Cavelier Pauline, Attwell David
Department of Physiology, University College London, Gower Street, London WC1E 6BT, UK.
Neurosci Lett. 2007 Jan 29;412(2):95-100. doi: 10.1016/j.neulet.2006.10.040. Epub 2006 Nov 22.
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.
神经递质向突触囊泡的积累由液泡质子ATP酶提供能量。我们在此表明，在脑片中，除非囊泡周转率增加，否则应用H(+) -ATP酶抑制剂巴弗洛霉素或 concanamycin 并不能有效地耗尽谷氨酸能囊泡中的递质。囊泡能量学模拟表明，要么巴弗洛霉素和 concanamycin 从囊泡内部作用于H(+) -ATP酶，要么在H(+) -ATP酶被抑制后囊泡膜电位得以维持。
