Previous experiments suggested the possibility of a short-term sound stimulus-evoked and transient increase in DPOAE amplitudes. This phenomenon is possibly due to the complexity of the outer hair cells and their efferent control system and the different time scales of regulatory processes. A total of 100 healthy subjects ranging from 18 to 40 years of age with normal hearing and normal DPOAE values in the range of 781–4000？Hz were recruited in the study. Diagnostic DPOAE measurements were performed after short-term sound exposure. We proposed a 10？sec, 50？dB sound impulse as the most effective stimulus for clinical practice between 40 and 60？sec poststimulus time to detect the aforementioned transient DPOAE increase. We developed a procedure for detection of this transient increase in DPOAE by the application of a short-term sound exposure. The phenomenon was consistent and well detectable. Based on our findings, a new aspect of cochlear adaptation can be established that might be introduced as a routine clinical diagnostic tool. A mathematical model was provided that summarizes various factors that determine electromotility of OHCs and serves as a possible clinical application using this phenomenon for the prediction of individual noise susceptibility. 1. Introduction The outer hair cells play a crucial role in the mammalian cochlea. These cells are part of a complex system that is necessary to detect low intensity sounds as well as to provide a self-defense against high intensity sounds [1]. In the mammalian cochlea, there is a complex mechanism, also known as cochlear amplification that provides the capability of detecting sounds of threshold intensity. Otoacoustic emission is also the result of active outer hair cell (OHC) motility, also known as electromotility [2–4]. Beyond the fast motility of OHCs (electromotility), these cells also exhibit an additional slow change in cell shape (slow motility). Slow motility is presented by cell shortening, which is assumed to play a protective role against loud sounds [5–9]. The slow motility of OHCs can modify the axial and lateral wall stiffness of cells decreasing the magnitude of their electromotile responses [7–9]. The slow motility of OHCs and the resultant cell stiffness changes can be considered as an intrinsic regulatory mechanism of OHCs. This mechanism is mechanically evoked, and it is independent from electromotility but depends on the presence and concentration of [Ca2+]i and is also linked to the metabolic modification of cytoskeletal structure [7–10]. Furthermore, the axial and lateral wall
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