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


     
 

This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
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 Labrecque, G. F.
Right arrow Articles by Baird, B.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Labrecque, G. F.
Right arrow Articles by Baird, B.

The Journal of Immunology, Vol 142, Issue 1 236-243, Copyright © 1989 by American Association of Immunologists

ARTICLES

Antigen-triggered membrane potential changes in IgE-sensitized rat basophilic leukemia cells: evidence for a repolarizing response that is important in the stimulation of cellular degranulation

GF Labrecque, D Holowka and B Baird
Department of Chemistry, Cornell University, Ithaca, NY 14853.

We have studied Ag-induced membrane potential changes of rat basophilic leukemia cells by using the potential-sensitive dye, bis-(1,3- diethylthiobarbiturate)trimethineoxonol. A rapid membrane depolarization is triggered by a multivalent Ag, and it has a bell- shaped dose dependence that parallels the degranulation response but not the extent of cross-linking of the IgE-receptor complexes. As the temperature is reduced from 37 degrees C, this depolarization response slows and decreases in magnitude until complete inhibition is observed at 15 degrees C, similar to the temperature dependence previously observed for the Ag-stimulated rise in cytoplasmic Ca2+ and for degranulation. The results imply that a highly temperature-dependent step subsequent to Ag binding and cross-linking is necessary for the depolarization response. A partial return to the resting potential is seen to follow the depolarization response to Ag. This repolarization process is inhibited by quinidine.HCl and Ba2+ in parallel with an inhibition of the degranulation response. Repolarization is not affected by 4-aminopyridine or by the absence of K+ in the external buffer. These data suggest that the repolarization is caused by a previously uncharacterized K+ channel.


This article has been cited by other articles:


Home page
 J. Immunol.Home page
E. Shumilina, R. S. Lam, F. Wolbing, N. Matzner, I. M. Zemtsova, M. Sobiesiak, H. Mahmud, U. Sausbier, T. Biedermann, P. Ruth, et al.
Blunted IgE-Mediated Activation of Mast Cells in Mice Lacking the Ca2+-Activated K+ Channel KCa3.1
J. Immunol., June 15, 2008; 180(12): 8040 - 8047.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Cell Physiol.Home page
R. Sullivan, S. K. Koliwad, and D. L. Kunze
Analysis of a Ca2+-activated K+ channel that mediates hyperpolarization via the thrombin receptor pathway
Am J Physiol Cell Physiol, November 1, 1998; 275(5): C1342 - C1348.
[Abstract] [Full Text] [PDF]

Home page
 J. Biol. Chem.Home page
C. Wofsy, U. M. Kent, S.-Y. Mao, H. Metzger, and B. Goldstein
Kinetics of Tyrosine Phosphorylation When IgE Dimers Bind to FC[IMAGE] Receptors on Rat Basophilic Leukemia Cells
J. Biol. Chem., September 1, 1995; 270(35): 20264 - 20272.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
This Website Copyright © 1989 by The American Association of Immunologists, Inc. All rights reserved.
All Contents Copyright © 1989 by The American Association of Immunologists, Inc. All rights reserved.