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The cochlear amplifier was first proposed in 1948 by T. Gold[1]. This was around the time when Georg von Békésy was publishing articles observing the propogation of passive travelling waves in the dead Cochlea.

Thirty years later the first recordings of emissions from the ear were captured by D.T. Kemp[2]. This was confirmation that such an active mechanism was present in the ear. These emissions are now termed otoacoustic emissions and are produced by what we call the Cochlear amplifier.

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. In such a model, a lop sided pressure about the Organ of Corti is hypothesized which actively adds to the passive traveling wave to form the active traveling wave. Perhaps the most popular example of this model was defined by Neely, S.T. and Kim, D.O.[3]. The definition of the active traveling waves require forward and backward traveling waves to be generated in the Cochlea, as proposed by Shera, C.A. and Guinan, J.J.[4].

Contention still surrounds the existence of the active traveling wave. Recent experiments conducted by T. Ren[5] show that emissions from the ear occur with such a fast response that the slowly propagating active traveling waves can not exist. The only explanation for fast emission propagation is the dual of the active traveling wave, the active compression wave. Active compression waves were proposed as early as 1980 by P.J. Wilson[6] due to older experimental data. However were widely disregarded by the research community until stronger experimental proof confirming these early experiments against the active traveling wave were produced.

Thirty years after Kemp's experimental proof of the existence of Gold's Cochlear amplifier and sixty years after the proposal of Gold's Cochlear amplifier, the active compression wave Cochlear amplifier was defined by M.R. Flax and W.H. Holmes[7][8]. In this model the active pressure is equal on both sides of the Organ of Corti and this produces very fast propagating pressure waves which generate extra activity within the Cochlea and emissions through the middle/outer ear.

Other explanations for the active processes in the inner ear exist[9][10][11] however these explanations are not as popular and old as the active traveling wave and active compression wave Cochlear amplifier models.


  1. Gold 1948 : Hearing. II. The Physical Basis of the Action of the Cochlea
  2. Kemp 1978 : Stimulated acoustic emissions from within the human auditory system
  3. Neely and Kim 1986 : A model for active elements in cochlear biomechanics
  4. Shera 1999 : Evoked otoacoustic emissions arise by two fundamentally different mechanisms: A taxonomy for mammalian OAEs
  5. Ren 2006 : Group Delay of Acoustic Emissions in the Ear
  6. Evidence for a cochlear origin for acoustic re-emissions, threshold fine-structure and tonal tinnitus
  7. Flax 2008 : PhD - The active compression wave cochlear amplifier
  8. Flax and Holmes 2008 : Introducing the compression wave cochlear amplifier
  9. Bell 2004 : The cochlear amplifier as a standing wave: "Squirting" waves between rows of outer hair cells{?}
  10. Braun 1994 : Tuned hair cells for hearing, but tuned basilar membrane for overload protection: evidence from dolphins, bats, and desert rodents
  11. other references to proposed active processes not included here.
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