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.