The cochlear amplifier is a positive feedback mechanism within the cochlea that provides acute sensitivity in the mammalian auditory system.
[1] The main component of the cochlear amplifier is the outer hair cell (OHC) which increases the amplitude and frequency selectivity of sound vibrations using electromechanical feedback.
[5] This was around the time when Georg von Békésy was publishing articles observing the propagation of passive travelling waves in the dead cochlea.
The first modeling effort to define the cochlear amplifier was a simple augmentation of Georg von Békésy's passive traveling wave with an active component.
[7] The existence of otoacoustic emissions is interpreted as implying backward as well as forward traveling waves generated in the cochlea, as proposed by Shera and Guinan.
Recent experiments[9] show that emissions from the ear occur with such a fast response that the slowly propagating active traveling waves can not explain them.
Active compression waves were proposed as early as 1980 by Wilson[10] due to older experimental data.
[12] In the mammalian cochlea, wave amplification occurs via the outer hair cells of the organ of Corti.
The somatic motor is the OHC cell body and its ability to elongate or contract longitudinally due to changes in membrane potential.
[13] Because the cell body is not in direct contact with any structure and is surrounded by the fluid-like perilymph, the OHC is considered dynamic and able to support electromotility.
Contrary to previous research, prestin has also been shown to transport anions; the exact role of anion-transport in the somatic motor is still under investigation.
Upon BM deflection downwards hyperpolarization of the OHC results, and intracellular chloride ions bind allosterically causing prestin expansion.
A nonlinear capacitance (NLC) results which leads to a voltage-induced mechanical displacement of prestin into an elongated or contracted state as described above.
Positive deflection of the tip links stretches them in the direction of the tallest stereocilia, causing MET channel opening.
Channel closure ceases the transduction current and increases the tension in the tip links, forcing them back in the negative direction of the stimulus.
The entering current first increases and then quickly decreases due to myosin's release of tension of the tip link and subsequent closing of channels.
Experiments have shown that in reduced extracellular calcium, the myosin motor tightens, resulting in more open channels.