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Ca2+-activated Cl− currents are dispensable for olfaction

2011; Nature Portfolio; Volume: 14; Issue: 6 Linguagem: Inglês

10.1038/nn.2821

1546-1726

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

Advanced Chemical Sensor Technologies

Calcium-activated chloride currents are thought to amplify the olfactory signal during the transduction process. Here the authors identify Ano2 as the critical channel in both main olfactory epithelium and in the vomeronasal organ. Surprisingly, disruption of Ano2 did not reduce performance in an olfactory behavioral task, suggesting that olfaction does not actually depend on these channels. 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 ∼40%, 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.