Nitric oxide activates a potassium current in olfactory receptor neurons from Caudiverbera caudiverbera and Xenopus laevis.
The putative role of nitric oxide (NO) in the physiology of olfactory receptor neurons (ORNs) is controversial. Here we report that pulses of NO caused an outward current in voltage-clamped isolated olfactory neurons. The I-V relation of this effect, its sensitivity to charybdotoxin and its dependence on external potassium suggest that NO activates a K(+)-conductance. As blockers of soluble guanylyl cyclases failed to affect the current, we conclude that NO opens K(+)-channels in a cGMP-independent manner.
Schmachtenberg
O
O
Departamento de Biología, Facultad de Ciencias, Universidad de Chile, Casilla 653, Santiago, Chile.
Bacigalupo
J
J
D000818:Animals; D001001:Anura; D002772:Cholera Toxin / Q000494:pharmacology; D006454:Hemoglobins / Q000494:pharmacology; D066298:In Vitro Techniques; D008564:Membrane Potentials / Q000187:drug effects; D009569:Nitric Oxide / Q000502:physiology*; D020030:Nitric Oxide Donors / Q000494:pharmacology*; D009599:Nitroprusside / Q000494:pharmacology; D009603:Nitroso Compounds / Q000494:pharmacology; D018034:Olfactory Receptor Neurons / Q000187:drug effects / Q000502:physiology*; D015221:Potassium Channels / Q000187:drug effects / Q000502:physiology*; D014982:Xenopus laevis
D006454:Hemoglobins; C118603:NOC 12; D020030:Nitric Oxide Donors; D009603:Nitroso Compounds; D015221:Potassium Channels; D009599:Nitroprusside; D009569:Nitric Oxide; D002772:Cholera Toxin