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Calcium mediates the NO-induced potassium current in toad and rat olfactory receptor neurons

O Schmachtenberg1, J Bacigalupo

  • 1Department of Biology, Faculty of Science, University of Chile, P.O. Box 653, Santiago, Chile, and Millenium Institute for Advanced Studies in Cell Biology and Biotechnology (IASBB) at University of Chile, Santiago, Chile.

The Journal of Membrane Biology
|May 17, 2000
PubMed

Insights

Nitric oxide (NO) activates a calcium-dependent potassium (K+) current in olfactory neurons. This NO-induced current results from calcium influx, suggesting a role for NO signaling in vertebrate olfaction.

Area of Science:

  • Neuroscience
  • Cell Physiology
  • Sensory Systems

Background:

  • Nitric oxide (NO) is a signaling molecule with diverse physiological roles.
  • Olfactory receptor neurons (ORNs) are responsible for detecting odors.
  • The role of NO in vertebrate olfactory signaling remains largely unexplored.

Purpose of the Study:

  • To investigate the effect of nitric oxide (NO) on ion currents in amphibian olfactory receptor neurons.
  • To elucidate the mechanisms underlying NO-induced currents in ORNs.
  • To determine the physiological relevance of NO signaling in vertebrate olfaction.

Main Methods:

  • Whole-cell patch-clamp recordings from dissociated amphibian and rat ORNs.
  • Stimulation with NO-donor sodium nitroprusside.
  • Application of K+ and Ca2+ channel blockers (tetraethylammonium, iberiotoxin, nifedipine, cadmium).
  • Calcium imaging to assess intracellular Ca2+ changes.
  • Focal stimulation and experiments with cAMP-gated channel blockers.

Main Results:

  • NO activated a K+ current sensitive to K+-channel blockers, indicating a Ca2+-dependent K+ conductance.
  • NO-induced currents were abolished by Ca2+-channel blockers and reduced by lowering external Ca2+.
  • Ca2+ imaging revealed a transient increase in intracellular Ca2+ upon NO stimulation.
  • NO-induced Ca2+ influx, not via ciliary transduction channels, mediated the activation of the Ca2+-dependent K+ conductance.
  • Similar effects were observed in rat ORNs.

Conclusions:

  • Nitric oxide activates a Ca2+-dependent K+ conductance in vertebrate olfactory receptor neurons.
  • This activation is mediated by NO-induced Ca2+ influx, likely through non-canonical pathways.
  • NO signaling plays a significant role in the physiology of vertebrate olfaction.

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