Sodium-dependent Potassium Channels in Leech P Neurons

Sodium-dependent Potassium Channels in Leech P Neurons In leech P neurons the inhibition of the Na+-K+ pump by ouabain or omission of bath K+ leaves the membrane potential unaffected for a prolonged period or even induces a marked membrane hyperpolarization, although the concentration gradients for K+ and Na+ are attenuated substantially. As shown previously, this stabilization of the membrane potential is caused by an increase in the K+ conductance of the plasma membrane, which compensates for the reduction of the K+ gradient. The data presented here strongly suggest that the increased K+ conductance is due to Na+-activated K+ (KNa) channels. Specifically, an increase in the cytosolic Na+ concentration ([Na+]i) was paralleled by a membrane hyperpolarization, a decrease in the input resistance (R in) of the cells, and by the occurrence of an outwardly directed membrane current. The relationship between R in and [Na+]i followed a simple model in which the R in decrease was attributed to K+ channels that are activated by the binding of three Na+ ions, with half-maximal activation at [Na+]i between 45 and 70 mM. At maximum channel activation, R in was reduced by more than 90%, suggesting a significant contribution of the KNa channels to the physiological functioning of the cells, although evidence for such a contribution is still lacking. Injection experiments showed that the KNa channels in leech P neurons are also activated by Li+. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png The Journal of Membrane Biology Springer Journals

Sodium-dependent Potassium Channels in Leech P Neurons

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Publisher
Springer Journals
Copyright
Copyright © 2006 by Springer Science+Business Media, Inc.
Subject
Life Sciences; Human Physiology; Biochemistry, general
ISSN
0022-2631
eISSN
1432-1424
D.O.I.
10.1007/s00232-005-0816-x
Publisher site
See Article on Publisher Site

Abstract

In leech P neurons the inhibition of the Na+-K+ pump by ouabain or omission of bath K+ leaves the membrane potential unaffected for a prolonged period or even induces a marked membrane hyperpolarization, although the concentration gradients for K+ and Na+ are attenuated substantially. As shown previously, this stabilization of the membrane potential is caused by an increase in the K+ conductance of the plasma membrane, which compensates for the reduction of the K+ gradient. The data presented here strongly suggest that the increased K+ conductance is due to Na+-activated K+ (KNa) channels. Specifically, an increase in the cytosolic Na+ concentration ([Na+]i) was paralleled by a membrane hyperpolarization, a decrease in the input resistance (R in) of the cells, and by the occurrence of an outwardly directed membrane current. The relationship between R in and [Na+]i followed a simple model in which the R in decrease was attributed to K+ channels that are activated by the binding of three Na+ ions, with half-maximal activation at [Na+]i between 45 and 70 mM. At maximum channel activation, R in was reduced by more than 90%, suggesting a significant contribution of the KNa channels to the physiological functioning of the cells, although evidence for such a contribution is still lacking. Injection experiments showed that the KNa channels in leech P neurons are also activated by Li+.

Journal

The Journal of Membrane BiologySpringer Journals

Published: Jan 1, 2005

References

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