Carboplatin, a second-generation antineoplastic drug, is much less ototoxic than cisplatin in humans and many laboratory animals. However, when a moderate dose of carboplatin is administered to chinchillas, it can selectively destroy inner hair cells (IHCs) and type-I ganglion neurons without damaging the outer hair cells (OHCs). One of the earliest signs of injury from carboplatin is damage to type I, spiral ganglion neurons. Selective destruction of IHCs has no effect on the cochlear microphonic (CM) potential and distortion product otoacoustic emissions (DPOAEs). However, very high doses of carboplatin can destroy both OHCs and IHCs resulting in a decline in CM and DPOAE amplitude. In cases where carboplatin partially destroys the IHCs, the auditory nerve fibers that contact the residual IHCs have normal thresholds and tuning, but their spontaneous and driven discharge rates are reduced. These results suggest that OHCs are responsible for the sharp tuning and exquisite sensitivity of the cochlea. IHC loss leads to a reduction in neural input (i.e., sensory deprivation) to the central auditory system. Surprisingly, although the neural input to the central auditory system is reduced, evoked response amplitudes recorded from the auditory cortex are often enhanced. These results indicate that when the neural input to the central auditory brain is reduced, the central auditory system compensates for the reduced input by increasing its gain.