Prestin and Motility of the Cochlear Outer Hair Cell

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.

The effects of bFGF on the calicum influx in OHCs / 中国药理学通报

AIM To examined the effect of bFGF on the calcium influx in outer hair cells (OHCs) and its antagonistical effects with streptomycin. The aim of the study is to explore the mechanism of acute ototoxicity of streptomycin and antagonism of bFGF. METHODSE The OHCs of guinea pig were isolated using an enzyme machine methods and loaded with 10 ?mol?L -1 Fluo 3/AM for 30 min at 37℃,then cultured 60 min at room temperature. Individual Fluo 3 loaded OHCs were examined with a confocal microscope (ACAS Ultima, USA) using a 20? objective lens and linear scan mean. The fluorescent images, collected every 5 sec for 300 s, were stored in a computer. The fluorescent intensity of the images were analyzed by the software cooperated with the confocal microscope, and a function curve showing the change trend of fluorescent intensity with time was obtained. RESULTS The OHCs [Ca 2+ ] i hold steady within the process of normal extracellular liquid perfusion. OHCs [Ca 2+ ] i increased when perfused 100 mmol?L -1 high potassium media(10/11) and normal media containing 1 nmol?L -1 bFGF(9/9), but the OHCs [Ca 2+ ] i don't changes in high potassium free calcium media(7/7) and free calcium media containing 1 nmol?L -1 bFGF(8/8). After treated by 1 mmol?L -1 streptomycin, the OHCs [Ca 2+ ] i increased 0/12, 4/8 respectively when perfused high potassium media and bFGF media. And after treated by 1 nmol?L -1 bFGF, high potassium media make OHCs [Ca 2+ ] i increased more obviously and keeping longer time. After treated by 1 mmol?L -1 streptomycin, respectively, 0 1,1 and 10 nmol?L -1 bFGF make 4/11,6/9 and 12/12 OHCs [Ca 2+ ] i increasing when perfused high potassium media. CONCLUSION High potassium media and bFGF perfusion can result in increasing of OHCs [Ca 2+ ] i ,and OHCs [Ca 2+ ] i increase rooted in the calicum influx, there is synergic effects between high potassium and bFGF. The streptomycin can block the process of calcium influx induced by high potassium media and the block effects can be antagonized by bFGF, and the antagonistical effects have bFGF concentration dependence.