|
|
|
|
|
|
|
||
The Journal of General Physiology, Vol 92, 219-237, Copyright © 1988 by The Rockefeller University Press
ARTICLES |
B Ribalet, GT Eddlestone and S Ciani
Department of Physiology, Ahmanson Laboratory of Neurobiology, University of California, Los Angeles 90024.
K channels in the cell membrane of the insulin-secreting RINm5F cell line were studied using the patch-clamp technique in cell-attached patch mode. With 140 mM K in the pipette, two channels displaying different conductive and kinetics properties were observed. A voltage- independent, inward-rectifying, 55-pS channel was active at rest (no glucose, -70 mV), but was almost completely inhibited by 5 mM glucose. A 140-pS channel was seen in the absence of glucose only after cell membrane depolarization with high (30 mM) K. This channel was voltage dependent, with a linear slope conductance between -60 and +60 mV, and was completely inhibited only by greater than 15 mM glucose. The former channel we identify as an ATP-sensitive channel previously described in excised patches and refer to it as the K(ATP) channel. The latter, because of its large conductance and voltage-dependent kinetics, will be referred to as the maxi-K(V) channel, adopting a nomenclature previously used to classify highly conductive K channels (Latorre, R., and C. Miller, 1983, Journal of Membrane Biology, 71:11-30). In addition to glucose, mannose and 2-ketoisocaproate, which also initiate insulin secretion and electrical activity in the islet beta cell, reduced the activity of both the K(ATP) and the maxi-K(V) channel. Lactate and arginine, which potentiate but do not initiate insulin secretion or beta cell electrical activity in normal islets, each caused a large reduction in maxi-K(V) channel activity, without consistently affecting the activity of K(ATP) channels. Another agonist that potentiates insulin secretion and electrical activity in normal cells, the tumor-promoting phorbol ester TPA, blocked maxi-K(V) channel activity while stimulating the activity of the K(ATP) channel, thereby implicating phosphorylation in the control of channel activity. These results indicate that metabolic substrates that initiate electrical activity and insulin secretion in normal beta cells reduce the activity of both the K(ATP) and the maxi-K(V) channel, while potentiating agents reduce only the maxi-K(V) channel. The possible role of these two channels in the processes of initiation and potentiation of the beta cell response is discussed.
CiteULike 
Complore 
Connotea 
Del.icio.us 
Digg 
Reddit 
Technorati What's this?
This article has been cited by other articles:
|
|
 |
|
  T. Haug, R. Olcese, L. Toro, and E. Stefani Regulation of K+ Flow by a Ring of Negative Charges in the Outer Pore of BKCa Channels. Part II: Neutralization of Aspartate 292 Reduces Long Channel Openings and Gating Current Slow Component J. Gen. Physiol., July 26, 2004; 124(2): 185 - 197. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 Z.-W. Li, J. P. Ding, V. Kalyanaraman, and C. J. Lingle RINm5f Cells Express Inactivating BK Channels Whereas HIT Cells Express Noninactivating BK Channels J Neurophysiol, February 1, 1999; 81(2): 611 - 624. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 H. KURIYAMA, K. KITAMURA, T. ITOH, and R. INOUE Physiological Features of Visceral Smooth Muscle Cells, With Special Reference to Receptors and Ion Channels Physiol Rev, July 1, 1998; 78(3): 811 - 920. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. Branstrom, S. Efendic, P.-O. Berggren, and O. Larsson Direct Inhibition of the Pancreatic beta -Cell ATP-regulated Potassium Channel by alpha -Ketoisocaproate J. Biol. Chem., June 5, 1998; 273(23): 14113 - 14118. [Abstract] [Full Text] [PDF]
|
|
|
|
