Hearing research
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The outer hair cells (OHCs) are thought to be the dominant source of distortion product otoacoustic emissions (DPOAEs) in the mammalian cochlea; however, little is known about the quantitative relationship between reduction in DPOAE amplitude and the degree of inner hair cell (IHC) and OHC loss. To examine this relationship, we measured the DPOAE input/output functions in the chinchilla before and after destroying the IHCs and/or OHCs with carboplatin. Low-to-moderate doses (38-150 mg/kg, i.p.) of carboplatin selectively destroyed some or all of the IHCs along the entire length of the cochlea while sparing the OHCs. ⋯ DPOAE amplitude at 9.6 kHz decreased at the rate of 4.1 dB for every 10% loss of OHCs. At 7.2 and 4.8 kHz, DPOAE amplitude decreased 3.1 dB and 2.4 dB per 10% OHC loss, respectively. These results indicate that OHCs are the dominant source of DPOAEs.
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We have previously shown that acute electrical stimulation of the auditory nerve using charge-balanced biphasic current pulses presented continuously can lead to a prolonged decrement in auditory nerve excitability (Tykocinski et al., Hear. Res. 88 (1995), 124-142). This work also demonstrated a reduction in electrically evoked auditory brainstem response (EABR) amplitude decrement when using an otherwise equivalent pulse train with a 50% duty cycle. ⋯ These differences in the extent of the recovery between the continuous waveform and both the 50% duty cycle and AM waveforms were statistically significant for both 400 and 1000 pulses/s stimuli. Consistent with our previous results, the stimulus changes observed using AM pulse trains were rate dependent, with higher rate stimuli evoking more extensive stimulus-induced changes. The present findings show that while stimulus-induced reductions in neural excitability are dependent on the extent of stimulus-induced neuronal activity, the use of an AM stimulus paradigm further reduces post-stimulus neural fatigue.
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Neural activity plays an important role in the development and maintenance of sensory pathways. However, while there is considerable experience using cochlear implants in both congenitally deaf adults and children, little is known of the effects of a hearing loss on the development of the auditory cortex. In the present study, cortical evoked potentials, field potentials, and multi- and single-unit activity evoked by electrical stimulation of the auditory nerve were used to study the functional organisation of the auditory cortex in the adult congenitally deaf white cat. ⋯ Even at saturation intensities the degree of synchronisation was less than observed when recording from auditory brainstem nuclei. Taken together, in these auditory deprived animals basic response properties of the auditory cortex of the congenitally deaf white cat appear similar to those reported in normal hearing animals in response to electrical stimulation of the auditory nerve. In addition, it seems that the auditory cortex retains at least some rudimentary level of cochleotopic organisation.