：
Cavelier, Pauline;Attwell, David
神经递质在突触小泡中的积累由液泡质子 ATP 酶提供动力。我们在此表明，在脑切片中，应用 H(+)-ATP 酶抑制剂巴弗洛霉素或刀那霉素并不能有效地消耗递质的谷氨酸能囊泡，除非囊泡周转增加。囊泡能量学模拟表明巴弗洛霉素和刀那霉素从囊泡内部作用于H(+)-ATP酶，或者在H'-ATP酶被抑制后维持囊泡膜电位。 (c) 2006 Elsevier Ireland Ltd. 保留所有权利。
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.