Prestin and Motility of the Cochlear Outer Hair Cell

다국어 초록 (Multilingual Abstract)

Introduction



Hearing sensitivity in normal mammals is drastically improved by about 40 dB by a cochlear amplifier, which is involved with mechano-electrical transduction (MET) located within the stereocilia on the apex of the cells modulating receptor potentials in response to hair cell bundle deflection,1,2,3,4,5,6,7) and electromotility placed in the outer hair cell (OHC) lateral wall triggering changes in the OHC length in response to the receptor potentials.4,8,9,10) While MET has been observed in both inner and outer hair cells of non-mammals and mammals, electromotility has been only observed in OHC of mammals. Recently, it has reported that OHC electromotility requires a voltage-dependent membrane based motor protein, prestin which is a member of solute carrier (SLC) 26 anion transporter family.11,12) That is, the presence of prestin is essential for the OHC electromotility and for cochlear amplification. Therefore, this paper deals with the recent studies identifying the relationship between prestin and electromotility, the recent findings of the structure and function of prestin, and the recent prestin-related topics.


OHC Electromotility and Cochlear Amplification

When acoustic signals reach the ear, they evoke the motion of the basilar membrane containing a single row of inner hair cells and three rows of OHC, which deflects the hair cell bundle located in the stereocilia by opening of the transduction channels.13,14,15) When the hair cell bundle deflects to the tallest stereocilia, the transduction channels open and allow K+ and Ca2+ ions into the OHC, which leads to an increase of the hair cell receptor potential resulting in depolarization.16) When the hair cell bundle deflects to the opposite direction, the channels close and outflow the ions out of the OHC, which leads to a decrease of the hair cell receptor potential resulting in hyperpolarization. The hair cell receptor potential drives to change the length of the OHC soma.4) Depolarization causes the OHC to contract along its longitudinal axis while hyperpolarization causes it to expand. The modulation of the length of OHC leads to the change of the basilar membrane vibration. In summary, the increased OHC receptor shortens the OHC (thick) and moves up the basilar membrane (BM) while the decreased OHC receptor elongates (thin) the cell and moves down the BM.4) This motility of the OHC is unique to only mammals. Therefore, in mammals, the OHC motility is necessary for cochlear amplification. Fig. 1 show the feedback loop which is involved with cochlear amplification in terms of the mechano-electrical transduction, electromotility, and efferent feedback from the brain.17)

Motility and Unique Structure of OHC

The change of OHC length in response to electrical stimulation was first observed by Brownell, et al.8) who reported that depolarization by current leads to the OHC contraction and hyperpolarization by current leads to the OHC elongation. The change of the OHC length produced by electrical stimulation has been termed electromotility. No other cell type in the mammalian cochlea displays electromotility. Therefore, electromotility is an only characteristic displayed exclusively by mammalian OHCs. The basic mechanisms of the OHC electomotility have been sought in terms of the OHC forces and the OHC stiffness because the axial stiffness of the OHC is itself voltage dependent.18)The OHC electromotility originates within the lateral wall of the OHC.19,20) The anatomic structure of the OHC is essential for the motility. The OHCs are very sensitive to the osmotic strength of the external solution because the OHCs swell in response to the hypo-osmotic solution while they shrink in response to the hyper-osmotic solution.21,22,23,24) Because of the cylindrical structure, swelling leads to the OHC contraction while volume shrinking leads to the cell elongation. Therefore, the change of osmolality produces changes in turgor pressure of the OHC.
The struct...

다국어 초록 (Multilingual 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.

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