Vesicular ATPase Inserted into the Plasma Membrane of Motor Terminals by Exocytosis Alkalinizes Cytosolic pH and Facilitates Endocytosis

Zhongsheng Zhang, Khanh T. Nguyen, Ellen Barrett, Gavriel David

Research output: Contribution to journalArticle

47 Citations (Scopus)

Abstract

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 (∼13 nM average peak increase in [H+]), followed by a prolonged alkalinization (∼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.

Original languageEnglish
Pages (from-to)1097-1108
Number of pages12
JournalNeuron
Volume68
Issue number6
DOIs
StatePublished - Dec 22 2010

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Exocytosis
Endocytosis
Adenosine Triphosphatases
Proton-Translocating ATPases
Cell Membrane
Neurotoxins
Action Potentials
Neurotransmitter Agents
Fluorescence
Membranes
Proteins

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

Vesicular ATPase Inserted into the Plasma Membrane of Motor Terminals by Exocytosis Alkalinizes Cytosolic pH and Facilitates Endocytosis. / Zhang, Zhongsheng; Nguyen, Khanh T.; Barrett, Ellen; David, Gavriel.

In: Neuron, Vol. 68, No. 6, 22.12.2010, p. 1097-1108.

Research output: Contribution to journalArticle

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