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J. Biol. Chem., Vol. 276, Issue 33, 31233-31237, August 17, 2001
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From the Departments of Medicine and Physiology,
Cardiovascular Research Institute, University of California, San
Francisco, California 94143-0521
A role for aquaporins (AQPs) in hearing has been
suggested from the specific expression of aquaporins in inner ear and
the need for precise volume regulation in epithelial cells involved in
acoustic signal transduction. Using mice deficient in selected aquaporins as controls, we localized AQP1 in fibrocytes in the spiral
ligament and AQP4 in supporting epithelial cells (Hensen's, Claudius, and inner sulcus cells) in the organ of Corti. To
determine whether aquaporins play a role in hearing, auditory brain
stem response (ABR) thresholds were compared in wild-type mice and transgenic null mice lacking (individually) AQP1, AQP3, AQP4, and AQP5.
In 4-5-week-old mice in a CD1 genetic background, ABR thresholds in
response to a click stimulus were remarkably increased by >12 db in
AQP4 null mice compared with wild-type mice (p < 0.001), whereas ABR thresholds were not affected by AQP1, AQP3, or AQP5
deletion. In a C57/bl6 background, nearly all AQP4 null mice were deaf,
whereas ABRs could be elicited in wild-type controls. ABRs in AQP4 null
CD1 mice measured in response to tone bursts (4-20 kHz) indicated a
frequency-independent hearing deficit. Light microscopy showed no
differences in cochlear morphology of wild-type versus AQP4
null mice. These results provide the first direct evidence that an
aquaporin water channel plays a role in hearing. AQP4 may facilitate
rapid osmotic equilibration in epithelial cells in the organ of Corti,
which are subject to large K+ fluxes during
mechano-electric signal transduction.
Impaired Hearing in Mice Lacking Aquaporin-4 Water Channels*
*
This study was supported by National Institutes of Health
Grants HL59198, DK35124, HL60288, and DK43840 and Grant R613 from the
National Cystic Fibrosis Foundation.The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
To whom correspondence should be addressed: Cardiovascular
Research Institute, 1246 Health Sciences East Tower, Box 0521, University of California, San Francisco, San Francisco, CA. 94143-0521. Tel.: 415-476-8530; Fax: 415-665-3847; E-mail:
verkman@itsa.ucsf.edu.
Copyright © 2001 by The American Society for Biochemistry and Molecular Biology, Inc.
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