|
|
|
|
|
|
|
||
The Journal of General Physiology, Vol 93, 765-783, Copyright © 1989 by The Rockefeller University Press
ARTICLES |
M Covarrubias, C Kopta and JH Steinbach
Department of Anesthesiology, Washington University School of Medicine, St. Louis, Missouri 63110.
We used selective inhibitors of the asparagine-linked oligosaccharide processing pathway to study the effect of sugar trimming on the functional properties of the nicotinic acetylcholine (ACh) receptor expressed in clonal mammalian BC3H-1 cells. Inhibitors of initial steps of the processing pathway (1-deoxynojirimycin[DNJ] and castanospermine[CS]) reduced the density of ACh receptors on the cell surface (3- to 5-fold) but their responsiveness to ACh was more reduced (5- to 10-fold). These results suggest that the function of the ACh receptor was altered. When the ACh receptors were expressed in the presence of DNJ or CS, analysis of ACh-evoked single-channel currents (- 100 mV and 11 degrees C) revealed an approximate threefold reduction in the opening rate (control: 600-650 s(-1)), treated: 130-250 s(-1)) and an approximate twofold reduction in the rate of agonist dissociation (control: 900-1,000 s(-1), treated: 400-500 s(-1)). In addition, the proportion of brief duration bursts (tau = 50-100 microseconds) was increased (1.5- to 2-fold) by treatments with DNJ or CS. In contrast, an inhibitor of a late processing step (swainsonine) did not produce such alterations. The single-channel conductance was not altered by any of the three inhibitors, and the slopes of log-log dose-response curves at low concentrations and desensitization did not appear to be affected. Each inhibitor altered the electrophoretic mobility of the ACh receptor subunits. We conclude that early sugar trimming can influence the kinetics of the nicotinic ACh receptor in BC3H-1 cells.
CiteULike 
Complore 
Connotea 
Del.icio.us 
Digg 
Reddit 
Technorati What's this?
This article has been cited by other articles:
|
|
 |
|
  J. Zhu, I. Watanabe, B. Gomez, and W. B. Thornhill Determinants Involved in Kv1 Potassium Channel Folding in the Endoplasmic Reticulum, Glycosylation in the Golgi, and Cell Surface Expression J. Biol. Chem., October 12, 2001; 276(42): 39419 - 39427. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 D. Shepherd and P. Brehm Two Types of ACh Receptors Contribute to Fast Channel Gating on Mouse Skeletal Muscle J Neurophysiol, December 1, 1997; 78(6): 2966 - 2974. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 W. R. Kem, V. M. Mahnir, R. L. Papke, and C. J. Lingle Anabaseine Is a Potent Agonist on Muscle and Neuronal Alpha-Bungarotoxin-Sensitive Nicotinic Receptors J. Pharmacol. Exp. Ther., December 1, 1997; 283(3): 979 - 992. [Abstract] [Full Text]
|
|
|
|
 |
|
 W. Phillips, C Kopta, P Blount, P. Gardner, J. Steinbach, and J. Merlie ACh receptor-rich membrane domains organized in fibroblasts by recombinant 43-kildalton protein Science, February 1, 1991; 251(4993): 568 - 570. [Abstract] [PDF]
|
|
|
|
|
|
A. Pabon, K. W. Chan, J. L. Sui, X. Wu, D. E. Logothetis, and W. B. Thornhill Glycosylation of GIRK1 at Asn119 and ROMK1 at Asn117 Has Different Consequences in Potassium Channel Function J. Biol. Chem., September 22, 2000; 275(39): 30677 - 30682. [Abstract] [Full Text] [PDF]
|
|
|
|
