| First Author | Zhang Z | Year | 2010 |
| Journal | Neuron | Volume | 68 |
| Issue | 6 | Pages | 1097-108 |
| PubMed ID | 21172612 | Mgi Jnum | J:167715 |
| Mgi Id | MGI:4879038 | Doi | 10.1016/j.neuron.2010.11.035 |
| Citation | Zhang Z, et al. (2010) Vesicular ATPase inserted into the plasma membrane of motor terminals by exocytosis alkalinizes cytosolic pH and facilitates endocytosis. Neuron 68(6):1097-108 |
| abstractText | Key components of vesicular neurotransmitter release, such as Ca(2+) 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 Ca(2+) influx elicited by action potential trains (12.5-100 Hz) evokes a biphasic pH change: a brief acidification ( approximately 13 nM average peak increase in [H(+)]), followed by a prolonged alkalinization ( approximately 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. |
