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This Article Full Text Full Text (PDF) Supplemental data All Versions of this Article: 583/3/1005    most recent jphysiol.2007.129601v1 Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Nickell, W. T. Articles by Kleene, S. J. Search for Related Content PubMed PubMed Citation Articles by Nickell, W. T. Articles by Kleene, S. J. Related Collections Neuroscience

¹ Department of Cell and Cancer Biology, University of Cincinnati, Cincinnati, OH 45267, USA

When olfactory receptor neurons respond to odours, a depolarizing Cl^– efflux is a substantial part of the response. This requires that the resting neuron accumulate Cl^– against an electrochemical gradient. In isolated olfactory receptor neurons, the Na⁺–K⁺–2Cl^– cotransporter NKCC1 is essential for Cl^– accumulation. However, in intact epithelium, a robust electrical olfactory response persists in mice lacking NKCC1. This response is largely due to a neuronal Cl^– efflux. It thus appears that NKCC1 is an important part of a more complex system of Cl^– accumulation. To identify the remaining transport proteins, we first screened by RT-PCR for 21 Cl^– transporters in mouse nasal tissue containing olfactory mucosa. For most of the Cl^– transporters, the presence of mRNA was demonstrated. We also investigated the effects of pharmacological block or genetic ablation of Cl^– transporters on the olfactory field potential, the electroolfactogram (EOG). Mice lacking the common Cl^–/HCO₃^– exchanger AE2 had normal EOGs. Block of NKCC cotransport with bumetanide reduced the EOG in epithelia from wild-type mice but had no effect in mice lacking NKCC1. Hydrochlorothiazide, a blocker of the Na⁺–Cl^– cotransporter, had only a small effect. DIDS, a blocker of some KCC cotransporters and Cl^–/HCO₃^– exchangers, reduced the EOG in epithelia from both wild-type and NKCC1 knockout mice. A combination of bumetanide and DIDS decreased the response more than either drug alone. However, no combination of drugs completely abolished the Cl^– component of the response. These results support the involvement of both NKCC1 and one or more DIDS-sensitive transporters in Cl^– accumulation in olfactory receptor neurons.

(Received 19 March 2007; accepted after revision 25 July 2007; first published online 26 July 2007)
Corresponding author S. J. Kleene: Department of Cell and Cancer Biology, University of Cincinnati, PO Box 670667, Cincinnati, OH 45267, USA. Email: steve{at}syrano.acb.uc.edu

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