Knowledge Bank

There is a growing body of evidence suggesting that cochlear de-afferentation can occur without accompanying outer hair cell (OHC) loss after noise exposure. Due to the high incidence of noise exposure in the United States, there is a need to develop assessments that can identify and monitor this de-afferentation in noise-exposed listeners. The current study was undertaken to investigate changes in the components of electrocochleography (EcochG) in the Fischer F344/NHsd rat in order to assess long-term cochlear deafferentation from hazardous noise. Changes in the action potential (AP) and cochlear microphonic (CM) input-output (I/O) functions were measured after noise exposure. The CM/AP ratio was examined to account for between-test differences since electrode differences and OHC damage would impact each component. Noise-induced cochlear de-afferentation was predicted to result in reduction of AP amplitude without change in the CM amplitude, thus resulting in elevation of the CM/AP ratio. Fischer 344/NHsd rats were exposed to a narrowband noise to induce permanent (PTS) or temporary threshold shifts (TTS). After exposure, the AP and CM I/O functions were measured once every 4 weeks for 24 weeks in order to assess long term cochlear de-afferentation. Results showed that the AP I/O function was depressed at all levels in ears with PTS. The CM/AP ratios revealed depression of the AP at weeks 8-24, indicating possible cochlear de-afferentation. In ears that experienced TTS, a recruitment-like effect was seen in the iii AP I/O function at 4 weeks, indicating OHC pathology. Subsequent AP decreases were seen over the 4-24 week testing period, indicating cochlear de-afferentation. This was also seen in the CM/AP ratio, which increased over time due to reduction in AP amplitudes. The I/O functions obtained from ears that had experienced TTS or PTS displayed patterns consistent with long-term cochlear de-afferentation. The findings indicate that components of EcochG are sensitive to possible de-afferentation of the cochlea after noise-exposure.