Journal
NEURON
Volume 68, Issue 6, Pages 1097-1108Publisher
CELL PRESS
DOI: 10.1016/j.neuron.2010.11.035
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Funding
- NIH [NS058888]
- Muscular Dystrophy Association [MDA112102]
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Key components of vesicular neurotransmitter release, such as Ca2+ influx and membrane recycling, are affected by cytosolic pH. We measured the pH-sensitive fluorescence of Yellow Fluorescent Protein transgenically expressed in mouse motor nerve terminals, and report that Ca2+ influx elicited by action potential trains (12.5-100 Hz) evokes a biphasic pH change: a brief acidification (similar to 13 nM average peak increase in [H+]), followed by a prolonged alkalinization (similar to 30 nM peak decrease in [H+]) that outlasts the stimulation train. The alkalinization is selectively eliminated by blocking vesicular exocytosis with botulinum neurotoxins, and is prolonged by the endocytosis-inhibitor dynasore. Blocking H+ pumping by vesicular H+-ATPase (with folimycin or bafilomycin) suppresses stimulation-induced alkalinization and reduces endocytotic uptake of FM1-43. These results suggest that H+-ATPase, known to transfer cytosolic H+ into prefused vesicles, continues to extrude cytosolic H+ after being exocytotically incorporated into the plasma membrane. The resulting cytosolic alkalinization may facilitate vesicular endocytosis.
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