Ca2+-activated Cl- currents are dispensable for olfaction

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

Research output: Contribution to journalArticle

142 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 1 2011

ASJC Scopus subject areas

  • Neuroscience(all)

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