Journal
NEURON
Volume 45, Issue 4, Pages 553-561Publisher
CELL PRESS
DOI: 10.1016/j.neuron.2005.01.012
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Funding
- NEI NIH HHS [R01 EY014596-03, R01 EY014596-01, R37 EY006837-15S1, R01 EY006837-17, R01 EY014596-02, R01 EY014596, R01 EY006837-18, R37 EY006837, R01 EY006837, R01 EY006837-16A1, R37 EY006837-15] Funding Source: Medline
- NIDCD NIH HHS [DC 06904, R01 DC006904, R01 DC006904-01] Funding Source: Medline
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In vertebrate olfactory receptor neurons (ORNs), the odorant-triggered receptor current flows through two distinct ion channels on the sensory cilia: Ca2+ influx through a cyclic nucleotide-gated (CNG) channel followed by CI- efflux through a Ca2+-activated anion channel. The excitatory CI- current amplifies the small CNG current and crucially depends on a high intracellular CI- concentration. We show here that a Na+-K+-2CI(-) cotransporter, NKCC1, is required for this CI- current, in that ORNs deficient in NKCC1 or incubated with an NKCC blocker (bumetanide) lack the CI- current. Surprisingly, immunocytochemistry indicates that NKCC1 is located on the somata and dendrites of ORNs rather than the cilia, where transduction occurs. This topography is remarkably similar to the situation in secretory epithelial cells, where basolateral CI- uptake and apical CI- efflux facilitate transepithelial fluid movement. Thus, a single functional architecture serves two entirely different purposes, probably underscoring the epithelial origin of the ORNs.
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