Ca2+-activated Cl- currents are dispensable for olfaction
Ca2+-activated Cl- currents are dispensable for olfaction
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DOI：
10.1038/nn.2821
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发表时间：
2011-06-01
影响因子：
25
通讯作者：
Jentsch, Thomas J.
中科院分区：
文献类型：
--
作者：
Billig, Gwendolyn M.;Pal, Balazs;Jentsch, Thomas J.
典型的嗅觉信号转导涉及激活环AMP激活的阳离子通道，使感受器神经元的纤毛去极化并升高细胞内钙离子。然后，钙激活可能比阳离子电流大十倍的氯离子电流，并被认为有力地放大了这一反应。我们鉴定AnocTamin2(AnocTamin2，也称为TMEM16B)是嗅觉感受器神经元的纤毛钙激活的氯通道。Ano2在嗅主上皮(MOE)和犁鼻器(VNO)中表达，也表达相关的Ano1通道。阻断小鼠的Ano2几乎消除了MOE和VNO中钙激活的氯电流。阻断Ano2仅使液相嗅觉反应减少约40%，不改变气相嗅觉反应，也不会降低嗅觉行为任务的表现。与目前的观点不同，环核苷酸门控阳离子通道不需要氯离子通道的促进就可以达到接近生理水平的嗅觉。
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 similar to 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.