| First Author | Rüsch A | Year | 1999 |
| Journal | Hear Res | Volume | 131 |
| Issue | 1-2 | Pages | 170-6 |
| PubMed ID | 10355613 | Mgi Jnum | J:55291 |
| Mgi Id | MGI:1337584 | Doi | 10.1016/s0378-5955(99)00030-1 |
| Citation | Rusch A, et al. (1999) Mechano-electrical transduction in mice lacking the alpha-subunit of the epithelial sodium channel. Hear Res 131(1-2):170-6 |
| abstractText | Sensory hair cells of the vertebrate inner ear use mechanically gated transducer channels (MET) to perceive mechanical stimuli. The molecular nature of the MET channel is not known but several findings suggested that the amiloride-sensitive epithelial Naf channel, ENaC, might be a candidate gene for this function. In order to test this hypothesis, we examined knockout mice deficient in the alpha-subunit of ENaC, and therefore in ENaC function. First, neonatal alpha ENaC(-/-) mice exhibited vestibular reflexes not different from wildtype littermates thus indicating normal vestibular function. We used organotypic cultures of cochlear outer hair cells from newborns to rescue the hair cells from the perinatal death of alpha ENaC(-/-) mice. When hair bundles of cochlear outer hair cells of alpha ENaC(-/-) mice were mechanically stimulated by a fluid jet in whole cell voltage clamp experiments, transducer currents were elicited that were not significantly different from those of alpha ENaC(+/-) or (+/+) cochlear outer hair cells. These results suggest that the vertebrate mechano- electrical transducer apparatus does not include the alpha- subunit of the epithelial Na+ channel. (C) 1999 Elsevier Science B.V. All rights reserved. |
