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1 Medicine, UNC - Chapel Hill, Chapel Hill, North Carolina, United States
2 CF Center, UNC - Chapel HIll, Medicine, Chapel Hill, North Carolina, United States
3 Howard Hughes Medical Institute and Department of Molecular Biology and Genetics, Johns Hopkins University, Baltimore, Maryland, United States
4 Medicine, CF Center, UNC - Chapel Hill, Chapel Hill, North Carolina, United States
5 Chapel Hill, North Carolina, United States; CF Center, UNC - Chapel HIll, Medicine, Chapel Hill, North Carolina, United States
6 HHMI/Johns Hopkins, United States; HHMI/Johns Hopkins
* To whom correspondence should be addressed. E-mail: bgrubb{at}med.unc.edu.
In normal nasal epithelium, the olfactory receptor neurons (ORNs) are continuously replaced through the differentiation of progenitor cells. The olfactory epithelium (OE) of the cystic fibrosis (CF) mouse appears normal at birth, yet by 6 months of age, a marked dysmorphology of sustentacular cells and a dramatic reduction in olfactory receptor neurons are evident. Electro-olfactograms (EOG) revealed that the odor-evoked response in 30 d old CF mice was reduced ~45%; in older CF mice, a ~70% reduction was observed compared to the wildtype (WT) response. Consistent with studies of CF airway epithelia, Ussing chamber studies of OE isolated from CF mice showed a lack of forskolin-stimulated Cl- secretion and a ~12-fold increase in amiloride-sensitive sodium absorption, compared to WT mice. We hypothesize that the marked hyperabsorption of Na+, most likely by olfactory sustentacular cells, leads to desiccation of the surface layer in which the sensory cilia reside, followed by degeneration of the ORNs. The CF mouse thus provides a novel model to examine the mechanisms of disease associated loss of olfactory function.
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