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CFTR-Regulated Chloride Transport at the Ocular Surface in Living Mice Measured by Potential Differences

From the Departments of Medicine and Physiology, Cardiovascular Research Institute, University of California San Francisco, San Francisco, California.

PURPOSE. To define the role of the cystic fibrosis transmembrane conductance regulator (CFTR) in Cl^– secretion at the mouse ocular surface in vivo.

METHODS. Open-circuit potential differences (PDs) across the fluid-bathed ocular surface were measured in anesthetized wild-type and cystic fibrosis (CF) mice in response to Cl^– ion substitution and transport agonists and inhibitors.

RESULTS. Basal ocular surface PD was –23 ± 1 mV (SE; 20 wild-type mice), depolarizing to –16 ± 2 mV after amiloride, then hyperpolarizing to –34 ± 3 mV after low Cl^–. CFTR activation by forskolin or a selective activator caused further sustained hyperpolarization to –50 to –60 mV. UTP produced a comparable but transient hyperpolarization. The CFTR inhibitors CFTR_inh-172 and GlyH-101 largely reversed agonist- but not low Cl^–-induced hyperpolarizations. PD in CF mice hyperpolarized by 2.1 mV after low Cl^– and was insensitive to CFTR activators or inhibitors.

CONCLUSIONS. CFTR provides a major pathway for mouse ocular surface Cl^– secretion, suggesting the application of CFTR activators as therapy for dry eye. Amiloride-sensitive Na⁺ transporters facilitate Na⁺ absorption. PD measurements provide a robust and reproducible means of assessing ocular surface ion transporting mechanisms.

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