Odorants suppress a voltage-activated K+ conductance in rat olfactory neurons

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Updated: Oct 19, 2026

Perforated Patch-clamp Recording of Mouse Olfactory Sensory Neurons in Intact Neuroepithelium: Functional Analysis of Neurons Expressing an Identified Odorant Receptor
10:16

Perforated Patch-clamp Recording of Mouse Olfactory Sensory Neurons in Intact Neuroepithelium: Functional Analysis of Neurons Expressing an Identified Odorant Receptor

Published on: July 13, 2015

F W Lischka1, J H Teeter, D Restrepo

  • 1Monell Chemical Senses Center, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA.

Journal of Neurophysiology
|July 13, 1999
PubMed

Insights

Odor stimulation in rat olfactory receptor neurons (ORNs) can activate cyclic nucleotide-gated (CNG) channels or inhibit a voltage-activated potassium current (IKo). This potassium channel modulation suggests a novel role for odorant-induced K+ conductance changes in olfactory signal transduction.

Area of Science:

  • Neuroscience
  • Olfactory Receptor Neuron Physiology
  • Signal Transduction

Background:

  • Odor stimulation of olfactory receptor neurons (ORNs) typically increases cAMP, opening cyclic nucleotide-gated (CNG) channels and causing depolarization.
  • While CNG channel activation is the primary known mechanism, other ion conductances may be modulated by odorants.

Purpose of the Study:

  • To investigate whether potassium (K+) conductances are modulated by odorants in mammalian ORNs.
  • To elucidate the role of K+ conductance modulation in olfactory signal transduction.

Main Methods:

  • Recording membrane current in rat ORNs using perforated-patch techniques.
  • Applying various odorants to stimulate ORNs and observing changes in ion conductance.
  • Characterizing the inhibited K+ conductance (IKo) pharmacologically and electrophysiologically.

Main Results:

  • Odorant stimulation elicited two main responses in rat ORNs: 30% showed CNG channel activation, while 55% exhibited inhibition of a voltage-activated K+ conductance (IKo).
  • The inhibited IKo shared characteristics with delayed rectifier K+ channels.
  • Odorant-induced IKo inhibition was specific, concentration-dependent, and showed a latency, indicating an indirect mechanism.

Conclusions:

  • Odorants can indirectly suppress a voltage-activated K+ conductance (IKo) in mammalian ORNs.
  • This suppression of IKo represents a significant, previously underappreciated mechanism in olfactory signal transduction.
  • Modulation of K+ conductances contributes to the complex processing of olfactory information.

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