Otoacoustic emissions (OAEs) are considered to originate from active cochlear processes involving the outer hair cells (OHC). These emissions are suppressed by activity in the efferent olivocochlear bundle (OCB) and following OHC damage caused by noise exposure or ototoxic drugs. Temporary enhancement of OAEs may occur following noise exposure, and permanent enhancement of emissions has been associated with primary afferent dysfunction in the auditory system. This suggests that there are active adaptation processes in the cochlea exist that could potentially compensate for loss of afferent input. We have used the anti-cancer drug carboplatin to induce selective inner hair cell (IHC) lesions in the cochleae of chinchilla and measured the elevation of auditory thresholds that occurred using brainstem responses (ABR). Following carboplatin treatment click evoked otoacoustic emissions (CEOAEs) were amplified from cochlear frequency regions, which demonstrated extensive IHC damage but apparently normal OHCs. These results support the theory that OHCs cells are involved in the production of these cochlear emissions but also provides further evidence that active adaptation processes exist in the cochlea. It is postulated that loss of afferent input reduces the activity in the medial efferent OCB resulting in de-suppression of OHC contractility. Enhanced OHC contractility could then produce amplification of CEOAEs.