Since the prestin protein is the key component of somatic motility, in previous experiments Zuo and his colleagues genetically knocked out prestin in mice and tested the effects on hearing. Those mice showed a hearing defect that indicated a malfunction of somatic motility. While the knockout experiments were strong evidence for the role of somatic motility, the affected mice also showed structural abnormalities in their outer hair cells, Zuo said, thus complicating the interpretation.
In the new experiments to more unequivocally establish the role of somatic motility, the researchers genetically altered mice to have only subtle alterations in the prestin protein. These alterations only compromised prestins function as an amplifier but did not otherwise affect the outer hair cell structure or function, the researchers analysis showed.
We found that these mice showed exactly the same kinds of hearing deficiency as the previous knockout mice, Zuo said. Therefore, we believe that these experiments eliminate criticism of our earlier experiments with the knockout mice. The new experiments, Zuo said, thus firmly establish that the dancing somatic motility of the outer hair cells is critical to cochlear amplification.
However, he noted, With this study we still cannot really exclude stereociliary motility from contributing to cochlear amplification, because eliminating somatic motility also reduces ciliary motility. So, it is not possible to totally isolate either form of motility. In fact, we hypothesize that the two mechanisms might work together in different aspects of amplification.
By finding prestins role in hearing Zuo and his colleagues may help scientists better understand the mechanisms of hearing loss. For example, an overdose of aspirin causes a high-frequency hearing loss by inhibiting prestins function, Zuo sa
|Contact: Carrie Strehlau|
St. Jude Children's Research Hospital