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Related Experiment Video

Updated: Jun 2, 2026

Flash Photolysis of Caged Compounds in the Cilia of Olfactory Sensory Neurons

Flash Photolysis of Caged Compounds in the Cilia of Olfactory Sensory Neurons

Published on: October 29, 2011

Ca2+-activated Cl− currents are dispensable for olfaction.

Gwendolyn M Billig¹, Balázs Pál, Pawel Fidzinski

¹Leibniz-Institut für Molekulare Pharmakologie (FMP)/Max-Delbrück-Centrum für Molekulare Medizin (MDC), Berlin, Germany.

Nature Neuroscience

|April 26, 2011

Summary

This summary is machine-generated.

Anoctamin2 (Ano2) is the primary calcium-activated chloride channel in olfactory neurons. Its absence significantly reduces but does not eliminate olfactory responses, challenging existing models of olfactory amplification.

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Area of Science:

Neuroscience
Olfactory receptor neuron physiology
Ion channel function

Background:

Olfactory signal transduction relies on cation channels and calcium-activated chloride currents.
Chloride currents are thought to amplify olfactory neuron depolarization and responses.
The specific chloride channel responsible for this amplification in olfaction remained unidentified.

Purpose of the Study:

To identify the ciliary Ca(2+)-activated Cl(-) channel in olfactory receptor neurons.
To investigate the role of this channel in olfactory signal transduction and behavior.

Main Methods:

Identification of Anoctamin2 (Ano2) as the Ca(2+)-activated Cl(-) channel in olfactory neurons.
Generation of Ano2-deficient mice to study the channel's function.
Electrophysiological recordings (electro-olfactograms) in the main olfactory epithelium (MOE) and vomeronasal organ (VNO).
Assessment of olfactory behavioral tasks in Ano2-deficient mice.

Main Results:

Ano2 was identified as the ciliary Ca(2+)-activated Cl(-) channel in the MOE and VNO.
Ano2 disruption in mice abolished Ca(2+)-activated Cl(-) currents in these tissues.
Ano2 deficiency reduced fluid-phase electro-olfactogram responses by approximately 40% but did not affect air-phase responses or olfactory behavior.
These findings suggest cyclic nucleotide-gated cation channels do not require Cl(-) channel boost for near-physiological olfaction.

Conclusions:

Anoctamin2 is the principal Ca(2+)-activated Cl(-) channel in olfactory neurons.
While important, Ano2 is not essential for all aspects of olfactory function or behavior.
The current understanding of olfactory signal amplification may need revision, as cation channels alone appear sufficient for significant olfactory capabilities.