Prestin and Motility of the Cochlear Outer Hair Cell.
- Author:
Chul Hee CHOI
1
Author Information
1. Department of Audiology and Speech-Language Pathology and Research Institute of Biomimetic Sensory Control, College of Medical Sciences, Catholic University of Daegu, Gyeongsan, Korea. cchoi@cu.ac.kr
- Publication Type:Review
- Keywords:
Outer hair cells (OHCs);
Electromotility;
Prestin;
Cochlear amplification;
OHC length;
Noise-induced hearing loss;
Ototoxicity
- MeSH:
Acoustics;
Animals;
Anti-Bacterial Agents;
Apoptosis;
Cell Membrane;
Hair;
Hearing;
Hearing Loss, Noise-Induced;
Humans;
Membrane Potentials;
Membranes;
Mice;
Mice, Knockout;
Noise;
Proteins
- From:Korean Journal of Audiology
2011;15(3):101-106
- CountryRepublic of Korea
- Language:English
-
Abstract:
The main objective of this study is to describe the role and function of prestin on cochlear amplification based on the relationship of electromotility and prestin in the outer hair cells (OHCs). After the finding of cochlear active process or amplification, OHCs have been received a lot of attention as a source of the cochlear amplification. In response to acoustic signals, the OHCs produce the receptor potentials resulting in changes in the length of the OHCs called electromotility. The electromotility originates within the lateral wall of the OHCs and relates to the unique structures of the OHCs. The OHC electromotility depends on particles of the lateral plasma membrane due to an area motor in the lateral plasma membrane. Recently, it has been reported that the electromotility requires a voltage-dependent membrane based motor protein, prestin. Prestin means fast in Italian. The presence of prestin is essential for cochlear amplification and electromotility. Prestin is a member of solute carrier 26 anion transporter family. Prestin is associated with the unique structure of the lateral wall of the OHCs. Prestin forms motor complexes with other proteins and lipids of the lateral wall sensing the transmembrane potential and generating force by changing its surface area. Recently, prestin knockout mice have been used to prove the presence of prestin. Prestin is required for electromotility of the OHCs and for cochlear amplification in normal hearing because targeted depletion of prestin in mice leads to loss of OHC electromotility and loss of hearing sensitivity up to 60 dB. In addition, recent studies have shown that the loss of cochlear amplification after intense noise exposure can result from damage to prestin and prestin involves in the process of aminoglycoside-induced apoptosis in OHCs. These show that prestin plays an important role in transducing apoptosis signals in response to antibiotics. Therefore, the presence of prestin is mandatory for cochlear active process and amplification in normal hearing.
