Abstract
Several members of the SLC26 gene family have highly-restricted expression patterns in the auditory and vestibular periphery and mutations in mice of at least two of these (SLC26A4 and SLC26A5) lead to deficits in hearing and/or balance. A previous report pointed to SLC26A7 as a candidate gene important for cochlear function. In the present study, inner ears were assayed by immunostaining for Slc26a7 in neonatal and adult mice. Slc26a7 was detected in the basolateral membrane of Reissner’s membrane epithelial cells but not neighboring cells, with an onset of expression at P5; gene knockout resulted in the absence of protein expression in Reissner’s membrane. Whole-cell patch clamp recordings revealed anion currents and conductances that were elevated for NO3 − over Cl− and inhibited by I− and NPPB. Elevated NO3 − currents were absent in Slc26a7 knockout mice. There were, however, no major changes to hearing (auditory brainstem response) of knockout mice during early adult life under constitutive and noise exposure conditions. The lack of Slc26a7 protein expression found in the wild-type vestibular labyrinth was consistent with the observation of normal balance. We conclude that SLC26A7 participates in Cl− transport in Reissner’s membrane epithelial cells, but that either other anion pathways, such as ClC-2, possibly substitute satisfactorily under the conditions tested or that Cl− conductance in these cells is not critical to cochlear function. The involvement of SLC26A7 in cellular pH regulation in other epithelial cells leaves open the possibility that SLC26A7 is needed in Reissner’s membrane cells during local perturbations of pH.
Highlights
The extra-sensory epithelium of the inner ear consists of many cell types that contribute to the maintenance of the unusual composition of the cochlear and vestibular lumen
Slc26a4/pendrin mediates HCO32 secretion and Slc26a5/prestin is the motor protein that supports outer hair cell electromotility, which is a key element in selectivity and sensitivity of hearing [4]
The onset of expression occurred at post-natal day 5 (P5) (Figure 2), which corresponds to the onset of functional Na+ absorption in Reissner’s membrane [13]
Summary
The extra-sensory epithelium of the inner ear consists of many cell types that contribute to the maintenance of the unusual composition of the cochlear and vestibular lumen. The luminal fluid, endolymph, is very high in K+ (,150 mM) and low in Na+ (1 mM cochlea, 10 mM vestibule) and Ca2+ (25 mM cochlea, 250 mM vestibule), a composition that is essential to support transduction of sound and acceleration via the sensory hair cells [1]. It is known that Reissner’s membrane in the cochlea contributes to homeostasis of endolymph by glucocorticoidregulated absorption of Na+ [2,3], but other potential transport pathways in this epithelium have not yet been determined. Slc26a7 is a member of the Slc transporter family, two others of which have limited expression in the inner ear and which support critical physiological functions. Knockout of either of these genes in mice leads to deafness [5,6]
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