Ca2+-activated Cl- currents are dispensable for olfaction

Gwendolyn M. Billig, B. Pál, Pawel Fidzinski, Thomas J. Jentsch

Research output: Contribution to journalArticle

136 Citations (Scopus)

Abstract

Canonical olfactory signal transduction involves the activation of cyclic AMP-activated cation channels that depolarize the cilia of receptor neurons and raise intracellular calcium. Calcium then activates Cl- currents that may be up to tenfold larger than cation currents and are believed to powerfully amplify the response. We identified Anoctamin2 (Ano2, also known as TMEM16B) as the ciliary Ca2+-activated Cl- channel of olfactory receptor neurons. Ano2 is expressed in the main olfactory epithelium (MOE) and in the vomeronasal organ (VNO), which also expresses the related Ano1 channel. Disruption of Ano2 in mice virtually abolished Ca2+-activated Cl - currents in the MOE and VNO. Ano2 disruption reduced fluid-phase electro-olfactogram responses by only 440%, did not change air-phase electro-olfactograms and did not reduce performance in olfactory behavioral tasks. In contrast with the current view, cyclic nucleotide-gated cation channels do not need a boost by Cl- channels to achieve near-physiological levels of olfaction.

Original languageEnglish
Pages (from-to)763-769
Number of pages7
JournalNature Neuroscience
Volume14
Issue number6
DOIs
Publication statusPublished - Jun 2011

Fingerprint

Vomeronasal Organ
Olfactory Mucosa
Smell
Cations
Cyclic Nucleotide-Gated Cation Channels
Olfactory Receptor Neurons
Calcium
Cilia
Cyclic AMP
Signal Transduction
Air
Neurons

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

Ca2+-activated Cl- currents are dispensable for olfaction. / Billig, Gwendolyn M.; Pál, B.; Fidzinski, Pawel; Jentsch, Thomas J.

In: Nature Neuroscience, Vol. 14, No. 6, 06.2011, p. 763-769.

Research output: Contribution to journalArticle

Billig, GM, Pál, B, Fidzinski, P & Jentsch, TJ 2011, 'Ca2+-activated Cl- currents are dispensable for olfaction', Nature Neuroscience, vol. 14, no. 6, pp. 763-769. https://doi.org/10.1038/nn.2821
Billig, Gwendolyn M. ; Pál, B. ; Fidzinski, Pawel ; Jentsch, Thomas J. / Ca2+-activated Cl- currents are dispensable for olfaction. In: Nature Neuroscience. 2011 ; Vol. 14, No. 6. pp. 763-769.
@article{07c9ea5c3e794cbbb1bc47ba55eda295,
title = "Ca2+-activated Cl- currents are dispensable for olfaction",
abstract = "Canonical olfactory signal transduction involves the activation of cyclic AMP-activated cation channels that depolarize the cilia of receptor neurons and raise intracellular calcium. Calcium then activates Cl- currents that may be up to tenfold larger than cation currents and are believed to powerfully amplify the response. We identified Anoctamin2 (Ano2, also known as TMEM16B) as the ciliary Ca2+-activated Cl- channel of olfactory receptor neurons. Ano2 is expressed in the main olfactory epithelium (MOE) and in the vomeronasal organ (VNO), which also expresses the related Ano1 channel. Disruption of Ano2 in mice virtually abolished Ca2+-activated Cl - currents in the MOE and VNO. Ano2 disruption reduced fluid-phase electro-olfactogram responses by only 440{\%}, did not change air-phase electro-olfactograms and did not reduce performance in olfactory behavioral tasks. In contrast with the current view, cyclic nucleotide-gated cation channels do not need a boost by Cl- channels to achieve near-physiological levels of olfaction.",
author = "Billig, {Gwendolyn M.} and B. P{\'a}l and Pawel Fidzinski and Jentsch, {Thomas J.}",
year = "2011",
month = "6",
doi = "10.1038/nn.2821",
language = "English",
volume = "14",
pages = "763--769",
journal = "Nature Neuroscience",
issn = "1097-6256",
publisher = "Nature Publishing Group",
number = "6",

}

TY - JOUR

T1 - Ca2+-activated Cl- currents are dispensable for olfaction

AU - Billig, Gwendolyn M.

AU - Pál, B.

AU - Fidzinski, Pawel

AU - Jentsch, Thomas J.

PY - 2011/6

Y1 - 2011/6

N2 - Canonical olfactory signal transduction involves the activation of cyclic AMP-activated cation channels that depolarize the cilia of receptor neurons and raise intracellular calcium. Calcium then activates Cl- currents that may be up to tenfold larger than cation currents and are believed to powerfully amplify the response. We identified Anoctamin2 (Ano2, also known as TMEM16B) as the ciliary Ca2+-activated Cl- channel of olfactory receptor neurons. Ano2 is expressed in the main olfactory epithelium (MOE) and in the vomeronasal organ (VNO), which also expresses the related Ano1 channel. Disruption of Ano2 in mice virtually abolished Ca2+-activated Cl - currents in the MOE and VNO. Ano2 disruption reduced fluid-phase electro-olfactogram responses by only 440%, did not change air-phase electro-olfactograms and did not reduce performance in olfactory behavioral tasks. In contrast with the current view, cyclic nucleotide-gated cation channels do not need a boost by Cl- channels to achieve near-physiological levels of olfaction.

AB - Canonical olfactory signal transduction involves the activation of cyclic AMP-activated cation channels that depolarize the cilia of receptor neurons and raise intracellular calcium. Calcium then activates Cl- currents that may be up to tenfold larger than cation currents and are believed to powerfully amplify the response. We identified Anoctamin2 (Ano2, also known as TMEM16B) as the ciliary Ca2+-activated Cl- channel of olfactory receptor neurons. Ano2 is expressed in the main olfactory epithelium (MOE) and in the vomeronasal organ (VNO), which also expresses the related Ano1 channel. Disruption of Ano2 in mice virtually abolished Ca2+-activated Cl - currents in the MOE and VNO. Ano2 disruption reduced fluid-phase electro-olfactogram responses by only 440%, did not change air-phase electro-olfactograms and did not reduce performance in olfactory behavioral tasks. In contrast with the current view, cyclic nucleotide-gated cation channels do not need a boost by Cl- channels to achieve near-physiological levels of olfaction.

UR - http://www.scopus.com/inward/record.url?scp=79960843311&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=79960843311&partnerID=8YFLogxK

U2 - 10.1038/nn.2821

DO - 10.1038/nn.2821

M3 - Article

C2 - 21516098

AN - SCOPUS:79960843311

VL - 14

SP - 763

EP - 769

JO - Nature Neuroscience

JF - Nature Neuroscience

SN - 1097-6256

IS - 6

ER -