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 e