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J Speech Lang Hear Res. 2009 Jun;52(3):745-54. doi: 10.1044/1092-4388(2008/07-0192). Epub 2008 Sep 19.

The cystic fibrosis transmembrane conductance regulator and chloride-dependent ion fluxes of ovine vocal fold epithelium.

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Department of Speech Communication Arts and Sciences, Brooklyn College of The City University of New York, 2900 Bedford Avenue, Brooklyn, NY 11210, USA.



Ion-driven transepithelial water fluxes participate in maintaining superficial vocal fold hydration, which is necessary for normal voice production. The authors hypothesized that Cl(-) channels are present in vocal fold epithelial cells and that transepithelial Cl(-) fluxes can be manipulated pharmacologically.


Immunohistochemical assays were used to identify cystic fibrosis transmembrane regulator Cl(-) channels in ovine vocal fold mucosae (n = 2). Electrophysiological responses of vocal fold mucosae (n = 80) to Cl(-) channel inhibitors and secretagogues were evaluated in an ovine model using a randomized controlled experimental design.


Cystic fibrosis transmembrane regulator channels were localized to the plasma membranes of epithelial cells. The Cl(-) transport inhibitor, diphenylamine-2-carboxylate, elicited a 30% decrease in mean short-circuit current (I(sc); n = 10). The secretagogue, isobutylmethylxanthine, yielded a 31.7% increase in mean I(sc) (n = 10). Another secretagogue, uridine triphosphate, elicited a 48.8% immediate and 17.3% sustained increase in mean I(sc) (n = 10). No sustained increases occurred following application of secretagogues to mucosae bathed in a low Cl(-) environment (n = 10), suggesting that responses were Cl(-) dependent.


The authors provide structural and functional evidence for the presence of a transepithelial pathway for Cl(-) fluxes. Pharmacological manipulation of this pathway may offer a mechanism for maintaining superficial vocal fold hydration.

[Indexed for MEDLINE]

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