Calcium Mediates the NO-induced Potassium Current in Toad and Rat Olfactory Receptor Neurons

Calcium Mediates the NO-induced Potassium Current in Toad and Rat Olfactory Receptor Neurons Nitric oxide (NO) activates a K+ current in dissociated amphibian olfactory receptor neurons. Using the patch-clamp technique in its whole-cell mode and stimulation with puffs of the NO-donor sodium nitroprusside, we further studied this effect and show that it was sensitive to the K+-channel blockers tetraethylammonium and iberiotoxin, indicating the activation of a Ca2+-dependent K+ conductance. The Ca2+-channel blockers nifedipine and cadmium abolished the NO-induced current, and lowering external Ca2+ reduced it significantly. Ca2+ imaging showed a transient fluorescence increase upon stimulation with NO, and after blockade of K+ currents, an NO-induced inward current could be measured, suggesting that the activation of the Ca2+-dependent K+ conductance is mediated by Ca2+ influx. LY83583, a blocker of the ciliary cAMP-gated channels, did not affect the current, and experiments with focal stimulation indicated that the effect is present in the soma, therefore Ca2+ is unlikely to enter via the transduction channels. Finally, we show that NO exerts an effect with similar characteristics on olfactory receptor neurons from the rat. These data represent the first evidence that NO activates a Ca2+-dependent K+ conductance by causing a Ca2+ influx in a sensory system, and suggest that NO signaling plays a role in the physiology of vertebrate olfactory receptor neurons. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png The Journal of Membrane Biology Springer Journals

Calcium Mediates the NO-induced Potassium Current in Toad and Rat Olfactory Receptor Neurons

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Publisher
Springer-Verlag
Copyright
Copyright © 2000 by Springer-Verlag New York Inc.
Subject
Life Sciences; Biochemistry, general; Human Physiology
ISSN
0022-2631
eISSN
1432-1424
D.O.I.
10.1007/s002320001062
Publisher site
See Article on Publisher Site

Abstract

Nitric oxide (NO) activates a K+ current in dissociated amphibian olfactory receptor neurons. Using the patch-clamp technique in its whole-cell mode and stimulation with puffs of the NO-donor sodium nitroprusside, we further studied this effect and show that it was sensitive to the K+-channel blockers tetraethylammonium and iberiotoxin, indicating the activation of a Ca2+-dependent K+ conductance. The Ca2+-channel blockers nifedipine and cadmium abolished the NO-induced current, and lowering external Ca2+ reduced it significantly. Ca2+ imaging showed a transient fluorescence increase upon stimulation with NO, and after blockade of K+ currents, an NO-induced inward current could be measured, suggesting that the activation of the Ca2+-dependent K+ conductance is mediated by Ca2+ influx. LY83583, a blocker of the ciliary cAMP-gated channels, did not affect the current, and experiments with focal stimulation indicated that the effect is present in the soma, therefore Ca2+ is unlikely to enter via the transduction channels. Finally, we show that NO exerts an effect with similar characteristics on olfactory receptor neurons from the rat. These data represent the first evidence that NO activates a Ca2+-dependent K+ conductance by causing a Ca2+ influx in a sensory system, and suggest that NO signaling plays a role in the physiology of vertebrate olfactory receptor neurons.

Journal

The Journal of Membrane BiologySpringer Journals

Published: Jan 31, 2014

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