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Published on: February 21, 2016
Olfactory epithelia exhibit progressive functional and morphological defects in CF mice
Barbara R Grubb1, Troy D Rogers, Heather M Kulaga
1CF/Pulmonary Research and Treatment Center, The University of North Carolina, Chapel Hill, NC 27599-7248, USA. bgrubb@med.unc.edu
American Journal of Physiology. Cell Physiology
|April 13, 2007
Summary
Cystic fibrosis (CF) mice show olfactory dysfunction due to abnormal sodium absorption in the nasal epithelium, leading to reduced olfactory receptor neurons. This mouse model offers insights into olfactory deficits in CF patients.
Area of Science:
- Neuroscience
- Genetics
- Physiology
Background:
- Olfactory receptor neurons (ORNs) in normal nasal epithelium undergo continuous replacement.
- Cystic fibrosis (CF) mouse olfactory epithelium (OE) develops sustentacular cell dysmorphology and ORN reduction by 6 months of age.
Purpose of the Study:
- To investigate the mechanisms behind olfactory dysfunction in CF mice.
- To characterize the physiological changes in the OE of CF mice.
Main Methods:
- Electroolfactography to measure odor-evoked responses.
- Ussing chamber studies to assess ion transport in OE.
- Histological examination of OE morphology.
Main Results:
- CF mice exhibited significantly reduced odor-evoked responses (45% at 30 days, 70% in older mice) compared to wild type (WT).
- OE from CF mice showed impaired forskolin-stimulated Cl(-) secretion and a 12-fold increase in amiloride-sensitive Na(+) absorption compared to WT.
- Evidence of sustentacular cell dysmorphology and ORN reduction in 6-month-old CF mice.
Conclusions:
- Abnormal Na(+) hyperabsorption by olfactory sustentacular cells in CF mice likely causes surface layer desiccation and subsequent ORN degeneration.
- The CF mouse serves as a valuable model for studying the mechanisms of olfactory loss associated with CF and other diseases.
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