Mechano-electrical transduction in mice lacking the α-subunit of the epithelial sodium channel

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 Na + channel, ENaC, might be a candidate gene for this function. In order to test this hypothesis, we examined knockout mice deficient in the α-subunit of ENaC, and therefore in ENaC function. First, neonatal αENaC(−/−) 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 αENaC(−/−) mice. When hair bundles of cochlear outer hair cells of αENaC(−/−) 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 αENaC(+/−) or (+/+) cochlear outer hair cells. These results suggest that the vertebrate mechano-electrical transducer apparatus does not include the α-subunit of the epithelial Na + channel.