Non-linear aspects of outer hair cell transduction and the temporary threshold shifts after acoustic trauma.

The 200-Hz cochlear microphonic potential (CM) and the compound action potential (CAP) of the auditory nerve evoked by tone-bursts were recorded in the basal turn of the cochlea of anaesthetised guinea pigs, before and after exposure to traumatic high-frequency tones that produce a temporary threshold shift (TTS) in this cochlear region. The drop in CM and the TTS were highly correlated, suggesting that it is the disruption of the outer hair cells generating the CM that causes the TTS. The previously measured rise in endocochlear potential and drop in organ of Corti K+ levels suggest that the TTS is due to a temporary closure of outer hair cell mechanoelectrical transduction (MET) channels, which produces a drop in the mechanical sensitivity of the organ of Corti, due to disruption of the active process provided by outer hair cells. The time course of the onset and recovery of TTS is consistent with a kinetic folding and refolding of MET channels over a time course of hours and days. Mathematical modelling of this putative channel folding suggests that TTS recovery may be accelerated by the presentation of additional sounds during the recovery period. We present electrophysiological data (CM and CAP measurements) showing that this accelerated recovery occurs. Using two-tone complexes (phase-locked 5- and 10-kHz traumatic tones, and 10-kHz traumatic tones with 25-Hz bias tones), we also show that the mechanisms producing TTS are non-linear and asymmetric, and that the greatest 'trauma' occurs when the hair bundles of outer hair cells are deflected away from the basal body of these cells (i.e. in the direction normally causing hyperpolarisation of the cell membrane potential).