Onset and offset responses from inferior colliculus and auditory cortex to paired noisebursts: inner hair cell loss.

Thirteen adult chinchillas were anesthetized with ketamine/acepromazine and tungsten electrodes were placed in the right inferior colliculus (IC) and auditory cortex (AC). A reference electrode was implanted in the anterior cranium. Following a recovery period, AC and IC responses to left ear stimulation were obtained from unanesthetized animals resting in a passive restraint inside a sound-attenuating booth. After the first recording, the animals were injected with carboplatin (75 mg/kg). Four to five weeks later, a second recording was made. Stimuli were 50 ms duration (0 ms rise and fall time), 80 dB SPL noiseburst pairs. In one group of seven animals, the gap time varied from 1 to 64 ms. In a second group of six animals, the gap time ranged from 0.25 to 64 ms in order to determine gap threshold. The responses were amplified (10000x) and filtered from 10 to 3000 Hz. Each response was the average of 100 stimulus presentations. The dependent variables were the latency of the initial positive peak and the amplitude of the response from initial positive peak to the following negativity. Following the second recording, all animals were sacrificed, the cochleas harvested, and cochleograms were obtained by counting outer hair cells (OHCs) and inner hair cells (IHCs). For the onset response to the second noiseburst of each pair, response amplitudes decreased and latencies increased with decreasing gap time. For a 64 ms gap time, the IC response approached the latencies and amplitudes seen for the onset response to the single noiseburst or first noiseburst in the pair (herein called "baseline" values), while the AC response latency approached baseline values, but AC amplitude did not. Interestingly, the offset responses to the first noiseburst were not present at gaps of less than 8 ms, while the onset responses to the second noiseburst were typically present at gaps of 1-2 ms. Cochleograms revealed a normal (or near-normal) complement of OHCs, and IHC loss averaging roughly 30-40% in apical regions and increasing to 60-70% in more basal regions (compared to normative data). Following carboplatin, the latencies of IC onset responses were delayed by several tenths of a millisecond, with the greatest pre- versus post-carboplatin latency shift occurring at short noiseburst gaps. AC response latencies were largely unaffected by carboplatin. IC onset response amplitudes were reduced following carboplatin, while AC onset responses were similar to pre-carboplatin values. IC offset response latencies to the first noiseburst were increased post-carboplatin, while AC offset response latencies varied little from pre-carboplatin values. IC and AC offset response amplitudes to the first noiseburst were decreased post-carboplatin.