Highlights d Prestin is considered to be expressed exclusively in outer hair cells of the inner ear d The current study shows that prestin is expressed in cardiomyocytes d Prestin serves to amplify actin-myosin force generation in cardiomyocytes d Prestin serves a broader cellular motor function
The extracellular potential of excitable and nonexcitable cells with respect to ground is ϳ0 mV. One of the known exceptions in mammals is the cochlear duct, where the potential is ϳ80 -100 mV, called the endocochlear potential (EP). The EP serves as the "battery" for transduction of sound, contributing toward the sensitivity of the auditory system. The stria vascularis (StV) of the cochlear duct is the station where the EP is generated, but the cell-specific roles in the StV are ill defined. Using the intermediate cell (IC)-specific tyrosinase promoter, under the control of diphtheria toxin (DT), we eliminated and/or halted differentiation of neural crest melanocytes after migration to the StV. The ensuing adult transgenic mice are profoundly deaf. Additionally, the EP was abolished. Expression of melanocyte early marker and Kir4.1 in ICs precedes the onset of pigment synthesis. Activation of DT leads to loss of ICs. Finally, in accord with the distinct embryology of retinal pigmented cells, transgenic mice with toxigenic ablation of neural crest-derived melanocytes have intact visual responses. We assert that the tyrosinase promoter is the distinct target for genetic manipulation of IC-specific genes.
Background: KCNE3 is tentatively associated with inner ear diseases, but its functions are unknown. Results: Null deletion of Kcne3 produces profound changes in the excitability of auditory neurons. Conclusion: KCNE3 regulates the magnitude of K ϩ conductances responsible for maintaining the electrical phenotype of
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