The JI
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     
 

This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Campo, B.
Right arrow Articles by North, R. A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Campo, B.
Right arrow Articles by North, R. A.
The Journal of Immunology, 2003, 170: 1167-1173.
Copyright © 2003 by The American Association of Immunologists

Sustained Depolarization and ADP-Ribose Activate a Common Ionic Current in Rat Peritoneal Macrophages 1

Brice Campo, Annmarie Surprenant and R. Alan North2

Institute of Molecular Physiology, University of Sheffield, Sheffield, United Kingdom

Phagocytosis is associated with large changes in the membrane potential of macrophages, but the functional significance of this is unknown. Whole cell recordings were made from rat peritoneal macrophages. Sustained (>30 s) depolarization of the cells progressively activated a conductance that remained high (several nanoSeimens) for several tens of seconds. This current: 1) was linearly dependent on potential between -100 and +50 mV; 2) reversed close to 0 mV in a physiological external solution; 3) could also be carried in part by N-methyl-D-glucamine (PNMDG/PNa 0.7), chloride (PCl/PNa 0.5), or calcium (PCa/PNa 1.3); and 4) was blocked by intracellular ATP (5 mM) or ADP (10 mM) and by extracellular lanthanum (half-maximal concentration 1 mM). A current with all the same properties was recorded in cells when the intracellular solution contained ADP-ribose (10–300 µM) or {beta}-NAD (1 mM) (but not any other nucleotide analogs tested). The results suggest that prolonged depolarization leads to an increased intracellular level of ADP-ribose, which in turn activates this nonselective conductance(s).




This article has been cited by other articles:


Home page
 J. Leukoc. Biol.Home page
E. F. Vernon-Wilson, F. Aurade, L. Tian, I. C. M. Rowe, M. J. Shipston, J. Savill, and S. B. Brown
CD31 delays phagocyte membrane repolarization to promote efficient binding of apoptotic cells
J. Leukoc. Biol., November 1, 2007; 82(5): 1278 - 1288.
[Abstract] [Full Text] [PDF]

Home page
 J. Physiol.Home page
T. Schilling, F. Lehmann, B. Ruckert, and C. Eder
Physiological mechanisms of lysophosphatidylcholine-induced de-ramification of murine microglia
J. Physiol., May 15, 2004; 557(1): 105 - 120.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Lung Cell. Mol. Physiol.Home page
A. B. Mackenzie, H. Chirakkal, and R. A. North
Kv1.3 potassium channels in human alveolar macrophages
Am J Physiol Lung Cell Mol Physiol, October 1, 2003; 285(4): L862 - L868.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
This Website Copyright © 2003 by The American Association of Immunologists, Inc. All rights reserved.
All Contents Copyright © 2003 by The American Association of Immunologists, Inc. All rights reserved.