| Literature DB >> 17123716 |
Pauline Cavelier1, David Attwell.
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.Entities:
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Year: 2006 PMID： 17123716 PMCID： PMC6930131 DOI： 10.1016/j.neulet.2006.10.040
Source DB: PubMed Journal: Neurosci Lett ISSN： 0304-3940 Impact factor: 3.046