The effects of click level, click rate, and level of background masking noise on the inferior colliculus potential (ICP) in the normal and carboplatin-treated chinchilla.

Carboplatin produces a selective loss of inner hair cells in chinchilla, substantially reducing the amplitude of the compound action potential. A key question that arises from these experiments is: What effect does a reduction in IHC-eighth-nerve fiber input have on the central auditory nervous system? This investigation evaluated the inferior colliculus potential (ICP) in chinchillas treated with carboplatin. The left ear was surgically destroyed and a recording electrode was placed in the left inferior colliculus. Following thirteen days of recovery time, the ICP was recorded in the awake animal. Click level was varied from 10-20 to 80 dB pSPL. Click rate was varied from 10 to 1000 Hz using both conventional averaging and a cross-correlation procedure. Broadband masking noise was varied from 30 to 70 dB SPL with click level held constant at 80 dB pSPL. The dependent variables were the positive peak latency and peak-to-following trough amplitude of the evoked potential. Following baseline studies, the animals were administered carboplatin (50 mg/kg IP) and retested two weeks later. Prior to carboplatin administration, there was an increase in ICP latency and a decrease in ICP amplitude with decreasing stimulus level, increasing rate and increasing noise level. Mean ICP threshold was 30 dB pSPL. Following carboplatin administration, there was little change in threshold or peak latencies. In contrast, the amplitude of the ICP was reduced on average by one-third, although this effect varied considerably across animals. The magnitude of this amplitude decrement was not strongly dependent on click level, click rate, or the level of background noise.

Incomplete recovery of chicken distortion product otoacoustic emissions following acoustic overstimulation.

Distortion product otoacoustic emissions (DPOAEs) were measured in chickens before and after exposure to a 525-Hz pure tone (120 dB SPL, 48 h). The exposure caused extensive hair cell loss and destroyed the tectorial membrane along the abneural edge of the basilar papilla in the low-to-mid-frequency region of the cochlea. Although the lesion was restricted, DPOAEs were greatly depressed at all frequencies immediately after the exposure. The high-frequency DPOAEs gradually recovered to preexposure values after the exposure; however, there was little or no improvement in DPOAEs at test frequencies equal to or slightly above the exposure frequency even after 16 weeks of recovery. By 28 days of recovery, the previously damaged region of the basilar papilla had been repopulated by hair cells and the lower honeycomb layer of the tectorial membrane had regenerated, but not the upper fibrous layer. The upper fibrous layer of the tectorial membrane was still missing after 16 weeks of recovery and the region of damage corresponded closely to the frequency regions where the DPOAEs were depressed.