Mammalian spontaneous otoacoustic emissions are amplitude-stabilized cochlear standing waves.
Mammalian spontaneous otoacoustic emissions (SOAEs) have been suggested to arise by three different mechanisms. The local-oscillator model, dating back to the work of Thomas Gold, supposes that SOAEs arise through the local, autonomous oscillation of some cellular constituent of the organ of Corti (e.g., the "active process" underlying the cochlear amplifier). Two other models, by contrast, both suppose that SOAEs are a global collective phenomenon--cochlear standing waves created by multiple internal reflection--but differ on the nature of the proposed power source: Whereas the "passive" standing-wave model supposes that SOAEs are biological noise, passively amplified by cochlear standing-wave resonances acting as narrow-band nonlinear filters, the "active" standing-wave model supposes that standing-wave amplitudes are actively maintained by coherent wave amplification within the cochlea. Quantitative tests of key predictions that distinguish the local-oscillator and global standing-wave models are presented and shown to support the global standing-wave model. In addition to predicting the existence of multiple emissions with a characteristic minimum frequency spacing, the global standing-wave model accurately predicts the mean value of this spacing, its standard deviation, and its power-law dependence on SOAE frequency. Furthermore, the global standing-wave model accounts for the magnitude, sign, and frequency dependence of changes in SOAE frequency that result from modulations in middle-ear stiffness. Although some of these SOAE characteristics may be replicable through artful ad hoc adjustment of local-oscillator models, they all arise quite naturally in the standing-wave framework. Finally, the statistics of SOAE time waveforms demonstrate that SOAEs are coherent, amplitude-stabilized signals, as predicted by the active standing-wave model. Taken together, the results imply that SOAEs are amplitude-stabilized standing waves produced by the cochlea acting as a biological, hydromechanical analog of a laser oscillator. Contrary to recent claims, spontaneous emission of sound from the ear does not require the autonomous mechanical oscillation of its cellular constituents.
Shera
Christopher A
CA
Eaton-Peabody Laboratory of Auditory Physiology, Massachusetts Eye and Ear Infirmary, 243 Charles Street, Boston, Massachusetts 02114, USA. shera@epl.meei.harvard.edu
D000818:Animals; D003051:Cochlea / Q000502:physiology*; D006801:Humans; D008322:Mammals; D015233:Models, Statistical; D017711:Nonlinear Dynamics; D017084:Otoacoustic Emissions, Spontaneous / Q000502:physiology*; D011336:Probability; D013018:Sound Spectrography