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Neurotransmitter depletion by bafilomycin is promoted by vesicle turnover

Cavelier, P; Attwell, D; (2007) Neurotransmitter depletion by bafilomycin is promoted by vesicle turnover. NEUROSCI LETT , 412 (2) 95 - 100. 10.1016/j.neulet.2006.10.040.

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Abstract

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.

Type: Article
Title: Neurotransmitter depletion by bafilomycin is promoted by vesicle turnover
DOI: 10.1016/j.neulet.2006.10.040
Keywords: glutamate, synaptic transmission, veratridine, potassium, VESICULAR GLUTAMATE TRANSPORTER, GAMMA-AMINOBUTYRIC-ACID, SYNAPTIC VESICLES, FUNCTIONAL RECONSTITUTION, HIPPOCAMPAL-NEURONS, SIMULATED ISCHEMIA, RECEPTOR OCCUPANCY, ENERGY-DEPENDENCE, RAT HIPPOCAMPUS, V-ATPASES
UCL classification: UCL > Provost and Vice Provost Offices
UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences
UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Life Sciences
UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Life Sciences > Div of Biosciences
UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Life Sciences > Div of Biosciences > Neuro, Physiology and Pharmacology
URI: http://discovery.ucl.ac.uk/id/eprint/122713
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