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REPORT
Department of Cell Biology, Neurobiology, and Anatomy, University of Cincinnati, Cincinnati, Ohio
Submitted 12 September 2005; accepted in final form 28 November 2005
When stimulated with odorants, olfactory receptor neurons (ORNs) produce a depolarizing receptor current. In isolated ORNs, much of this current is caused by an efflux of Cl–. This implies that the neurons have one or more mechanisms for accumulating cytoplasmic Cl– at rest. Whether odors activate an efflux of Cl– in intact olfactory epithelium, where the ionic environment is poorly characterized, has not been previously determined. In mouse olfactory epithelium, we found that >80% of the summated electrical response to odors is blocked by niflumic acid or flufenamic acid, each of which inhibits Ca2+-activated Cl– channels in ORNs. This indicates that ORNs accumulate Cl– in situ. Recent evidence has shown that NKCC1, a Na+-K+-2Cl– cotransporter, contributes to Cl– accumulation in mammalian ORNs. However, we find that the epithelial response to odors is only reduced by 39% in mice carrying a null mutation in Nkcc1. As in the wild-type, most of the response is blocked by niflumic acid or flufenamic acid, indicating that the underlying current is carried by Cl–. We conclude that ORNs effectively accumulate Cl– in situ even in the absence of NKCC1. The Cl–-transport mechanism underlying this accumulation has not yet been identified.
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